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In Evolutionar Biology, Epigenetics has become part of the explanations for changes in the phenotype across generations. But can these changes directed to specific phenotypic traits along many generations be converted into DNA mutations?
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Epigenetic changes via expression of appropriate long non coding RNAs serve advantageous answers to harmful inner and outer environmental stimuli as a quick means of adaptation. When the danger of DNA stability is high along many generations, the defensive epigenetic changes may be converted into DNA mutations. In extreme danger of DNA derangement quick (defensive) mutations may occur even in tumor cells exposed to endocrine disruptors (Suba Z. 2017, Suba Z. 2018, Suba Z. 2020).
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Kindly discuss your ideas and viewpoints on the origin of life and the RNA world hypothesis.
What are the contradictory views on why researchers are still unsure about the origin of life through RNA or such analogous molecular intermediate pre-cursors preceding its existence?
"The general notion of an “RNA World” is that, in the early development of life on the Earth, genetic continuity was assured by the replication of RNA and genetically encoded proteins were not involved as catalysts. There is now strong evidence indicating that an RNA World did indeed exist before DNA- and protein-based life. However, arguments regarding whether life on Earth began with RNA are more tenuous. It might be imagined that all of the components of RNA were available in some prebiotic pool and that these components assembled into replicating, evolving polynucleotides without the prior existence of any evolved macromolecules. A thorough consideration of this “RNA-first” view of the origin of life must reconcile concerns regarding the intractable mixtures that are obtained in experiments designed to simulate the chemistry of the primitive Earth. Perhaps these concerns will eventually be resolved, and recent experimental findings provide some reason for optimism. However, the problem of the origin of the RNA World is far from being solved, and it is fruitful to consider the alternative possibility that RNA was preceded by some other replicating, evolving molecule, just as DNA and proteins were preceded by RNA." - Robertson and Joyce
[This is as per the explanation by Michael P Robertson and Gerald F Joyce in the article: "The origins of the RNA world." published in the Cold Spring Harb. Perspect. Biol. 4, a003608 (2012).]
The scientific community must resolve this contradicting conjecture through rational discussion and debate backed by strong experimental evidence on what must be the pre-cursor molecule to the Origin of Life if it is not RNA!
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One of the issues that is holding the concept of an RNA world back from being more scientifically useful - irrespective of whether there ever was such a thing - is that we don't use the idea in the scientific way it was intended. Just like any other prebiotic scenario, it is not (nor has it ever been) a scientific hypothesis. In fact, scenarios are usually not intended as such. Scenario authors from all niches (including RNA world) have pointed out that scenarios themselves are untestable. However, they guide thinking and allow to conceive of hypotheses that are testable. If we go through the old literature we find very explicit passages to support this fact.
For the specific authors advanced in the question, G.F. Joyce and L.E. Orgel, we have a passage from 1999 in "prospects for understanding the origins of the RNA world". (The RNA World 2nd ed. 49-77).
"The presumed RNA World should be viewed as a milestone, a plateau in the early history of life on earth. So too, the concept of an RNA World has been a milestone in the scientific study of life's origins. Although this concept does not explain how life originated, it has helped to guide scientific thinking and has served to focus experimental efforts."
You can find this point of view expressed in foundational work for all niches related to the popular scenarios today. But you can also find it for scenarios most people in origins have never heard of. E.g. the idea that celllular life started with terpenoids found in G. Ourisson and Y. Nakatomi's "the terpenoid theory of the origin of cellular life: the evolution of terpenoids to cholesterol. (1994) Chem & Biol. 1 11-23".
"The hypothesis provides an attractive way of ordering the terpenoids: like all evolutionary theories, it cannot be tested directly. The ideas summarized here do, however, suggest a multitude of experiments having some bearing on the fundamental and fascinating question: how did the first cells appear? We hope to carry out some of them."
A related line of thought - but highly influential - is the exposition by Harold J. Morowitz from 1992 in his book "Beginnings of Cellular Life: Metabolism Recapitulates Biogenesis". If we go to the conclusion, we find this explicit clarification on the distinction between a genuine scientific theory and a scenario:
"at this stage of the thought process, it is important to focus on the hypothesis that intermediary metabolism recapitulates prebiotic chemical evolution. This hypothesis is not a strictly vulnerable theory in the Popperian sense, but it does provide us with a valuable heuristic method for using modern knowledge of biochemistry to search for events that have left their trace. If the intermediary metabolism of autotrophs does not recapitulate biogenesis, then the discontinuities will have to be explained."
More than 2 decades back, many authors made a clear distinction regarding this nuance. Scenarios are here to help: they guide thinking and design experiments. They only guide thinking in a scientifically meaningful direction as long as we can easily abondon scenarios and enthusiastically continue replacing them with new, more informed scenarios. A situation where a scenario gets entrenched and where researchers treat it as a scientific hypothesis is - by construction - hard to escape.
In fact, this is exactly the situation that many researchers have described around the 80s, when criticism mounted against the prebiotic broth scenario. The passage from Wächtershäuser's 1988 "Theory of a Surface Metabolism" is telling:
"The prebiotic broth theory has received devastating criticism for being logically paradoxical (11, 135), incompatible with thermodynamics (11, 144, 160), chemically and geochemically implausible (134, 136, 144), discontinuous with biology and biochemistry (160), and experimentally refuted (135, 160). The reason for the tenacity with which it is retained as accepted dogma has been forcefully and clearly stated by Scherer (126): "If this rejection is substantiated, there will remain no scientifically valid model of the selforganization of the first living cells on earth."
Clearly, the broth scenario had overstayed its welcome. One reason for this is that its 'claims' (which for a scenario can only be speculations) were too much in contradiction with claims from fields of science that do not suffer the same restrictions when it comes to testing and refuting their theories. One example of a very controversial idea that can be found in Haldane's formulation of a broth scenario, is the purported necessity of a long, highly functional protein randomly emerging from a soup, as an extremely rare event: we expect this to be prohibitively unlikely and hence a far from parsimonious explanation.
Quite a few of the critiques voiced against the prebiotic broth scenario are equally valid critiques of some scenarios we have today, including RNA world.
The RNA world is an old and multifaceted concept. There are contrasting formulations that make different claims (to be interpreted as speculations) about history. As with the prebiotic broth scenario (and any scenario), it has raised genuine scientific objections. These have remained largely unadressed, in spite of its long dominance.
It is instructive to bear in mind that scenarios don't come from nowhere. They're fairly detailed speculations about purported historical events. To make them, each author makes assumptions. Some of these concern speculations that later became testable, e.g. about chemistry and physics. You will find different scenario authors make different assumptions and different arguments (and flaws therein). There's an inevitable bias here with respect to the fields an author is trained in. Some of the foundational assumptions in popular scenarios like RNA world are at least 50 years old, but some unchallenged assumptions date back to a literature that is more than a century old. A time before IUPAC, modern quantum mechanics, genetics, and so forth.
That has been enough time to forget that scenarios like RNA world are by construction not testable hypotheses and that they were not intended as such. Scenarios are here to guide thinking, to inspire experiments. The best thing a scenario can do for us, is generate insights that spur us to change the way we think and thereby necessitate replacing our old scenarios with new ones, and repeat the cycle. The science coming out of the community today is a lot more conducive to doing that than previously.
The same cannot be said for the rather myopic RNA-centric framing of a question in the cited passage, which attempts to elevate RNA world to more than a scenario. Rather than forcing ourselves to think about the rather narrow and outdated proposal by Joyce and Robertson, ("consider the alternative possibility that RNA was preceded by some other replicating, evolving molecule"), it is more productive to critically revisit all the things that have been assumed and argued when the concept of an RNA world was conceived and how which of these premises are considered valid or plausible today, and which ones back then. Is there a formulation of RNA world for abiogenesis that is logically sufficient? And if so is it logically necessary that abiogenesis proceeded this way?
It is also instructive to check how much of the logic was sound. e.g. the rhetorical tricks employed in RNA world introduce all sorts of hidden assumptionsm.
As an example of the latter: some still justify an RNA world by the party trick 'chicken-and-egg' question 'protein or RNA, which came first?', only to conclude with 'RNA, it encodes proteins' and hastily conclude with an even stronger 'RNA-first' for abiogenesis. 'chicken-and-egg' fallacies are nothing new in origins. In fact, they were already identified as such long ago. E.g. in chapter 8 of "Seven Clues to the Origin of Life (1985)" by Cairns-Smith, there's an illustrated passage detailing that these types of paradoxes in origins frame the question in a manner that prevent us from considering scaffolds.
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The fact is that even the so-called simple organisms such as E. coli are very complex enterprises with all sorts of things going on together. There is plenty of scope for accidental discoveries of effective new combinations of subsystems. It seems inevitable that every so often an older way of doing things will be displaced by a newer way that depends on a new set of subsystems. It is then that seemingly paradoxical collaborations may come about.
To see how, consider this very simplified model - an arch of stones: This might seem to be a paradoxical structure if you had been told that it arose from a succession of small modifications, that it had been built one stone at a time.
scaffolds that starts like this:
This might seem to be a paradoxical structure if you had been told that it arose from a succession of small modifications, that it had been built one stone at a time. How can you build any kind of arch gradually? The answer is with a supporting scaffolding. In this case you might have used a scaffolding of stones. First you would build a wall, one stone at a time:
Then you would remove stones to leave the 'paradoxical' structure.
"
It should be noted that in 2022, even in RNA-world, very few scholars remain that find RNA-first a convincing idea. As a scenario, however, it is not useless: it is instructive to consider what the underlying ideas are that at some point in time made such a highly specific idea compelling to so many of us.
A fixed motif in scenario papers is to start explicitly and implicitly assuming a few things about what chemistry can and cannot do and some properties of abiogenesis. These sort of assumptions used to be spelled out routinely, also outside scenario papers. Let me give two examples.
The original 1953 paper for the "Frank Model" "on spontaneous asymmetric synthesis", has the passages
".. the defining property of a living entity the ability to reproduce its own kind ...
confining attention to chemical molecules, the complexity of any having this essential property of life is likely to be great enough to make it highly improbable that it has a centre of symmetry."
(*I should point out that Frank makes an important error here: the capacity for molecular reproduction is not a molecular property but a property of a reaction network. If we add an additional thermodynamic criterion this property is autocatalysis and we can then check this claim from the IUPAC definition: https://goldbook.iupac.org/terms/view/C00876. It turns out there are trivial ways to make small networks that have this property https://chemrxiv.org/engage/api-gateway/chemrxiv/assets/orp/resource/item/60c74d67469df42226f44295/original/emergent-autocat-animation.gif.)
The point to retain here is that Frank considers it to be generally accepted that one can assume this property to be prohibitively rare in chemistry. This belief was wideheld, and we can e.g. read in "the units of selection" (1970) by Lewontin a summary on scientific views on abiogenesis
"The present view ... Since there was no autocatalysis, there was no reproduction or heredity and so no possibility of natural selection."
The coacervates in Oparins scenario were notably invoked to adress this issue.
When it comes to assumptions in scenarios, this systematically involved conjecturing that chemistry 'in the wild' intrinsically and deterministically becomes a 'mess', undergoing no meaningful complexification, and for which no reproduction and evolution can reasonably be expected. From there, it appears that no process of abiogenesis should conceivably occur naturally, and thereafter some specific sequence of exceptional events is proposed as plausible, because it appears to be the sole contender.
Let us make more explicit why this is not an innocent procedure:
We still find our understanding of 'basic chemistry' to be plagued with limitations and long-lived misinterpretations (e.g. 2 days ago we learned that methyl substitution destabilizes radicals instead of the textbook knowledge that it stabilizes them ).
Moving beyond the basics, we by and large lack a lot of formal theory, experiment, or even a simple reference frame for the things that happen then. Joyce and Robertson honor the tradition of purporting from the outset that 'chemistry in the wild' becomes an intractable mess. The issue is that we don't know at all if that's the case. We cannot assume this from the outset, we need to extensively study it. We require extensive experiments and theory and a reference frame for all the phenomenology associatied with complex systems (e.g. multiple components, compartments, multiple forms of nonequilibrium driving, length scales, time scales).
In making the routine assumption of 'messy, intractable chemistry that can neither complexify nor multiply', we have decided in advance that, once we finally understand 'chemistry in the wild' with its 'so-called intractible mixtures', it cannot have any bearing on abiogenesis. Let alone explain it.
That is a disproportionately bold conjecture about fundamental science, and a very consequential one: all historical scenarios - RNA world being one out of many - have been justified by formulating conjectures of this sort (many authors also insist on other properties, e.g. chemistry being deterministic). Clearly, it should be the first priority of everyone in the field to test this conjecture, by extensively and rigorously studying complex chemical systems as an end in itself. If the conjecture is correct, it provides an important validation for historical scenario approaches. If the conjecture turn out wrong, we are in a much better position to conceive of more scientifically informed scenarios, but potentially the approach will change entirely.
In presenting it as such, I am making it appear as if it could be an open question whether the chemical conjectures underpinning our scenarios in origins may be true or not. In fact, we have learned quite a few things in the meantime. And some clumsy mistakes were made elsewhere.
- Determinism:
When it comes to chemistry being deterministic (a key tennet of e.g. Sutherlands scenario and Wächtershäusers surface metabolism): upon critical evaluation of what is known of basic chemistry this idea becomes unacceptable, especially when considering the chemical processes on the surface of a planet, as opposed to a quick reaction in pyrex.
1) insofar as it is reproducible, modern chemistry owes much of it to big strides of standardization in glassware, methodology, synthesis protocols (e.g. usage of stirring bars).
2) lab chemistry exhibits many forms of contingency. This is particularly the case when it comes to phase behavior, e.g. habit modification, polymorphism. Aspirin purportedly has 8 reported polymorphs, phenobarbitone 13.
3) glassware is cleaned between reactions, thereby making successive reactions in the same glassware independent. In nature, this property of independence is absent. In fact, effort to make an evolutionary classification of minerals are rooted in the opposite: that certain minerals start to form conditional on the presence of certain others. (https://pubs.geoscienceworld.org/msa/ammin/article/104/6/810/570840/An-evolutionary-system-of-mineralogy-Proposal-for)
- Autocatalysis:
A first issue to get out of the way is the misconception that autocatalysis is prohibitively rare. A prominent PI in origins (RNA world, not a chemist) told me that chemists throughout history have found exactly one example. Claims about the contents of a literature one cannot realistically have read in a lifetime is a common error we can find in the origins literature. Below are some reviews.
I should stress that these reviews discuss examples from a few niches in chemistry. These reviews do at least allow to have 100s of counterexamples to dubious claims about no autocatalysis in chemistry, but it's only a small fraction. Virtually all branches of chemistry have regular reports of autocatalysis, but very few focus on autocatalysis in its own right. And hence most branches do not review their reported examples.
By critically examining the IUPAC definitions, one can show that autocatalysis is dramatially more widespread than long thought. In part, this is because the definition applies to a wealth of situations where the term is not routinely employed. By examinging the requirements of autocatalysis as an emergent network property, one can demonstrate that this property emerges particularly readily in a heterogeneous / multicompartment context. With the disclaimer that I'm an author I refer to the following:
- Messy chemistry:
Refreshing counterexamples are afforded by the literature on systems chemistry and dynamic combinatorial libraries.
In the context of origins, a recent work that is greatly aiding in fixing our misconceptions is : https://www.nature.com/articles/s41557-022-00956-7
Where a reaction of purported immense complexity is found to exhibit highly reproducible and ordered behavior as function of environmental inputs. How chemistry exactly works on this level is still poorly understood. I think I do, but it'll have to await peer review. But we cannot in good scientific conscience take for granted anymore that chemistry becomes messy and intractable. When we do the experiments, we see something very different.
in conclusion, I want to come back to the final point of the question
"The scientific community must resolve this contradicting conjecture through rational discussion and debate backed by strong experimental evidence on what must be the pre-cursor molecule to the Origin of Life if it is not RNA!"
No. The sientific community should strive to do what it can justify scientifically. Those that find it fruitful to relegate the RNA world - which is not a hypothesis - are justified in doing so. Notably because it is is founded on scientifically refuted premises and logical errors.
Those that find ways to make it fruitful to keep it are justified in doing so: it's a scenario, one can draw inspiration from it. Perhaps a thoroughly altered version can be developed that fixes previous issues.
Above all else, RNA is an amazing molecule that has been used for fundamental research that concerns everyone in origins, and will continue to do so irrespective of how serious the RNA world scenario is still taken.
What the origins of life community needs, first and foremost, however, is concern itself with more important matters.
Complex chemistry needs to be studied thoroughly on an experimental and theoretical level.
New scenarios are needed. And these scenarios should no longer require chemistry to have properties it doesn't have, and vice versa. These scenarios should also explicitly be appraciated for what they are, an for what they're not. They're here to help, to guide thinking, inspire experiments, produce testable predictions, update our beliefs. They are not scientific hypotheses in and of themselves.
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The phrase “evolutionary success” sometimes appears in scientific productions. However, the concept seems to be based primarily upon quantitative data. For instance, Rodents are said to be “evolutionarily successful” because about 40% of Mammals are Rodents (about 2000 species out of 5000 Mammal species). In the same view, seed plants are considered “evolutionarily successful” because most modern-day plants produce seeds.
In this perspective, multicellular organisms are sometimes considered as having had little evolutionary success, if not being anecdotal, because they are hugely outnumbered by unicellular prokaryotes. As Gould stated: “We live now in the ‘age of bacteria’”.
Nevertheless, I was wondering whether such a vantage point was not biased. As a matter of fact, why consider that being successful necessarily means being numerous? There are no known animals able to run as fast as cheetahs: does that not make cheetahs evolutionarily successful? In a much more anthropocentric way, no known organism displays such a big brain as ours: does this make us a success of evolution?
Should we prefer qualitative assessments over quantitative ones?
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Success is a subjective term. The use of subjective terms is a problem in science - See discussion "Terms ambiguity in research - Pros and Cons" (https://www.researchgate.net/post/Terms_ambiguity_in_research-Pros_and_Cons).
When you apply the term "success" to something with a long history, like "biological evolution," new problems arise with that subjectivity. A lot would depend on which timeframe you choose. Here is an example. Suppose you have selected the number of descendants' branches counted by the number of species as a criterion of evolutionary success. Then you have to choose the timeframe to which you want to apply this criterion. The winners would be different for different timeframes. If the timescale is when life exists on Earth, the apparent winner is the first common ancestor of all living things. What would happen if you chose one billion years as the timeframe. Then the winner would be different if you apply this timeframe to the beginning of life on Earth or recent times.
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I am searching for good recordings of distress calls emitted by American crocodiles, in particular by hatchlings. The longer the better. If not, also distress call recordings of other crocodilian species are fine.
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Differences in distress: Variance and production of American Crocodile ( Crocodylus acutus ) distress calls in Belize
Visit to that article
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I want to use BEAST to do EBSP analyses with two loci. I open two "input.nex" files in BEAUti to generate a "output.xml" file (In the Trees panel select Extended Bayesian skyline plot for the tree prior), and then run BEAST. I do not know if this is right and I do not know what to do next. I can not construct the trend of demographic history in Tracer just like BSP. I got one log file but two trees files (for each locus), and I do not know how to import both tree files into Tracer.
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One of the best websites to find the answers to these questions is the following link:
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Dear All,
I am struggling with a constant problem with a csv extension while preparing data for MuSSE model analysis: have tried to do a bunch of stuff to fix a problem but no success - always the same thing ("All names must be length 1"). I would very grateful for your help! :)
library(diversitree) dat="MuSSE_hosts.csv" dat<- read.table("MuSSE_hosts.csv", header=TRUE, dec=".", sep=",", row.names=1) mat <- dat[,2:ncol(dat)] lik.0 <- make.musse.multitrait(tree, mat, depth=0) Error in check.states.musse.multitrait(tree, states, strict = strict, : All names must be length 1
Thank you a lot in advance!
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Thank you a lot for your help!
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I am planning on starting grad school in about a year and a half but you can never start researching project advisors too soon!
I am interested in investigating the use of fungal parasites of insects such as Cordyceps in integrated pest management. Unfortunately, this seems to be an unpopular field of study, as so far in my searches I have only seen professors who study plant-insect relationships in IPM, but not fungal-insect relationships in IPM. Ideally, I am hoping to stay on the west coast of the US. My undergraduate background is in ecology and evolutionary biology, but I am currently broadening my skills in molecular lab techniques.
Faculty pages on university websites cannot always represent the scope of a professor's research interests. That said, can anyone recommend a recommend a colleague of theirs who might be looking for graduate students in a year and a half, and with a background in mycology, entomology, and IPM?
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I work with entomopathogens fungus in biological control with avocado, berries and citrus pest. But I'm in Mexico, Universidad de Guadalajara.
In the USA, the Californian Universities has a lot of tradition about thouse topics (Berkley, Riverside, Davis, etc)
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Suppose you discovered a gene from an organism that is unique and cannot fit to any extant and extinct organism in the planet, what does it imply to evolutionary biology? Explain.
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Those genes are called orphan genes (https://en.wikipedia.org/wiki/Orphan_gene) and they are widespread. The thing is: it doesn't pose a problem for the theory of evolution. The theory is so strong, that it rather poses a problem for the genes, so to say: we must find an explanation how those genes can arise (the wikipedia article mentions some hypotheses).
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Even tigers and lions kill just to survive. Lions kill other lions' cubs just because of "the egoistic gen". However, we kill - yearly (!) - hundreds and hundreds million of animals just for our food (and we most likely are successors of fruits-eating animals, as, e.g., also Pan paniscus are) and for mere entertainment (so called "hunting" - the same predators' "virtue" ) and simply disgusting pleasure (furs). We are keeping them in frightening conditions in meantime. (As if they were not living soul persons just as we all are?) And we kill them for nothing in millions just under suspection of slightest endangering for our own health:
In early November, the Danish government announced a plan to slaughter 15 million mink due to emerging fears of the COVID-19 mutation, which could be transmitted from these animals to humans. At a press conference held on November 4, Prime Minister Mette Frederiksen announced that twelve people had contracted the mutant virus and added that mink are "considered a threat to public health".
15 mln vs. 12 - isn't it a clear evidence of presumption of Homo sapiens sapiens
to be actually the most predatory (and beyond compare measure EXTRAORDINARY) of species of whole the Multiverse, therefore?
Photo from:
Dania. Władze wybiły norki. Teraz ich truchła wychodzą z ziemi (wprost.pl)
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Animals kill other animals just to feed themselves and nothing else, so why shouldn't we be like them?
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Are there any cyclical animal populations in the tropic?
I've been writing an evolutionary biology hypothesis, that claims that cyclical animal populations are actually a population-wide multi-year hormone cycles; not that different from menstrual cycles: https://www.researchgate.net/project/80-year-generational-hypothalamic-hormone-cycle-spanning-across-4-generations
The current assumption is that the annual changes in daylight enables the "counting" of years for biology, but since the amount of daylight is quite stable in the tropic, the "counting" of years wouldn't be possible there. This is why I'm asking: are there any cyclical animal populations in the tropic? The requirements are that the cycle is multi-year and has similar characteristics compared to the other cyclical populations (of lemmings, voles, hares, etc.)
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Of couse, there is cyclical animal population variantoin in hole planet due periodic elleven years variation in solar irradiation
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Good day. A simple two-day field activity will be done in an island. Currently, I am thinking to use a single family of gastropods in mangrove, compare color and measurements of of the shells between habitats (such as ground gastropods vs. gastropods on mangrove leaf and trunk and branches). Please advise. Thanks.
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Another experiment was to remove calling treefrogs from their calling site and displace them by 0.5m, 1.0m, 2m, 5m, etc. and observe the length of time needed for the frog to return. It is best to mark the frog to be sure the same individual is the one re-occupying the "vacated" calling site. It is surprising how little time is required for a return from 5m in some species, for example. This can be followed up by introducing clear plastic barriers on the homeward path and quantifying the barrier size that actually blocks the frog's successful return (small barriers are easily negotiated in some species).
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I am currently an undergraduate student (major in biological science) who is looking for a Master of Science in Plant Systematics and Evolution Biology aspects. My result in university is quite good but then I have no prior experience in doing research. I have a strong interests in evolutionary biology in plants, and I really hope that I can polish my scientific knowledge and research skills by studying master. Can anyone recommend me some suggestions regarding the following questions?
Any institute that you recommend me to do my Master in Plant Science?
Does lack of experience in research deprive you of Master admission?
Any suggestion that can help me?
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Shivaji University, Mumbai is the right option to Pursue Master Degree. It is one of the best University having good Plant Taxonomists in Department of Botany. Professors from Shivaji University Contributed a lot in discovering new plant taxa. Instead of M.Phil, I suggest to enroll Ph.D in B.S.I, under the supervision of any Scientist instead of Universities. For molecular systematics, Delhi University is the right one for M.Sc and Ph.D.
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I was wondering if, in evolutionary biology terms, dreaming is a synapomorphy for a certain delimitated group of animals. If you can point me out a textbook or papers to read more about it, I will appreciate it. Thank you
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I've tried several programs (e.g. TreeView, FigTree, MEGA, Archaeopteryx, Mesquite) but they just display node numbers and branch lengths. I'm using the software SYMMETREE to infer diversification rate shifts on particular nodes within a tree. Results refer to "branch numbers" which, according to the manual, can be displayed using MacClade. However, I´m not using a Mac OS platform.
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Yes, ape in R is a good option
For the sake of providing a direct answer to the SPECIFIC question you asked, the following R code will do exactly what you require, and output the tree to a PDFfile in your current working directory
library(ape)
tree = read.nexus(file="path\to\file")
tree_export = "tree.pdf"
pdf(file=tree_export, width=6, height=6)
plot(tree, cex =0.5, use.edge.length=FALSE)
axisPhylo()
edgelabels(cex = 0.25, width = 0.1)
dev.off()
depending on your tree structure just play around with the "cex"and "width" parameters to make the branch numbers readable, the above peramters are reasonable starting points.
The above code assumes your tree is in Nexus format. For the commonly used Newick format do this:
library(ape)
tree = read.tree(file="path\to\file")
tree_export = "tree.pdf"
pdf(file=tree_export, width=6, height=6)
plot(tree, cex =0.5, use.edge.length=FALSE)
axisPhylo()
edgelabels(cex = 0.25, width = 0.1)
dev.off()
i.e. swap "read.nexus" for "read.tree" function
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I have a phylogeny and two categorical traits (one binary, one multi-state) mapped to its tips. My claim is that there is a correlation in their phylogenetic distribution, i.e. that they evolved in concert, or dependently.
How can I test that formally?
I have tested for phylogenetic signal using Fritz' D (Fritz & Purvis 2010,)
of which there is plenty. But I am stumped on how to show that there is a correlation in presence/absence of one trait and the state of another. I can visualise that in a traitgram/phylomorphospace plot in phytools, but that doesn't give me a number that says "these are not independent".
In principle, phylogenetic independent contrasts (Felsenstein 1985) could be used to test for correlation, right? But PIC is for continuous characters, not categorical ones.
I have found phylogenetic logistic regression (Ives & Garland 2010, https://academic.oup.com/sysbio/article/59/1/9/1723322), but this is only for binary traits. I have read the "Analysis of Phylogenetics and Evolution in R" (Paradis 2012) and "Modern Phylogenetic Comparative Methods and Their Application in Evolutionary Biology" (Garamszegi (Ed.) 2014) books and googled myself to perplexion. I hope someone more knowledgeable can help me!
Many thanks in advance.
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Rutger is quite right. You have an 18-parameter model with dependence, and an 8-parameter model without dependence. You can compute the lnL_18 (for the dependence model) and lnL_8 (for the independence model), and use a likelihood ratio test with likelihood ratio chi-square = 2(lnL_18 - lnL_8) with 10 degrees of freedom (for the null hypothesis that the dependence model and the independence model fit the data equally well).
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Recently, Christopher Monit, Richard A. Goldstein & Greg J. Towers published an article entitled 'ChromaClade: combined visualisation of phylogenetic and sequence data' in BMC Evolutionary Biology volume 19, Article number: 186 (October, 2019).
In all respects this looks like a very interesting tool to analyze sequence data and phylogenies. Has anyone tried it? Could you comment on the outputs please?
Thanks for your time.
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Brian Thomas Foley, would you mind sharing some of the tools you've employed to visualize amino acid mutations on a phylogenetic tree? I am having trouble running ChromaClade
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Who gives the last word about the evolutionary process, genetics or ecology?
In other words, are ecological interactions driven by any genetic phenomenon? Or is it genetics that has been molded by ecology?
[I’m a Brazilian biologist and writer. I write about science – I have just released a new book, O que é darwinismo (What is Darwinism, in Portuguese) – and would like to know the opinion of colleagues from other countries (from any field of scientific knowledge).]
See also What do you think about fitness, adaptation and natural selection? (https://www.researchgate.net/post/What_do_you_think_about_fitness_adaptation_and_natural_selection)
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Nobel Prize winner Niko Tinbergen observed in his now classic 1963 paper, "On the aims and methods of ethology" (Zeitschrift fur Tierpsychologie 20: 410-433) that in order to adequately analyze observed patterns of behavioural ecology in a species, it is necessary to distinguish between *ultimate* and *proximate* causative factors. Ultimate factors include: i) the *function* (or "adaptive value") of a behaviour, and ii) the "phylogeny" (or evolutionary history) of a behaviour; proximate factors include: i) *ontogeny* (or behavioural changes related tp growth and development), and ii)*proximate conditions* (i.e., that which has happened in the recent past and that which is going on under current ecological conditions). So, what is needed in trying to gain insight on biological evolution is an holistic perspective that incorporates *both* genetics and ecology. A perfect example of the value of this integrated approach is the need for up-to-date data in both the genetic and ecological realms in order to deal with conservation biology issues.
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Hello. I am looking for a cheaper alternative to propionic acid which I can use for breeding Drosophila. I am currently teaching Evolutionary Biology and I would like my students to conduct experiment using Drosophila melanogaster. I would like them to breed these flies, expose them to different conditions and see if there are changes in their morphology. I think this would be a great experience for my Biology students to do this experiment.
I have tried using vinegar as alternative during my previous classes last semester but it was not very effective and we have acquired poor results.
Thank you.
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The propionic acid is in the fly food as a general microbial inhibitor, I have been able to get away without it as long as some other preservative is present (e.g. methylparaben/Tegosept, but this might not be cheaper).
If you really want to save on cost, you might be better off going with some oldschool way, like culturing flies on a banana/yeast mix (see attachment). I would keep an eye out for mold and bacteria though.
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Can someone provide suggestions on which methods / softwares can perform fast and reliable estimates of diversification rates (speciation - extinction) using very large phylogenetic trees (> 10 000 tips)? 
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BAMM, LASER, and APE
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"There has been a long and bitter controversy as to whether groups as cohesive wholes can serve as targets of selection. The answer is “it depends.” There are different kinds of assemblages of individuals (“groups”), some of which do and others which do not qualify as targets of selection." Ernst Mayr
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Mr. Pegman; Selection of any kind might lead to what is called an adaptation - that is, in hindsight, we can see that some phenotype is under positive selection and the reproductive status of the population improves. That's all.
Creation and design have no place whatsoever is any scientific discussion. The propositions are either untestable or have been disproven so many times that is tiresome to dwell on them. Best regards, Jim Des Lauriers
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According to the theory of natural selection, selected clone of bacteria are capable of tolerating specific stress factors. But when does this selection happen? Does it happen before the exposure to particular factor? Or is it a consequence of exposure to a particular factor? Is the specific clone of bacteria inherently resistant to that specific stress factor or does it acquire resistance following exposure to that particular factor?
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Thanks for all the tips! This was extremely helpful
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I want to work on scientific investigation (Ecology+Genetics) and community based conservation of two threatened species i.e. the Himalayan Gray Langur and the Himalayan Musk deer in western Himalayan areas of Pakistan. Can any body would like to guide me that which can be the funding resources for these researches?
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Take a look at the The Mohamed bin Zayed Species Conservation Fund: https://www.speciesconservation.org/
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I do not have network publisher a paid component of this software.
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You should download stable version, link works.
Kiavash
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Hello People
I am extracting host DNA from fecal samples. However, feces contains lot of microbes and their DNA too gets extracted during DNA extraction procedure.
I want to get rid/minimise the microbial DNA. It is causing a lot of issues in my PCRs (lots of misamplification). Is there an inexpensive method to do so?
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Yes this question can really only be addressed in a helpful manner with more information about your needs and unfortunately your budget. But basically eDNA techniques are emerging that allow simultaneous amplification/sequencing of all of the OTUs that successfully amplify, so by definition this approach uses universal primers for markers usually such as 16S rRNA and ITS, internally transcribed spacer region, or COI cytochrome c oxidase I, then the resulting sequences are blasted against NCBI database to determine biodiversity in the sample. But if you are using a more traditional PCR approach where you want to specifically amplify only certain target lineages, one possibility is use species of specific primers. Depending on the species of interest, this can be tricky if such PCR primers are not available, but you can design your own primers that specifically amplify only the species of interest, provided there are DNA sequences available for these taxa.
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Please respond to this quote above. This was written to me in response to a discussion on biological species concepts and evolutionary
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Hello Asif; If you intend to reply, think carefully about what your goal is. I used to engage in exchanges like the one you anticipate. I mistakenly thought that if I could explain some aspect of evolutionary theory or some particular data set, then I could help the person understand the general idea. That doesn't seem to be true. The issue is an ideological one, not a lack of information. Some years ago I wrote an essay intended to help science teachers with exactly this problem. Its title is "The Creation/Evolution Dispute: a Teacher's Handbook". Look it up on ResearchGate. Best regards, Jim Des Lauriers
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Hi all,
I am wondering if there was anyone interested in have a look at a draft of a follow up paper to my (and James Maclaurin's) 2016 paper 'The Value of Phylogenetic Diversity'. I am working on it just now. It would be good to get someone working on this project to have a look as it should be relevant. Here is the abstract.
Preserving the Tree of Life
Abstract
Biodiversity is a key concept in the biological sciences. While it has its origin in conservation biology it has become useful across multiple biological disciplines as a means to describe biological variation. It remains, however, unclear what particular biological units the concept refers to. There are currently multiple accounts of which biological features constitute biodiversity and how these are to be measured. I draw from the species concept debate to argue for a particular set of desiderata for “biodiversity” that is both principled and coheres with the concept’s use. Given these desiderata biodiversity should be understood as referring to difference quantified in terms of the phylogenetic structure of lineages, also known as the tree of life.
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I realise I never followed this up with the published paper. Here it is for anyone who is interested.
Lean, C. H. (2017). Biodiversity Realism: Preserving the tree of life. Biology & Philosophy, 32(6), 1083-1103.
Cheers,
Chris
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I would like to perform positive selection analysis among mammals. I am mostly interested in positive selection in humans and I have started off with around 100 mammals species and looking for a way to find the ideal number of species I can use to detect the selection.
I want to have a balance in the evolutionary distances between the species I will include: not too distant or not too divergent. Previous discussions give a minimum number of species to include in a positive selection analysis; however, not much information is given about the maximum number.
What is the appropriate number of species that should be used in positive selection analysis and what would be the maximum? Also, what interval of evolutionary distance should be used to be able to detect the positive selection and avoid false positives at the same time?
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Hello Ozge,
For selection analyses you want to be in a range where your rate of synonymous substitutions (dS) is not saturated. If this rate is too high then any methods based on dN/dS will not be appropriate.
In mammals, Rodents or Simian primates are great sets of species to detect signatures of selection (over 20 assembled genome in each). In general I would say that between 50-70My of evolution is a good amount for selection analyses in mammals.
As far as number of species, there is a great study by Sarah Sawyer's group that looked into this. I would recommend to aim for 20. If you are using likelihood methods you will run into computational hurdles with more species. But I would advise against using the entirety of mammals to run any type of selection.
I hope it helps.
Cheers,
Antoine.
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I remember quite some time ago I came across an interesting quote which I believe was attributed to the evolutionary biologist Theodosius Dobzhansky. If I recall right, it was in one of G.G. Simpson's books in which he was recounting some of the discussion around the time the modern synthesis of evolution was being formulated. The quote was something along the lines of "that's a wonderful story. But it's wrong." I have been trying to find what the exact quote was for reference but I do not think I have the original book where I saw it anymore. Any information on the context of this quote or if I have it wrongly attributed would be appreciated.
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If it helps, I believe it was a G.G. Simpson volume reminiscing about the history of the discipline and what he had seen during the crucial periods of formation of the modern synthesis. Or a biography of Simpson talking about the history of the modern synthesis.
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Citations that appear in the BODY of published papers contribute to metrics (e.g. h-index) that account for the impact of the work of a particular researcher. I acknowledge that the suitability of these indexes is debatable. In the meantime, I wonder why the citations that appear in Supporting Information (particularly those that refers to relevant methods and databases that were used in the papers) are not included in the calculation of such indexes.
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Yes! Hope journals will/are considering this issue.
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I'm aware of quite a few sites out there (e.g. morphobrowser, morphosource, nespos, evans) but I'm always looking for more.
In particular, I'm looking for ones that have CT scans high quality enough to do research with...i.e. the Digital Morphology Museum, KUPRI has a TON of amazing primate CT scans for free download. However, they're not particularly high quality, making it difficult to use for anything other than gross geometric measurements and/or teaching.
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The currently accepted value of the proportion of female births in large European-race populations is 0.485 (Bayesian Data Analysis, 3rd edition, Gelman et al.).
Do we know why the probability of being born male or female deviates from 0.5?
Thank you for your insights
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A clear treatment on the topic of sex ratios can be found in this book;
Charnov, E.L. 1982. The Theory of Sex Allocation. Princeton University Press.
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Hi,
I could list thousands of real world examples in which a cultural belief (e.g. Religion or political ideology ) in any particular area is attributing towards some form of social ill. However, I will only list one real world example for this case study, due in part, because cultural belief can cause some of the worst social pathological behavior to manifest and I,for one, wouldn't want to stir a psychological hornets nest. And that's why I've been very hesitant to get involved on a political level in the context of this case study. The reason I'm referring this case study to you ( the scientific community) is due to the fact that the more logical minds think about any particular problem the more probable a solution can be found to mitigate that problem.
Case Study:
A community is seriously contaminating the air they breath with toxic smoke (there isn't a "healthy" smoke). Whilst they do have the choice to not emit toxic smoke in there local environment.e.g. By using more cleaner technologies to heat there homes. They "choose" not to. The reasons why this form of social self harm exists (other than when there is no choice.e.g. Burn Coal or freeze) is only because of ignorance in most cases.
This ignorance is based on a central cultural presumption. A belief that blinds them from the facts, thus they act without due care and attention.
Fact 1.
The community (a significant percentage of the people in the community that contribute towards a negative health difference to the overall air quality) are choosing to behave in a way that, evidence has shown, seriously harms health ( e.g. Coal/wood smoke is far more toxic than cigarette smoke).
Fact 2.
They don't (are not cognitively indoctrinated too) accept the facts due to a habitual cognitive bias ( driven in part by a religious upbringing in which they are indoctrinated in such away that they avoid certain facts that contradicts their central premise (belief/opinion) and or ideological/financial incentive).
Fact 3.
local industry actively promotes ( and part takes) in the ritual of burning stuff in the local environment and is financially motivated to promote the burning of wood and coal.
Fact 4.
The culture is comparably wealthy in so that most (if not all) do not even consider the alternative cleaner options. New homes are built and coal fire places and or wood burners are installed.
Fact 5. The local governing bodies are part of the coal/wood burning culture thus are not interested in mitigating the problem (e.g. Smoke control regulations).
Fact 6. Some of the narratives promoted by local business ( financially associated within the tree to burning wood economy) suggest that burning wood for heating is a sustainable method to mitigate climate change.i.e. Tree's fix Carbon from the air and burning wood releases the carbon back into the Air ( and in local peoples lungs). Whilst this narrative is correct, they then go on to add the "carbon neutral" narrative, which is completely incorrect. For example, it takes a lot of industry (predominantly a diesel driven industry) to grow tree plantations and get those tree's processed and into houses as logs. Furthermore, the conifer tree plantations take up most of the forested areas of the local landscape and being of a monoculture design, are not self sustaining in the long term.e.g. Loss of fertile soils and loss of the carbon ( carbon capture cycle. Thus on a large scale disruptive to the ecosystem ).
So given the particulates (sorry, pun intended), the particulars of this case, does anyone have any suggestions what methods could be used in order to reduce smoke emissions thus improve the general health of the area. Other than replacing the entire culture with more intelligent thoughtful people, I'm at a loss in how to help these poor "souls" out.
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Gary;
Start casting about for your credible voice now. That voice can use all of the background information, literature research, and legwork that you can provide as a "good lieutenant". By providing that kind of quiet support the public face of your effort is less likely to burn out and will also gain confidence in the validity of the effort.
I, and others, started working on the preservation of a tract of land in this community and were pitted against entrenched real estate development interests. The strategy that I've suggested to you is the one we used. Progress was glacially slow with plenty of setbacks and some crucial "victories". The faces have mostly changed but the goal remained. Now, 40 years later that tract of land, and an area that doubled the total area, is about to be placed in permanent conservancy. This old war-horse is mostly out to pasture but still feels the warm joy of seeing a good thing through to a happy conclusion. As you pointed out, it took far longer than it should have. But in hindsight that's OK.
Best, Jim Des Lauriers
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(THE ANSWER: I asked the question and now, on June 30, 2019, it is answered to my satisfaction by the knowledgeable people who contribute here and especially by Aleš Kralj, Jun 28, 2019 , who asserted that evolution is fundamentally unpredictable. The Theory of Evolution as it is used here refers to “macroevolution.” A theory is expected to both explain and predict; the theory of evolution only explains. The theory of evolution is not a theory and it is suggested calling it a working hypothesis: the working hypothesis of evolution.
With the question answered to my satisfaction, I am now leaving the discussion. You may wish to continue.)
Science is based on observations. Empirical relationships between observations are called laws. For example, a graph of the position of an object vs. time is an expression of a law.
Theory is based on things you cannot measure; for example, one cannot measure momentum or energy, but only calculate them. If the imaginary things can be used to predict laws or observations you have a theory. If your theory cannot predict something that is observed …. or predicts something that is not observed . . . forget-about-it..... the theory not the observation! If your theory can not predict anything, the theory cannot be tested . . .why did you bother in the first place? Theories come and go. Scientists hide theories that do not work. ... What does oxygen mean? . . . is oxygen really needed to make an acid? That theory has come and gone. Where did phlogiston go?
Do you believe in the Theory of Evolution? What can you predict right now from the Theory of Evolution? What new species will be discovered?
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@ Md Zafar Alam Bhuiyan
@Hamid Gadouri
@ Everyone and Anyone
Here I would hope for a discussion based only on “natural” philosophy. Not a discussion that in anyway involves theology, or any other school of knowledge.
Basically is there a “Theory of Evolution” or only empiricism?
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Can a FigTree file is compatible and reproduced in R software? Also, can anyone give me some links or reference for trait mapping in phylogenetic trees?
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The best way to answer the question about what kinds of files can be opened in R software is to find the relevant Task View on CRAN. Below I've copied what the Phylogenetics Task View says about reading trees into R. As for ancestral state estimation, the literature is quite large and several of the recent, most flexible methods for quantitative traits, are not implemented in R. A nice recent summary/tutorial that emphasizes methods that are available in R is by Liam Revell, the author of the phytools package: http://www.phytools.org/eqg2015/asr.html
As for getting trees into R, from the Task View:
Getting trees into R : Trees in R are usually stored in the S3 phylo class (implemented in ape), though the S4 phylo4 class (implemented in phylobase) is also available. ape can read trees from external files in newick format (sometimes popularly known as phylip format) or NEXUS format. It can also read trees input by hand as a newick string (i.e., "(human,(chimp,bonobo));"). phylobase and its lighter weight sibling rncl can use the Nexus Class Library to read NEXUS, Newick, and other tree formats. treebase can search for and load trees from the online tree repository TreeBASE, rdryad can pull data from the online data repository Dryad. RNeXML can read, write, and process metadata for the NeXML format. PHYLOCH can load trees from BEAST, MrBayes, and other phylogenetics programs (PHYLOCH is only available from the author's website). phyext2 can read and write various tree formats, including simmap formats. rotl can pull in a synthetic tree and individual study trees from the Open Tree of Life project. The treeio package can read trees in Newick, Nexus, New Hampshire eXtended format (NHX), jplace and Phylip formats and data output from BEAST, EPA, HyPhy, MrBayes, PAML, PHYLDOG, pplacer, r8s, RAxML and RevBayes. phylogram can convert Newick files into dendrogram objects.
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I have a phlyogenetic tree (see attachment). In the legend, it is written that the distance scale represents the number of differences between the sequences.
My question is how can I read/interpret this figure?
For example, How close is Protein A-1 to B-4?
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Hi Arman,
As other people suggested, all the explanation should be in the legend of the figure. Often, the number on the scale should be the percentage of genetic variation. For example, if this was the case of your figure, the scale would suggest a 0.2 (20%) genetic variation for the length of the scale. However, in this case you would not be able to have a total distance >1. For phylogenetic studies, this length would be usually much shorter, with a scale bar at about 2-5%. However, this is not always the case, and that's why scale bars should always be explained under the figures.
In your example, "number of differences between the sequences" is to say the least incomplete (and it is not your fault for not understanding). They may be referring to something they explained better in the text? Maybe "differences" is referring to specific sites in the protein?
Also, just to be sure it is clear, I showed in the figure how to calculate the distance between the proteins. You have to consider the full length of both the branches up to the point these are connected (in RED in the attached figure). In your case, the branches A-1 and B-4 are connected only at the base of the tree. Therefore the distance between them is APPROXIMATELY 12 times the scale bar, or 2.4 "differences". In case you need a more precise measurement, however, you would need to create a distance matrix using the sequences that have been used to generate the tree.
Hope this will be helpful!
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Anyone know how to interpret the matrix of distance genetic whose analysis were performed in the software MEGA 5.0 (Tamura et al. 2011) using the pairwise method with the p-distance model?
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If you multiple those values per 100 you will get the percentage of difference (0.7% and 25%).
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If the gRNA works, chances are there is a small indel at the cutting site, but how frequent will this happen? Can I use the length difference as an indicator of gRNA efficiency.
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Hi Lu,
the chances just depend if the plasmid transfection/nucleofection of the RNP were successful. If the gRNA is properly designed (PAM sequence, uniqueness, etc.) it will always cut. Repair after NHEJ is totally random, and usually about 1 -10 bp are deleted but insertions are not rare either. Therefore, the length in difference cannot be an indicator for gRNA efficiency as, as long there has been been some indel and you verify it by sequencing that the target protein is disrupted, all gRNA are equally efficient.
I let you this interesting Addgene blogsite: http://blog.addgene.org/crispr-101-non-homologous-end-joining
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Woese and Fox (1977) stated that "phylogenetic relationships cannot be reliably established in terms of noncomparable properties" and that "a comparative approach that can measure degree of difference in comparable structures is required." What I don't understand is if this only applies to living (=extant) organisms or if one can determine (infer?) phylogenetic relationships even between fossils...
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The idea that DNA sequences swamp out morphological characters simply by virtue of their greater number of characters is not necessarily true. DNA is almost always very homoplastic, and if there is a good morphological signal in the data, it usually prevails. In my experience, morphology and molecules for my group (butterflies) are usually in agreement with one another. See
Simonsen, T. J., N. Wahlberg, A. V. Z. Brower, and R. de Jong. 2006. Morphology, molecules and fritillaries: approaching a stable phylogeny for Argynnini (Lepidoptera: Nymphalidae). Insect Syst. Evol. 37:405-418.
Wahlberg, N., M. F. Braby, A. V. Z. Brower, R. de Jong, M.-M. Lee, S. Nylin, N. E. Pierce, F. A. H. Sperling, R. Vila, A. D. Warren, and E. Zakharov. 2005. Synergistic effects of combining morphological and molecular data in resolving the phylogeny of butterflies and skippers. Proc. R. Soc. Lond. B 272:1577-1586.
Brower, A. V. Z., N. Wahlberg, J. R. Ogawa, M. Boppre, and R. I. Vane-Wright. 2010. Phylogenetic relationships among genera of danaine butterflies (Lepidoptera: Nymphalidae) as implied by morphology and DNA sequences. Systematics and Biodiversity 8:75-89.
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Dear Sir,
As a part of interest, I wanted to know the details of Hypothesis that One prokaryote engulfed the other bacteria and during the course of evolution other bacteria remained as symbiont latter we call it as Mitochondria.
Would you please elaborate this concept.....
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I highly recommend anything written by Lynn Margulis, as this idea was her original concept a long time before it was generally accepted by the scientific community!
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I mean cases that are not results of parallelism or convergent evolution.
We presented an example of Devonian ammonoids, but I have never heard of other good examples published since.
Monnet, C., Klug, C. & De Baets, K. (2011): Parallel evolution controlled by adaptation and covariation in ammonoid cephalopods. BMC Evolutionary Biology, 11 (115): 1-21.
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Hi, Christian,
I think that a good example may be the fact of enucleated red blood cells in the lungless salamanders (Plethodontidae). This trait is independent of similar situation in mammals.
Regards,
Alexey
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I have 12 species from same genus. For supermatrix approach we generally use the multiple sequence alignment single copy orthologs sequences then concatenate them and remove the badly aligned columns and generate ML trees. In my case I got around 2000 single copy orthologs that I used.
To add outgroup species, do I first need to cluster the outgroup sequences with my 12 species sequences? If the reply is yes, then I wonder it may decrease the number of single copy orthologs as they are the possibly the part of core genome and I suppose probably they all not will be present in outgroup or may be removed by MCL clustering because of less similarity than others.
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I agree perfectly with Brian sometimes if you do not have specific problem being an out group also used to make a direction to the tree is better to use a mid point rooting that is a sort of average of a probable root due at a probable ancestor
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I have once been asked about the methods for studying ancient DNA, and I am rather naive for knowing too little about studies on Ancient DNA. I am hoping to receive more information about sequencing Ancient DNA (Again other than mtDNA and Chloroplast DNA) for studying ancient samples. In particular Human samples.
(Assume we're gonna study them through pedigree diagram, are there any more specific methods for studying the Ancient DNA samples: Such as Haplotypes)
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Thanks for replying and I'm really sorry about the late reply!
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How can I explain this?
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Hi. Jmodeltest is best for your work, Ofcourse Mega6 or 7 version has Modeltest and based on your sequences, you can select the best model.
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I am trying to understand the molecular evolution of a gene family that composes of only two members (let's say X1 and X2). I have looked into the genomic neighborhoods of X1 and X2 in various species using Genomic Alignments in Ensembl and constructed a genomic neighborhood illustration of other genes flanking X1 and X2. However, my Blast searches didn't detect X2 in some fish species. When I looked into the genomic neighborhood of X2 in these fish species, I saw another X1 like sequence instead. I am thinking that maybe X2 was converted into X1 after the duplication event, but how can I prove that? My assumption may be stupid because I am not very experienced with genetics and concepts of evolutionary biology, but any help would be appreciated.
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Your assumption is reasonable. Another possibility is simply that one of the genes has been lost. Some fish species have had 2 rounds of genome duplications and afterwards lost some of the duplicated genes. Doing a synteny analysis, as Abhishek Kumar also recommended, would enable you to distinguish between gene loss and gene conversion.
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With HIV-1 phylogenies we quite often have data sets where we know important details about the true evolutionary history. For one example, with a local transmission chain such as husband to wife to infant chain we can often know for certain who was infected first and the dates of transmission events etc. In other cases the rough epidemiology is known so that we can tell that an epidemic spread out from a point source introduction.
Very often, or perhaps always given certain relative levels of diversity involved, the phylogenetic trees produced from a data set show a misrooting of one or more subclades which essentially turns that subclade "inside out" by putting the more diverse sequences rooted to the outgroup. The explanation seems to be the "long branches attract problem". In the father->mother->infant case for example, the sequences from the infant often appear on a branch in between the father and mother, when we know for certain that this is "out of order".
What I want is a tool that allows me to "fix" a known misrooting of a clade, and then calculate the likelihood value (or other such measurement) of the "correct" tree vs the misrooted tree. I can provide sample data sets and tree results to anyone who is interested in this.
 
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I just want to add: the CAT-like models for maximum likelihood are C10 to C60, which are supported in IQ-TREE. So you can use this when PhyloBayes is too slow. We also just published an approximation, which speeds up the analysis under such model without loss of accuracy:
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What were the general inferences concluded after the phylogeny reconstruction?
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Check the attached articles.
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I'm using mlcoalsim in order to compare the observed distribution of four summary statistics (neutrality tests) with those obtained from nine different demographical models. Nevertheless, the probability that simulated values be smaller than or equal to the observed values is the same for all nine models (including the standar coalescent model). I suspect that my models are not well inputed (for instance, I'm not sure how to transform times from years to 4N generations. I assumed that t =r/4N; where t is the time in 4N generations and r is the number of generations) or they are not really different. I would be grateful If someone could help me and give me some advices to make a succesfull simulation with mlcoalsim (feel free to write me in Spanish or English). 
Thank you in advance.
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Remember always that you are modeling phylogenetic relationships, not evolution. Evolution is not necessarily dichotomous as in hierarchic cluster analysis (of which cladistics is a variant) or Markov chains. Cladistics is also blind to ancestor-descendant relationships. The optimal model in cladistics is the most probable or most credible generation of a dichotomous tree that is not found in nature.
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I read several papers where researchers use several strains of same species for analysis of recombination or selection pressure however there are few papers in which researchers use the multiple species belong to one 'Genus' not the multiple strains belong of one 'Species'. What difference is expected in the result and how it can be interpreted.
I want to know how my pathogenic organism 'Xyz abcde' is evolved (recombination and selection pressure). 5 different strains of 'Xyz abcde' is sequenced while 9 organism in Genus 'Xyz' is sequenced.
Which dataset I should use to proceed and why? How it will make differences in the analysis?
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I agree with Brian Thomas Foley above that the choice of strains from same/different species/genera eventually will reject the divergence level.
The power of your analyses for selection and recombination will be affected by divergence as it defines how much information you have in your data. If your sequences are too diverse, or if your sequences are too close then you ar unlikely to find a signal (low power). There are many publications by now that have shown this, including some from my own: Anisimova et all 2001, 2002, 2003 and Anisimova and Yang 2007.
So divergence is one factor. Another factor to consider is what type of sampling you have and how well it corresponds to your actual question. Do you have mixed population and species data? Are you interested in lineage-specific effects? Are you interested in detecting episodic selection. Are you contrasting your sets of strains by some criteria (e.g., pathogeneicity or environment, etc.)? Basically, you can analyse any sample set, but the success of your analysis will depend on what specifically questions you are asking and whether your sample is the best one to provide information to answer these questions. So there you have to be careful what tests to set up and how to interpret them. I don't know if this helps, but I don't know specifically your scenario.
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Why internal stop codons appear during process of submission of COX-I or cyto b partial gene sequences to NCBI? And how can we get rid of them? This happened even if the nucleotide sequences are same as of other closely related species already submitted to the gene bank. How can we submit sequences if such error conditions persist?
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If you have partial sequences for protein coding genes, it is likely that they do not start at the first codon position. If that is the case, and you count the triplets from the very first nucleotide, it will lead to a frameshift in the codons, and stop codons are likely to occur. One way of obtaining the right frame is to compare your partial sequence to a fully sequenced gene in a closely related species and see if you can determine the position of the first nucleotide in your partial sequence. Once that is determined, you can then obtain the right coding frame in your sequence and you should then be able to avoid getting any premature (internal) stop codons.
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I need to get some primers, but due to logistic we can not put the in the suitcase and we have to transport them in the hand luggage. We assume we have to use a coolpack, but the flight will take 4 or 5 hours, does anyone know if there would be any effect on the primers? 
Thank you very much !
Kind regards, Mara
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I have generally received primer stock (powder form) in room temperature and I leave them at RT until I dissolve them in water to prepare a stock solution.  If you are transporting primer solution, it is still not a problem to transport them in Ice. The cool pack works for few hours anyway. They are being very stable, they should be fine even in room temperature. 
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While calculating the evolutionary divergence as computing pairwise distance, (using p-distance methods and Maximum Composite Likelihood model), the values ranged between 0.002-0.138 (p-distance) and 0.001-0.109 (ML) for between individuals of the same species, and for different species. I have got these value as distance matrix table using MEGA 7 software by inserting the nucleotide sequence of COI gene of 661 bp length. Can somebody tell me what are the actual threshold values of the evolutionary divergence calculated by the above said methods to delimit the distinct species? I mean at which values of these distances we would say that these two species/individuals are of distinct species?
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I would emphasize even more strongly than the previous respondents that speciation is a process where subpopulations establish their own independent evolutionary trajectories, and any notion of a threshold difference is only a rough approximation at best.  As an example, back in the '90s I was doing a postdoc where I was sequencing mtDNA of macaque monkeys.  At that time we discovered that rhesus monkeys had major haplotypes differing by about 3%.  A very well known evolutionary biologist from the American Museum of Natural History assured me that we had made a mistake because the threshold for species elimination was 1% for mtDNA.  Since then a different species of macaque has been found to contain mtDNA sequences that differ by about 9%.  Macaques have relatively extreme female philopatry, which explains this unusual observation, but it highlights the folly of assuming an arbitrary threshold of difference.
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I am trying to understand what drives bioerosion by grazing organisms.  I understand that algae are a major food source, but there are often problems in the literature distinguishing between basic herbivory grazing and BIOEROSIONAL grazing.  My question is specifically related to what controls bioerosional grazing in reefs with depth, especially related to food sources.  Please let me know if you can help. 
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I have aggression scores which are categorical. I'm interested to see how aggression levels of individuals change over trials (time). I made a random slope random intercept model for boldness scores which are continuous and visualized using the sjPlot package in R. I'm wondering if the same can be applied for categorical response variables. I have been searching along these lines for quite some time, and since my knowledge in statistics is very basic, I don't know if I found anything useful. Any help would be much appreciated. Thanks! Bharat
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Thanks much Andrew. Much appreciate your help. I'm looking for ways to do what you suggested. Any suggestions on links/articles that you may know of will be helpful.
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Hi,
I have a morphological trait measured in three different populations and I want to know how this character evolved. All the three populations are recent and I do not have information of this character in related or ancestral species. I do have information of the heritability, population size and variability of the trait within the population.
My questions are:
- How can I test if this trait evolved by natural selection?
- Can I do this with a single trait? and with only three almost current populations?
- Is it necessary to evaluate other possible evolutionary (other than natural selection) mechanisms if I want to make a valid conclusion?
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Hi,
In addition to the other suggestions, You could try to estimate population genetic differentiation for morphological traits (Qst) between your populations and compare with corresponding Fst estimate (using any molecular marker available). If Qst is significantly larger than Fst you could consider that the difference is caused because natural selection is acting on your morphological trait. There are several studies using Qst/Fst and you can get a typical experiemntal design from them.
Alternatively you may study variation on morphological trait and estimate its relation with fitness (any component) following Arnold and Wade 1984 methodology. If fitness is working on your trait you should find  higher fitness estimate for certain range of the trait distribition...
Best
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Why transition from moneocious to Dioecious and different forms of  Dioecious were found in some plant families? Is this an evolutionary adaptation or due to some other reasons?
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I advise you to read:
Plant Breeding Systems by A. J. Richards, second edition 1997; Chapman & Hall. 
I think this will help you better understand the evolution of plant breeding systems. 
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Hi everybody,
For my study, I need several life history traits:
- size of organisms
- number of offspring
- longevity
- their reproduction
and so on...
So I'm looking for databases for protist, plants, fungi, metazoa... I know this database: http://genomics.senescence.info/species/. Do you know any other?
Thank you very much.
Benoît
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Hi everybody,
Thank you very much for your answers. I will check all your links and come back to you soon.
Cheers,
Benoît
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Since amino acids are degenerate in nature, the amount of variation will be higher than its respective nucleotide sequence so will it make sense to construct a phylogeny tree using the protein code?
Also, how different should the sequences be from each other to be marked as a different lineage or under a different internode?
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As usual in science, it depends on the aim of your study. If you are trying to unveil the taxonomy of an unknown species, I would suggest you to work with 16S for bacteria/archea and 18S for eukaryotes.
If you are studying protein coding genes, as mentioned by Dr. Kumar, it might be more reliable to work with aminoacidic sequences (or translated nucleotidic sequences), as they have a higher information content ( 5x fold).
About the threshold of similarity in clustering sequences, it mostly based on experience on the sequences you are working with. It depends if you are working with nucleotides or coding sequences, the expected divergence between sequences, the evolutionary rate (K) of that region and the evolutionary distance between organisms that harbour the sequences. On top of that, there is also the aim of the study. It is not the same comparing variations among closely related populations (high similarity is expected) than variants between sequences that belong to different orders.
I would suggest you to read the books and reviews of Dr. Felsenstein, to learn the best approaches to your problem, as well as the most common pitfalls.
Cheers.
JMC
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I need to obtain a substitution rates per site per lineage per Myr in order to calibrate a molecular dating of a phylogeny between individuals from different rivers in South america. I found just one paper at the moment to use that method,that paper is "South American rays came in with the sea", but at the moment it had been difficult to obtain it from any database. Maybe you can suggest me others readings, Thanks!
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Thanks so much!
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I need to reconstruct ancestral sequences in evolution of short peptides. Trying all possible models in FastML I obtained results that just didn't make much sense. In Mesquite there are currently no available likelihood models for protein evolution... 
For me this is a first experience in this field. You, who do have some experience with peptide (or more likely protein) evolution reconstructions, which programmme would you recommend to use?
Thanks
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Use MEGA7. The King of them all
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In other words, does any other reptile group have similar teeth? or maybe some sort of mammal incisors that look similar?
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Thanks for your answers! I was trying to convince an amateur collector that a particular tooth was not that of a dinosaur, but a mammal incisor.
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So, it's a common notion that must be only one haplotype of mtDNA in the organism, but may somebody knows examples when it is not true?
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Dear Oleksandr,
Regaring the frequence, it is hard to answer, Shokralla et al. 2014 found 10% of ambiguities in a large dataset of DNA barcodes (possibly numts or heteroplasmy). For numts, there seem to be no phylogenetic congruence with their presence/frequence, indeed, when examing two close congeneric species of beetles, we found one free of numts while the other was mush affected. (https://www.researchgate.net/publication/272359549_Ghost_mtDNA_haplotypes_generated_by_fortuitous_NUMTs_can_deeply_disturb_infra-specific_genetic_diversity_and_phylogeographic_pattern)
I hope this helps
Julien
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I am  working on a gene which thought to be increases stress tolerant in plant if up-regulated but evolutionary algorithms shows that gene is evolved by neutral evolution. Now i am confused, how neutral evolution leads to stress adaptation or it is by chance.
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Thanking you, sir. It will help me a lot . 
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I want to compare evolution rate between two set of data (morphological and reproductive traits) because the values of the reproductive traits is very small in compare with morphological traits (both of the same unit and scale [mm]), so I want to perform a log-log regression of species mean trait measurements on species mean thorax volume which I used it as the index of the body size, but I don't know how can I perform it. Thus, I am looking for help or potential collaborator.
 thanks for any suggestion.
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Transformation does not LEAD to skewed data; rather, transformation changes skewed data to normal :)
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The computation of phylogeny used to rely on sequence comparison (i.e. alignment). For genetically similar strains or species, there is typically only a few variations detectable in the aa/nt sequences of single-copy or selected gene list. On the other hand, the selection of gene list is also difficult. A prepared set of conserved genes can be efficient but may lead to bias. As an alternative, single-copy method can include more information, but a gene cannot be selected if it has no orthologs identified in the other strains/species. In case that recombination or horizontal transfer happened and even was involved in phenotype or adaptability of a pathogen, the transferred element would therefore not be included in the reconstruction of phylogeny. A problem in tracking the spread route can thus happen.
My question is: can it be possible to include genome recombination information into the reconstruction of phylogeny, or is there available method to select a suitable gene set for sequence alignment and phylogeny computation?
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The answers to your questions really depend a lot on what type of organism you are studying.  Horizontal transfer between bacteria is quite a bit different than horizontal transfer between mammals, for example.  Some viruses undergo recombination quite frequently, and others do not.  In some mammals we can be certain that there has been no gene flow between isolated populations for x number of years, and in other mammals we are not so certain of total isolation. 
Even with very clear speciation events, such as modern humans now being a completely separate species from Chimpanzees, we have evidence of incomplete lineage sorting in the distant past when the human lineage split from chimpanzees, and introgresssion in more recent splits such as Neanderthals with modern humans.
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I'm supplementing an already published genetic database with genes extracted from full mitochondrial genomes from genbank. I have all accession numbers for the complete genomes and I have previous gene sequences too.
I'm using R to do all the downloading and data management but i'm willing to use other open access tools to do the job. So far, my plan is to just download the full genome, replicate it in separate fasta files for each mitochondrial gene, align all the sequences for that specific gene and then trim sequences manually. I could also go genome by genome extracting the genes manually on genbank, but I figure there is a smarter and quicker way to do it.
I have never done anything like this, so I'm playing by ear here. Any tips are welcome.
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Found it: "AnnotationBustR: An R package to extract subsequences from GenBank annotations" Here: https://peerj.com/preprints/2920.pdf  
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like the title , i am dealing with some mtDNA sequences, and totally i have 76 partial mtDNA sequences, and have recognized 13 haplotypes from these samples, when i do these tests, which dataset should i  use? 
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Yes, as said previously you need to test the ENTIRE data set. However, once you have done that you can do specific analysis of unique haplotypes to provide information of the variation among the variants. 
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Hi all!
I'm looking for informations about the ontogeny and ossification of the parietal, on fossil and living vertebrates.
Thanks!
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Dear Alienor,
I would advice you to have a look at the studies of Hans Christian Bjerring here:
Especially interesting may be two of his articles (both are available for downloading directly from Research Gate):
and
Also, you may be interasted in the earlier studies by Gunnar Save-Soderbergh and Malcolm Jollie. Especially this one:
My best,
Alex
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Speciation is the splitting of a single species into two species and qualifies as a bifurcation phenomenon. Has bifurcation theory ever been applied to speciation? If so, how? Any published references?
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And yet another publication: http://emis.ams.org/journals/UIAM/PDF/41-67-88.pdf . So there are consideratios of this kind.
Best, Igor
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?
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I would further stir this pot by noting that from an epistemological perspective, the existence of common ancestors is an inference based on phylogenetic analysis of empirical data.  Monophyletic groups are discovered by assessing patterns of synapomorphy, which is the evidence that allows us to recognize them.  Homoplasy, in this regard, is simply patterns of character distribution that add extra steps to the most parsimonious tree because the features appear to arise more than once, or to be gained and then lost, in various taxa.  Common ancestors are hypothetical entites that reside at the internal nodes of the cladogram.
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Actually I am working with genome based metabolic network reconstruction. But I didn't get any success yet in using a software which can be handy to work with and if someone have used it before in their work please do mention while responding.
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Dear all,
I am revising a manuscript for PLoS ONE; it's a modeling study concerning effects of mass extinction on phylogenetic tree balance.  It's very similar to Heard & Mooers (2002), but background extinction and diversity-dependence have been added to the model so that the modeled tree recovers to an equilibrium size and then undergoes turnover while evolution continues.
In the discussion, I wanted to be very clear about the limitations of the results, and the conditions under which they would apply, so I raised the following points that the effects of mass extinction on tree balance would not be enduring IF:
i) how traits and rates evolve remain unchanged after the mass extinction
ii) the tree cannot continue to expand indefinitely after either reaching its pre-extinction size, or converging on a new equilibrium size
iii) trait values, and the rates that depend on them, are subject to hard limits that result in eventual erosion of trait/rate variance
iv) there is no mechanism for isolating slowly-diversifying clades from very rapidly-diversifying ones.
And the reviewer's comment was:
"Which raises the obvious question of whether these conditions prevail for real clades! This seems like a real gap in the MS."
Stick foot in mouth time. :(
It seems to me like what they want is a point-by-point justification of each of these, with citations.  I think I have (or can easily come up with) references to support points II) and III), but I'm having trouble with point I) and especially point IV.  Basically, what the last point is saying is that slowly-diversifying clades can continue to persist if they're isolated in some way (spatial/ecological, temporal etc.) from more rapidly-diversifying related clades.  In the model as I have it, no such isolating mechanism exists and so clades with the slowest diversification rates inevitably disappear as the simulation progresses.  (NOTE:  for point I), the original study provided no biological justification as to why they maintained constant parameters after their mass extinction event.)
Can anybody help me out here?  Can you suggest any study that demonstrates for a real clade that more slowly-diversifying members within that clade are somehow isolated from more rapidly-diversifying ones?
Thanks in advance,
Gabe
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I cannot help out with biological citations. And I guess what I write here will be a truism. Proving points I) - IV) for some system is a challenge in itself. If one only has contemporary data, then to be able to test such hypotheses other modelling assumptions will need to be made. And justifying them will be also just as difficult. Of course fossil data will help out but that will lead to other assumptions being necessary for e.g. calibration.
Without actually observing (and not estimating) the past we will always run into identifiability issues, and I have a strong feeling that at least parts of I) - IV) will have such issues.
Good luck!
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Some peoples believe that we can not discriminate subspecies inside a population because of no distinctive genetic differentiations.
There are some different concepts about Insects subspecies, Can we rely on separating subspecies inside a population by genetics? some poepole belive that there are no difference to accept various subspecies inside a population or species?
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