Science topic

Inbreeding - Science topic

The mating of plants or non-human animals which are closely related genetically.
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Hello.
I got results (vcf) from one of the selfing plant species using Illumina Rad-seq.
So I am interpreting the results with several tools.
But the results showed 'high' observed heterozygosity. It was almost ~ 1.
Also, Hs (subpopulation) and Ht (Total) also were high. It was almost 0.5.
In my opinion, the study species is selfing, so their inbreeding coefficients also should be near ~ 1.
However, their inbreeding coefficients were negative. I guess that their high value of heterozygosity causes it.
I used gatk and freebayes for variant calling, and then filtered loci with missing (95 %), individuals with missing (90 %), and minor allele frequency with 0.05.
Is there anything wrong with the results? or Is that possible?
or Did I miss something when calculating the heterozygosity?
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Byungwook Choi If the plant is allotetraploid, then I think it's almost certain that alignment of the duplicated regions is what's going on. My guess is that completely separating the paralogs without also failing to align heterozygous alleles is going to be challenging. Fortunately, if it is also highly selfing there shouldn't be many heterozygous sites either, so you might be able to find thresholds for calling variable sites that work. I'll leave it up to someone with more experience at genomic alignment than I have to provide specific advice on that, though.
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Academic inbreeding is the practice when Ph.D. holders are employed by the same institution that trained them. We invite you to participate in a survey about academic inbreeding in ecology. This survey aims to assess the effect of academic inbreeding on the scientific outputs of ecologists.
If you are an ecologist with Ph.D. and still researching, please share your opinion in the form available on the link below:
Completing the questionnaire will take ca. 5 minutes, the information you shared will be treated as confidential, and your identity remains anonymous.
The survey is available until September 30th, 2022.
Thank you for taking the time to contribute to our project. We have been circulating this survey on Twitter (https://tinyurl.com/22hhmt8z). Please feel free to share this survey with your colleagues in your institution or in your research network.
Best Regards,
Jana Růžičková & Zoltán Elek
Ecologists from ELKH-ELTE-MTM Integrative Ecology Research Group and ELHK Centre for Agricultural Research, Plant Protection Institute, Budapest, Hungary.
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Many thanks for your input!
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Hi,
I am asking a question regarding the inbreeding of western Tragopan by using GBS, but we have only 12 samples from a single valley, it may be enough for analysis, and which tool do we have to use for analysis? Please share your valuable comments and relevant pieces of stuff.
thanks
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I am following your project, this is conservation concern species that's why we are unable to collect the samples and rare as well. so we will try to best analysis by these samples,\.
thanks
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What do you think about the "academic inbreeding"? Academic inbreeding means former students being professors at the same university they were formed.
Does Academic Inbreeding Affect Scientific production? Does Academic Inbreeding Affect teaching?
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Spot on Shivam Maurya ! Academic inbreeding is as unhealthy as it is in plants and animals. You find a department fully staffed with former students who are all beholden the departmental chair who hired them. They dare not question what he/she says are the appropriate paradigms, theoretical and conceptual frameworks for the department. New and innovative ideas often find it difficult to take root in such a department. Inbreeding is the deliberate and often unethical prevention of applicants who are not former students from joining the teaching and research staff of a department. However, it is not inbreeding when all applicants (former students and those from elsewhere) compete for posts on an equal footing. Where there is open competition, it is very unlikely that you can find a department with 75% to 100% of its staff being former students.
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I am analyzing population structure of a fungal organism collected from various locations using RADseq data. For this purpose I ran few analyses, but want to focus on maximum likelihood phylogeny and estimation of inbreeding coefficient (Fis) here. Phylogenetic analysis identified three well supported clades within one population (similar branching was observed with phylogeny based on protein coding loci). When I estimate inbreeding coefficient using the same dataset as for the phylogeny I get a value of 0.009. These two results do not seem to agree with each other, since phylogeny seems to detect signature of subpopulation structure within this population, but Fis doesn't. What may explain this pattern?
Thanks for the ideas!
Olga
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If Population genetic indicators, such as allele and genotype frequencies, observed and expected heterozygosity, were calculated using the POPGENE VERSION 1.31.
The Wright Fixation Index (FIS), which is a measure of the difference between observed and expected heterozygosity. 0.009 is a relative indicator of population heterozygosity.
The tendency of the indicator to 0 also reflects the excess of heterozygotes (unrelated mating).
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USDA checks for promoters and transgenes in the final product (after selfing, backcrossing, etc.) before releasing it to the market. Do they check for every backbone in the vector? Do they check more than the standardized protocols for some known genes and fragments? Given that Agrobacterium-mediated transformation is random integration, is there a possibility that USDA can still miss some of the segments in their standardized protocol?
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Excellent question.
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I use the 'vegan' function in the R package 'diveRsity' to calculate the Inbreeding coefficient of populations with SSR data. However, ten of twenty-six values are negative. If there is something wrong with analyze. Many thanks for your help.
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Calling Fis inbreeding coefficient is often misleading. The fixation coefficient Fis is basically a metrix of HW departure, which can be negative, in case of excess of heterozygosity (as underlined above).
Reason for excess of heterozygosity with microsatellites, may be related to different phenomena, such as randomness (you may check if your Fis are significantly different from 0), inbreeding avoidance, or small effective population size in species with sexual differentiation.
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Hi, I am working on a theoretical quantitative genetics paper exploring rank distributions of parents and progeny based off of genetic (narrow heritability) , GXE, and environmental (random, maternal effects) influences. I want to test some data but public datasets of complete (not summarized by moments or correlations) data of parent-progeny phenotypes are hard to find.
Ideally, I would like a data set with animal ID, animal sex, sire and dam ID, sire and dam phenotype, and animal phenotype. Best case would be an approximately outbred population but I accept a lot of agricultural and lab animals have some inbreeding present so I can take what I can get a long as it is not a consciously inbred line or with frequent backcrossing, etc.
Also, the number of progeny per coupling is an important variable so animals with a moderate number of offspring (5-10) per female would be appreciated.
Thanks for any help.
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Thank you very much
Regards
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Hi everyone,
I have some GBS data from some populations of stoats, and would love some help interpreting the inbreeding coefficients from PLINK.
I have attached all of them, which I graphed per population.
Below are the outputs for --het and --ibc, all theoretically inbreeding coefficients.
This is GBS data, filtered on minor allele frequency and coverage so it's got good coverage and rare alleles are gone. ~6000 SNPs. I have some biological knowledge of the populations and feel pretty confident I know the relative diversity of each. The genome quality is excellent.
Den is Denmark, and probably in reality has the highest genetic diversity. UK likely has the next highest diversity ( these populations are both within the native range). Ire is Ireland, and with one individual here which we know is diverged from all others I think we will have lost most of its diversity in filtering. All other pops are introduced range (NZ). ARK and HUN are near each other, & should be about the same. TAR probably has the most diversity of the NZ samples. RAN is a moderately isolated island near ARK and HUN. WAI is a very isolated highly inbred population on an island.
I have diversity values for all of these based on previous micro satellite work, and HUN and ARK are about the same diversity, RAN is lower, and WAI is much lower.
It looks in most plots to me, unless I'm confused by Plinks outputs, that DEN is most inbred, followed by IRE and UK. If higher Fhat1 was less inbred, that plot would be what I would expect, but I think its the opposite? This could be ascertainment bias due to NZ dominating the sampling?
UK is most like the NZ ones because NZ stoats came from UK - therefore it's most likely I have retained SNPs in UK because my dataset is dominated by NZ variation. WAI should always have higher inbreeding than the other NZ populations I'm sure.
While WAI was a large proportion of the data, it's not more than half, so I don't think ascertainment bias should affect it that much. If as I said, fhat1 is reversed and higher = less inbred, lower = more, than we are all groovy. If not, what do you think caused this?
My guess is that possibly F is the most accurate here and useful, and it is an ascertainment bias for DEN, IRE that draw them up. There may be some sample quality issues with TAR adding some outliers with high inbreeding coefficients.
Other options are that the coverage stats are off and this has caused some funny results?
Any help greatly appreciated!
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--ibc calculates inbreeding coefficients for each sample and get the report as
--out plink.ibc
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Hello, I'm working on cyt-b sequence data, and I want to know the inbreeding situation of populations.
Does anyone know what software or formula could I use to calculate FIS or other coefficients that could reflect inbreeding?
I found most methods to calculate FIS are not for haploid sequences
Thanks a lot
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Fis is a measure of the average relatedness of the two parents of individuals in the population. Since mitochondrial sequences are inherited from just one parent, they do not provide this information. They can provide information on Gst (somewhat analogous to Fst) addressing the extent to which genetic variation is subdivided among populations, but you would need data from diploid nuclear loci to estimate inbreeding.
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I'm looking at wild horse populations and trying to map their relations. Ultimately I'd like to assess their relatedness and inbreeding coefficients. However, the most important component right now is mapping the populations' pedigrees.
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To find coefficient of relatedness and inbreeding coefficient huge data set accross genration is required. I use CFC software to find these two parameters from padegreed data of sheep maintained at organized sheep breeding farm of Kashmir.
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Some sunflower inbreds tend to produce multi heads after a few generations of inbreeding, which is undesirable trait. Which is the most efficient way to get rid if it.
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I with agree Dr. Ayoob Obaid Alfalahi because almost Rf lines have a multi headed as the same in Agricultural Research Center in Egypt.
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Hi,
I am doing a GWAS analysis of european bison's a dog's SNPs. Right now I am doing multiple data clean up, according to previous studies and what I have learned.
I was thinking, if it is ok to test HWE and discard data that does not fit if I am working with animals, where mating is controlled and inbreeding coefficient is high?
And what about tests for population structure etc.? It is obvious that there is going to be some structure in reintroduced and domestic animals. I don't want to loose any important data and I want to be sure, that I have done everything correctly.
Thank you for your help.
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Lenka Ungrová If your population is large enough, it is recommended to perform HWE test.
I feel these papers give you some insight into which decision might be right for you:
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I would like to transfer the Dat-Cre transgene (B6 background) into a outbred strain (SW) of mice. How can this be done? Do I start with a single breeding pair (Dat-Cre B6 x SW) and then for every generation I backcross with a new SW, or do I have to start with several Dat-Cre x SW breedings? Any help is much appreciated, I am trying to understand what I need to do.
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You may limit your trials to the facility available and conduct replicated trials with the remainder to have a large base population.
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I'm studying the parish records of a small village in the XVI-XVIII centuries, where endogamy is quite common
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I am also study on inbreeding. How ever my study focus on River Terrapin (Batagur affinis). All the best and keep in touch ya.
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Hello,
I wanted to find some information about the ant species Liometopum microcephalum but poorly didn‘t find any...
My questions are:
Is this Dolichoderinae species polygynous
Do they have a proper nuptial flight, if so how far do they fly to mate?
Do they mate in air or on ground leven/on a tree?
How likely is inbreeding in this species?
thanks a lot in advance.
Best regards,
Andre Leonhardt
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Hello Andre; I don't have a citation for L microcephalum but this paper might give you a lead.
R Hoey-Chamberlain, MK Rust, JH Klotz
A Review of the Biology, Ecology and Behavior of Velvety Tree Ants of North America. Sociobiology 60(1): 1-10 (2013)
Best regards, Jim Des Lauriers
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I am working on marker assisted backcross breeding in rice and during the foreground selection I can see the band in donor as well as recipient parent although it is of different band size. The donor parent is showing the amplification of target allele which is justified but why my recipient parent is showing the amplification in different position? which I am assuming it should not show any amplification.
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If in doubt, cut and sequence.
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I have a pedigree structure of F1 generation and assuming no inbreeding in the pedigree. How can I estimate dominance relationship matrix by using the pedigree structure ?
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Hope some of these files be useful.
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Hello everyone,
I have a question regarding Bi-parental QTL mapping. In my genotype data, three parents are involved, e.g., X, Y, Z. All my materials are inbred lines and double-haploids. So, the individuals I have are either X*Y or X*Z. My genotype data is A, B, H translated. So, A= Homozygous for parent A(AA), B= Homozygous for parent B(BB), H=Heterozygous(AB).X was considered to be as parent A and Y/Z was considered as parent B while doing the ABH translation.
I am using RQtl for the QTL mapping. I am confused, which cross type should I use? If I use “cross-type =DH” it shows warning messages as three genotypes are involved. Which cross type should I use? Should I replace all H with missing values so that R can read it as DH or it is ok if I use “F2” as cross-type?
Thank you very much .Any kind of suggestion would be highly appreciated.
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Zachary Stansell Thank you very much.I removed all H from my genotype data as my mapping population is a DH and I got some H because of out crossing. After that read.cross function worked! Thank you for your kind help
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Hello everyone!
I'm working with the WES data of a family with hypothyroidism and deafness with an apparently AD inheritance; our group haven't had identified the genes involved in the developing of this illnes, so, we are interested in investigating the consanguineous state of the patients in order to have more information to analyze this case.
I'm a beginner in this kind of studies, so if you have some tips on how to infer the possible consanguinity status of the patients I will very appreciate your contributions .
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Google Brain Team recently released DeepVariant which you can use as an alternative to GATK.
We implemented a reproducible version that was submitted to NF-Core (https://lifebit.page.link/UW58).
We also made it available in Lifebit (https://lifebit.page.link/os1m) if you want to try it with example parameters.
In practice, DeepVariant first builds images based on the BAM file, then it uses a DeepLearning image recognition approach to obtain the variants and eventually it converts the output of the prediction in the standard VCF format.
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Effective population size is the central of evolutionary science. Genetic gain in modern breeding program for quantitative traits largely depends on the effective population size of the elite lines that are being used as parents. Due to inbreeding most of the elite lines attain narrow genetic base over time. Moreover, crossing elites with diverged germplasms often produce low yielding lines. Under this situation, is it possible to breed effectively for many decades with relatively smaller effective population size of the parental population?
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If you start a breeding program with a population that has a small effective breeding number you are limiting what you can achieve. The biggest problem is not inbreeding, but genetic drift, whcih results in the loss of alleles and thus reduces genetic variance. Inbreeding can be a cause for concern and needs to be managed in any breeding program. The small genetic variance in populations with a small effective breeding numbner is what will limit the response to selection. You might be lucky, but it would be a risky bet since selective breeding programs take time and are expensive. A good example of what happens if you try to start a selective breeding program for increased growth in a population that was founded with a small effective breeding number can be found in Tave and Smitherman (1980)--on my RG site--and Teichert-Coddington and Smitherman (1988) Trans Am Fish Soc 117:297-300. There was little heritability for growth and selection could not improve it.
You mentioned crossing divergent lines often produces poor F1 hybrids. That is true. Hybrid vigor is due to dominance genetic variance and that is hit or miss. You cannot predict which crosses will nick and produce great hybrids and which will produce duds. You make crosses and see what happens.
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A large proportion of plants produced by selfing shows lethal characteristics due to inbreeding.
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Inbreeding depression has been reported in self pollinated crops for few characters in few crops. The negative genes that lead to inbreeding depression when homozygous can be removed from a population as the affected individuals die (or fail to breed) and take their negative genes with them.
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I am aware of the pedigree and kinship2 libraries in R, but functionality is limited. Programs like EASYPOP can save pedigree information but are not focused on simulation of pedigree parameters specifically. I am interested in looking at e.g. the impact of founder inbreeding levels (usually assumed to be zero) on kinship estimates in subsequent generations.
I am just asking before trying to do something from scratch. :)
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Use Vortex. You can use your pmx files as input and also provide microsatellite data. We did some simulations assuming different founder assumtions. Worked quite well.
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In my Ph.D research work i need to know n calculate inbreeding coefficient and depression in maize So to S5 generations and how its moving from generation to generation in case of half sibs, full sibs and selfed generation.....can suggest research paper r any reports , books ...
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Inbreeding coefficient is the probability that in an individual at any locus the alleles are identical by descent (IBD). The coefficient of inbreeding (F) of an offspring is equal to the coefficient of coancestry (f) between its parents. For Half-sibs you have Parent A, B, and C with alleles a1a2, b1b2, and c1c2 respectively, which give origin to individuals X and Y with alleles x1x2 and y1y2. Parents for X are A and B, while parents for Y are C and B. The coefficient of coancestry (f) for X and Y will be f_xy = 1/4(f_AC + f_AB + f_BC + f_BB) where f_AC = 1/4(P(a1=c1)+P(a1=c2) +P(a2=c1)+P(a2=c2)) [P = probability that allele a= be equal to allele c1], and f_BB = 1/4(P(b1=b1)+P(b1=b2)+P(b2=b1)+P(b2=b2)) = 1/4(1+F_B+F_B+1) = 1/2(1+F_X).
For full sibs it will be similar but parents A and B give origin to the individuals X and Y. I suggest you to check Rex Bernardo's Book, Breeding for quantitative traits in plants pages 35-44.
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Does anyone know of literature documenting unexpected cases of sterility or sub-fertility in wild populations of animals? I'm not looking for examples where there is known social suppression or sub-fertility due to disease or inbreeding. Even case studies would be useful. Thanks.
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thanks
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Pleiotropy occurs when one gene influences two or more seemingly unrelated phenotypic traits. (from Wikipedia)
(from Greek πλείων pleion, "more", and τρόπος tropos, "way")
Pleiotropy is a relatively obscure word but it is a concept with very deep implications. Some define is using "unrelated" and some "seemingly unrelated" and this itself illustrates the difficulties in understanding this concept.
There are 3 fundamental commonalities of biological systems that relate to pleiotropy:
1) Due to the economy of evolution by natural selection, components of systems and the systems themselves systems are multi-functional.
2) Due to advantages mediated by group interactions, components of systems and the systems themselves systems are interdependent.
3) Due to advantages mediated by group interactions, some proportion of beings are interdependent intra-specifically and extra-specifically.
We would like to affect desirable changes in the our evolution and the evolution of the beings we attempt to manage (crops, livestock, pets...). We have done this through selective breeding currently and in the past, and are focusing effort to do this is a directed focused manner currently though biotechnology.
Managing the our evolution and the evolution of the beings we manage is a brutal ugly endeavor. This oppositional process generates immeasurable amounts of suffering. The natural process is little better. The wild process is little better.
Natural or directed, efforts to control evolution are complicated by both pleiotropy and genetic bottlenecking. Both have left huge scars on mankind and the beings we try to manage.
Anything we actively or passively select for or against, will also actively or passively select for or against other traits and tendencies. These silent passengers may not manifest until certain environmental, dietary or social conditionals are met.
A readily observable example of this can be seen in "pure-bread dogs". Purebred dogs have a group of observable and silent traits associated with the breed, that make it readily distinguishable from other breeds. The amount of suffering, inbreeding, and bottle-necking that went into making these breeds is unimaginable. Now we have purebred dogs that look striking, are suited to certain tasks, and are relatively healthy when they are young. These are the criteria dog breeders chose when crafting the breed. These purebred dogs may breed "champions" but overall they are unhealthy at every age, and simply fall apart as they age. When we made purebreds there was a lot of baggage due to pleiotropy and genetic bottle-necking that came along for the ride.
We are currently engaging in intense directed and natural selection for privileged positions in human societies. We design complex testing systems people must compete to even be tested, and then must win to gain "advantage", all with the illusion of objectivity. But there is little objectivity and very specific traits are being selected for. The conditions we impose and those we give advantage to will have pleiotropic effects both on individuals and society.
Long term survival is is a balance between leveraging short and medium term advantages while at the same time maintaining enough diversity and flexibility to pass infrequent/random environmental or social conditionals which can present at any time. Even huge advantage and numerical represntation in a given environment and time means little if an environmantal conditional presents the day later that a species cannot pass and leads to extinction.
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Its understanding is a great tool in selection and to encourage local or indigenous desired breed.
I believe the understanding will help the evolutionary world and all life science researchers
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Hello dears
I want to design primers for validation of alleles in RIL population of two inbreed lines one is sensitive and second is resistance.
I have run the PCR of two lines and got the targeted sequence to identify the SNP and InDel. Now I want to distinguish the favourable allele variation in RILs.
Q1, how to design Primers ?
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You can use melt-curve based genotyping. Include a fluorescent dye in your PCR mix (I used SYBR Greener) and use a real-time PCR machine just for the melt-curve. You can easily detect small InDels and SNPS if your PCR products are SMALL (80-200 bp).
To design the primers, you need to know the DNA sequence that surrounds your SNP and/or Indels. I use Primer3 plus http://www.bioinformatics.nl/cgi-bin/primer3plus/primer3plus.cgi
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I am investigating on accessions of Brassica olearacea, which are in their fourth circle of reproduction in a gene bank. They show a reduced germination rate und different phenotypical symptoms. Does anyone of you has experiences with effects of the decrease of genetic diversity due to the seed bank conservation? What kind of phenotypical symptoms would be expected? How to counteract if some form of low diversity limit is reached?
Thank you for any comment!
Jannis
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Thank all of you for your advices!
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Hello dears
I would like ask that how I can calculate the SNP and InDel data cause I have done the multiple sequence alignment by using BioEdit software. here I have confusion cause I have used 300 inbreed lines of GWAS study. let me know please detail information .
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After aligning your libraries against the reference genome, you can also use SAMTOOLS (as an alternative to GATK's) for SNP and INDELs detection, but before doing so make sure you remove the PCR duplicates. The resulted file with the variants (VCF file) should be filtered accordingly (i.e based on the coverage) and finally you should annotate the SNPs and INDELs for your GWAS (you can use Annovar or snpEff for the annotation).
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If a pop. of 50 has high allelic diversity, low Ho, a moderately high F-index, does this indicate genetic drift, inbreeding and non-random mating? Would it be all three? Can't yo have non-random or selective mating without inbreeding? Could selective mating indicate high fitness? Thanks!
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First question you have to ask:
- can this relate to the some issues with the markers (null alleles in STR for instance)?
- if not, this can be typically explained by non-random mating / population structure/ Walhund effect. The use of inbreeding is tricky here in the sense where individuals are expected to be more more inbred than under HW; however at the population level, this does not imply any specific genetic drift.
So to answer to your questions (once your this does not relate to your markers):
- Does it indicate genetic drift? Not at population level. Inbreeding? Not at population level. Non-random mating. Yes, clearly
- Can't yo have non-random or selective mating without inbreeding? It depends how do you define inbreeding. If it is in the sense of genetic variability reduction at population level, non-random or selective mating does not necessarily imply inbreeding.
- Could selective mating indicate high fitness? In general the explanation is not this one, but without knowing the context it is difficult to say.
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Does inbreeding affect the equilibrium just like mutation, genetic drift and so on?
Thank you!
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Crow & Kimura. 1970. Introduction to Population Genetics Theory. p. 65.
Genotype      Frequency
AA                p^2*(1-f) + p*f
Aa                2pq(1-f)
aa                q^2*(1-f) + q*f
f is the inbreeding coefficient. With f=0 you have the standard HW proportions. With f=1 there are no heteozygous Aa.
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Hi.
The difference between expected and observed heterozygosity gives you the f coefficient which says you whether your population experiences inbreeding or not, right?
But since these differences between observed and expected heterozygosities are deviatons from H-W equilibium, are they also useful for assesing the effect of other evolutionary forces other than non-random mating? What other kind of information can you get from this difference? Does the wahlund effect deals with this difference? 
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Thanks for your answer! I will pay attention on Wahlund effects. So, is it expected that the number of observed heterozygotes will be low when you have a clear population structure?
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I have a large SNP dataset and am looking at differences in inbreeding in a several populations.
I've calculated per locus and average FIS per population in the R package, hierfstat. I also used the bootstrap method in hierfstat to calculate the 95% CI around the average FIS for each population.
I've also calculated the individual inbreeding coefficient (F) in PLINK.
For some populations the average individual inbreeding coefficient (per population) in higher than the average FIS and falls outside of the calculated 95% CI.
Can anyone tell me why (biologically) individual inbreeding might be higher than population-level inbreeding?
Cheers 
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Hi Lauren
F= 1-H0/He
and
(1-Fis)(1-Fst)=1-Fit
And depending on your hierarchichal structure, these terms will vary.. You can have a look at Arlequin manual to see different definition with different structures.
Pablo
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How are the effects of a polygamous mating system on inbreeding
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Polygamous mating system in a closed community or population may accelerate the inbreeding depression as the chances of two individual carrying the same gene mutation increases. 
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There are severals predictions about that populations with a history of inbreeding would show less inbreeding depression (because deleterious mutations had been purged) tha populations with little or no prior inbreeding.The history of inbreeding was inferred by severals methods, including average inbreeding coefficients, morphology flower and populations size, and others. Inbreeding depression was usually estimated by comparing fitness components in experimental inbred populations to noninbred populations and estimating of severals parameters in the populations.
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Hello everyone.
I am planning to study the genetic diversity and also the inbreeding level of insect population. 
at the moment, i had collected the insect samples from several sampling sites. Each samples had been bulked based on the sampling sites. Then, the samples were extracted and amplified using mitochondrion gene (COI) and did the sequencing. The sequence data had been availabe to generate the philogenetic tree.
i am bit confused, how can i utilise this data to calculate for the inbreeding level? is there any formula to calculate from the mitochondrion sequence?
Please post your valuable suggestions.
Thank you...
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Dear Yogo,
Unfortunately, sequencing COI isn't likely going to help you estimate inbreeding in your populations.  Because mitochondrial DNA is (usually) only inherited from the female parent, it's not possible to assess homozygosity in individuals through identify by descent (IBD) as it would be for diploid markers that are inherited from both parents.  Also, one of the reasons that COI is so useful for DNA barcoding is because of its tendency to be mostly invariant within species while often showing diagnostic differences between closely related species.  For the same reason, haplotype diversity within your populations is likely to be low, which could be misinterpreted as inbreeding but more likely reflects the characteristics of the gene itself. 
The best you can probably do with the COI sequences is estimate nucleon (h) and nucleotide (pi) diversity.  If you see much variation within or among your populations you may have evidence of either cryptic species or multiple evolutionary lineages within your species.  If there's enough variation, you may also be able to do a coalescent analysis to get at the historical demography of the populations and species, which could let you indirectly assess population-level coancestry (with some caveats).  If inbreeding is the main question you're wanting to address, you'd be better off to use diploid markers. 
Hope this helps!
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What is time point for use of in breed mice in in vivo infection study also how can we identify our experimental mice as are really in breed?
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Dear Ajay,
I found some valuable information for you,
Genetic background or strain determination must look at markers across the whole genome, so there is no simple test. The easiest would be to send your DNA to the Jackson labs and they will do this for you for around $200 (Last year price). if you have any other question, please don't hesitate to write me,
Affectionately,
Mehdi
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I am interested to undertake a study on determination of level of inbreeding in elephant population in an isolated habitat. The nature of study area is thick forest, hence collection of fecal samples  is the relevant approach to study Genetics of elephants. Anybody who is familiar and experienced in designing protocol of collection and analysis of DNA Fecal Samples. The population is not well known, population number is approximated 102 elephants. Thanks
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You have to collect the fresh dung samples for better result. Fresh samples (less than 24 hours freshness) has higher DNA quality than older samples. But you can consider collecting 2/3 days old samples too. You have to collect the dung's outer layer and store in 95% ethanol. 
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If inbreeding is followed for hybrids then for races which method is adopted?
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Dear Dr G.vishnu brindha Devi
Prima facie, when you cross hybrid you get 75% dominant (If it is not case of over dominance) and 25% recessive or If it is a  case of over dominance   you get 25%dominant 50% hybrid vigor and 25% recessive. For obtaining a desired hybrid you use marker for crossing certain genes
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Are there any methods for inbreed testing (laboratory tests) among of animals?
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Genetic background or strain determination must look at markers across the whole genome, so there is no simple test.  The easiest would be to send your DNA to the Jackson labs and they will do this for you for around $200.  Sorry, but that is about as easy and cheap as this will get. 
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I find significant positive Fis in a population I am not expecting to be inbred, could this be a true signal of inbreeding? or are the some factors that can cause a false signal of inbreeding in this population?
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In reality Fis is not really a signature of inbreeding... it's a signature of heterozygote deficit, which can be related to inbreeding. The reasons of positive Fis can be either related to markers or populations. Here are some possible explanations:
- with microsatellite, existance of null alleles
- population structure, related  to existance of subpopulation (wahlund effect), or preferential mating
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If genetic drift causes to homogeneous population with strong characters to survive in a particular environment, how does inbreeding lead that to a weak, unstable population...?
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Inbreeding has no effect on genetic drift. Inbreeding causes however stronger selection against recessive deleterious traits. Populations where deleterious genes become fixated as a consequence of random effects (genetic drift) may loose their viability (as seems to be the case for animals where only a few individuals are still alive) 
I do not know if this is the answer to the question posed, as this question is not very clearly stated...
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We developed more than 10, 1st generation primary hybrids using different parents. It is expected inbreeding and lethal, if they were selfed for generating F2 material. Are there any alternative methods or models?   
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For not letal hybrids it need to know the numbers of chromosome and used often only polyploid forms.
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Hello, I have used FSTAT for counting average Fis (inbreeding coefficient) per population. In some populations one locus is completely homozygous and FSTAT doesn't add it when counting average Fis for that population. I have a feeling that I should count that locus as Fis=1 and add it normally to the average. So if I have  for one population loci  with Fis 0.640,  -0.069, homozygous and  -0.297, should I average only those three non-homozygous as FSTAT did or should I average also with homozygous locus with Fis=1? Thank you!
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I suppose FSTAT is doing the right thing. The locus with Fi=1 is not contributing to diversity. However, since this Fi (=1) is an estimate, you can ask FSTAT to provide a 95% CI of this, and then possibly use the lower limit to get your average! 
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I am using dominant markers (AFLP) to assess the genetic diversity of a plant. I don´t have reliable information about the mating system, so I´d like to estimate gene diversity assuming both Hardy–Weinberg equilibrium and total inbreeding. POPGENE is supposed to do that, but when I do the analysis with the assumption of HWE or total inbreeding i get exactly the same results. What I am doing wrong?
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dear Ziva,
you should use AFLPSurv (http://www.ulb.ac.be/sciences/lagev/aflp-surv.html) which explicitly gives to options to calculate gene diversity of AFLP markers with the assumption of  either total inbreeding (option 1) or HWE (options 2..4), the latter again with different approaches to estimate allele frequencies.
regards
Walter
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There are classic examples of heterozygote superiority (e.g., the malarial resistance of individuals heterozygous for the sickle-cell gene). But, how common — across the genome and across taxa — is heterozygote superiority?
I can think of two crudely relevant data points. In a wide array of taxa well over 50% of loci are monomorphic (which suggests no heterozygote advantage at those loci). On the other hand, inbreeding depression implies a homozygote disadvantage, at least at some loci.
The reason I said these facts are crudely relevant is because of a 2002 paper by Derek Roff where he presents experimental evidence that inbreeding depression (in a cricket) results more from an increased incidence of harmful recessives than from a reduction in the frequency of beneficial heterozygotes. If that result generalizes it does not argue for the prevalence of heterozygote superiority. Any thoughts?
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Dear Steven, I think different topics might be slightly muddled in this question: 1) the heterozygote advantage in cases where the effect of a single gene on the phenotype is well known and has strong phenotypic effects, with 2) heterozygosity advantage as one of the mechanisms underlying inbreeding depression. The first case you mention, is not central to the final question you pose. In the second case, molecular ecologists tend to use heterozygosity measured in neutral markers to infer inbreeding levels in natural populations, or to reveal the strength of the associations between heterozygosity and fitness-related traits. Most often this refers to complex traits (affected by many genes) normally distributed and hence that are amenable of study using quantitative genetics techniques. Thus, when looking at empirical studies it is important to find-out what genes (coding, non-coding), the strength of their effects, the number of genes/markers and what type of trait (simple or complex) the researchers are dealing with.
First, sickle cell anemia is an example of heterozygote advantage, one of the mechanisms that allow the maintenance of genetic polymorphism through balancing selection. The other well-known mechanism is frequency-dependent selection (as in the peppered moth phenotypic change to melanic forms during the industrial revolution). Thus the heterozygote advantage of the sickle-cell gene is context-dependent and depends on the frequency of the protozoan parasite in the population; outside malaria infested areas there is no such heterozygote advantage. So for answering your first question “how common — across the genome and across taxa is heterozygote superiority?” you would have to first account as well for the context-dependency and reformulate your question as follows: “how common — across the genome, taxa, and environmental contexts (phenotype by environment interactions) is heterozygote superiority?”. But there is more to this, because the answer won't be the same for complex traits (dozens of genes) and simple traits (1 gene).
Second, and importantly, regarding your second point: inbreeding depression does exclusively imply a homozygote disadvantage; there are other potential mechanisms such as overdominance (with neutral markers you can also have associative overdominance). Inbreeding depression is just the reduction in fitness that happens with the increase in frequency of mating between related individuals (recognized by Darwin in 1868 and formally defined by Morton 1956). Roff’s 2002 empirical study supported the partial dominance hypothesis, which had been previously highlighted as the main underlying mechanism by the Charlesworth’s. It overall seems that the overdominance hypothesis has received significantly less support than the others (recessives, or mild recessives). 
I am unsure of at what level you want to explore this question further. If you want to dive more in the theory of quantitative genetics behind it go for the Charlesworth work, recent chapters by Bruce Walsh ( I think they are available online), Patrice David... If you are interested on heterozygosity-fitness correlations in wild populations (using neutral markers) you should start looking at Chapman 2011 (recent review in Mol Ecol), work from Amos, Aparicio, Balloux, Coltman, Coulson, Hansson, Keller, Ortego, Pemberton, Slate, etc… (these authors have also worked on the power of different heterozygosity-based measures). For papers showing heterozygosity on coding loci or allozymes on fitness traits such as growth or metabolic efficiency you should look at 70s-80s work on invertebrates. Mitton and Grant 1984 gives a good overview. Hope this helps.
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Taking several confounding factors, such as residence, SES, mothers age, populations, inbreeding etc how can we get an adjusted value and risk analysis (odds ratio). Which software is best for such analysis?
The reproductive features are: Fertility, mortality, sex ratio, selection intensity. For each of the reproductive feature please suggest an appropriate statistical model. 
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Hi. There are free and for purchasing options. Among the free options, I suggest you EpiInfo from www.cdc.gov it could be easy for you. R is a powerful free software, but it is complex. Among purchasing options, I think Stata is a balanced option between performance and cost. Best regards.
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Inbreeding coefficient
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Lethal equivalents from coefficient of inbreeding can be measured with your observations using General Linear Models (GLM) and Regression equations. Most of the researchers have found the fitness of population decline in proportion with increasing inbreeding coefficient (F).
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I have 21 inbred lines from one source and another 24 from a different source. Which mating design will be best in studying the gene action and combining ability of all these lines? Which statistical software is freely available for analysis?
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The final purpose is to get both line completely inbred?
The "classical way" is described extensively by Jackson Lab using 20 incrossing (did not found the original link)
Here a paper often quoted on the statistic
Abiola et al. 2003 PMID: 14634638
AND
Welsh et al. 2012 DOI:10.1534/g3.111.001784
Newer methods using 5 inbreed was established using genetic matching:
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Dear all,
We work with large families with mendelian inherited diseases. Parents of sick children are often related with each other. However, sometimes we do not know about the degree of relationship (e.g. second cousin or third cousin). Therefore we want to calculate inbreeding coefficients using SNP genotype data (AA, AB and BB). We use GenomeStudio. We tried Plink with `plink input report 2.1.3´ plug-in of GS but inbreeding coefficients had negative value. What do you think is the problem? Could you suggest another software or another way to calculate? Thanks.
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Dear Nehir,
I have a long-term experience working in highly inbred genetic isolates for mapping genes of complex diseases. I using several methods for F evaluation in the isolates , in the pedigrees and based on genome scanned STRs and SNPs.  Currently for SNPsw analyses I'm using Golden Helix SVS software that has much options, including HWE, coefficient of inbreeding etc. You can use it for evaluation of F (coefficient of inbreeding) based  on SNPs. If you will get negative F -this says about  larger number of observed heterozygotic subjects than expected. I have got such negative F as well but only in demographically younger genetic isolates (sec ondary isolates according Neel' (1992) definition)- negative F in this case says about 'younger' inbreeding (in latest generations) in comparison with positive F I observed in demographically ancient genetic isolates of indigeneous small ethnics that have traditional consanguneus marriages in their ancient history. Just one more note: F calculated by different methods will have different values, don't be confused with that. Hope, this information will be helpful for you. Best wishes
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My lab just finished gathering the phylogenetic microsatellite data on several populations of a plant species. After a quick and dirty initial analysis with GenAlex, we found six alleles across all the populations showing high mean heterozygosity and low mean Fis (negative values). The seventh allele is showing exactly the opposite with 100% homozygosity in every individual and population. I am just curious if anyone has ever come across this phenomenon before and what a reasonable genetic explanation may be for this fixation. Since we are speaking about microsatellite markers, I do not expect selection and genetic fixation of an allele at all, let alone across every population examined.
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I am guessing you mean 7 loci and not alleles. For the locus that is 100 percent homozygous, is it fixed for the same repeat in all populations? If so, that just means it is not variable and therefore doesn't provide any information.
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It seems there is hardly any difference between the founder effect and bottleneck effect that leads to the same conclusion that the alleles in the population are not subject to change and over time recessiveness can be due to inbreeding.
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Bottleneck effect and Founder effect are basically both names for the same phenomenon. When the effective population size of a group of individuals falls, the rate at which alleles identical by descent end up in the same individual increases = increased inbreeding and increase in the visibility of recessive alleles in the homozygous state and an possibly hence inbreeding depression etc. Bottleneck is a general term coined for several different cases of population number collapse; The Founder is one instance of the process associated with the phenomenon at the edge of a populations range when a few individuals 'move out' or occupy new territory and form the basis of an expanded population in the new range. So that that population suffers 'a bottleneck' or population constriction in numbers.
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The phenomenon of inbreeding increases the level of homozygotes for autosomal recessive genetic disorders and generally leads to a decreased fitness of a population known as inbreeding depression.
Inbreeding has been associated with increased risk of adverse prenatal outcomes including stillbirths, low birth weight, preterm delivery, abortion, infant and child mortality, congenital birth defects, cognitive impairments, malformations and many other complex disorders.
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You will have to obtain a measurement of how much an individual is inbred (for example, by genetic markers or by reliable lineage or marriage data several generations backwards) and then mesaure the outcomes of interest (for example, IQ) in each individual. With these measures you could conduct simple regression analysis to see whether (and how much) inbreeding is associated with IQ. I would, however, make sure to look for curvelinear associations, because strong outbreeding could, at least, teoretically have negative effects as well.
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For example, we are taking increasing value of inbreeding coefficients on X-axis and on any trait or disease prevalence on Y-axis.
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Carlos, are you an analytical chemist? Then you should have a look on biological, physcological, economical data. In all subjects (even hard core physics and astronomy) there are correlations that might be much much lower than 0.9 and those are still very very interesting, "significant" or relevant. It depends on the context. You should not give such general advices that turn out to be generally wrong.
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The phenomenon of inbreeding increases the level of homozygotes for autosomal recessive genetic disorders and generally leads to a decreased fitness of a population known as inbreeding depression which is a major objective in clinical studies.
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I think that the solution to this very real problem is counter intuitive to our cultural and societal norm/beliefs that we should marry and have children with those from similar cultural, religious, and ethnic backgrounds. In the animal kingdom, males often leave the family unit and breed with females in other groups. This adds strength to the species. Even though humans are not generally having children with immediate relatives, they tend to stay within their familiar group for social reasons. This is why we get thalasemia, tay saks, sickle cell, and other varied cancers and metabolic diseases. Our social practices have not caught up with our genetic needs.
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I am trying to figure out the best approach to determine the effect of fragmentation on the standing genetic variation in a population. We have the relatedness data of the individuals in the form of a family pedigree (20-30 years of data, ~500 individuals). This means we can estimate a relatedness matrix for all living individuals. Till now, the population has been allowed to freely mix, and did so often over long distances. However, changes in the environment is going to restrict these movements to a degree. The sub populations are going to be rather variable in size from a less than 10 to more than 150. We will get an estimate of the reduction in these movements. What I want to do is model/estimate what the effect is of these reduced movements on the standing genetic variation of the population as a whole. I am thinking of using some genetic drift principles to model these things. What would others suggest?
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I am not sure you can say much about SGV with only pedigree data. And depending on the degree of a barrier, you might not see very much in such a short period of time in terms of how your relatedness matrix correlates to habitat fragmentation.
But modelling drift is a good start - you could do some coalescence modelling of populations of different sizes with different degrees of migration and see if you can differentiate it from a null model.
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Because in available cultivated sunflowers there is a very very narrow genetic base. In that situation, how can we develop diverse inbred lines for different traits.
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hi dear Dr, Prakash; may be these are usefull;
1- Todorova, M., P. Ivanov, et al. (1997). "Doubled haploid production of sunflower (Helianthus annuus L.) through irradiated pollen-induced parthenogenesis." Euphytica 97(3): 249-254.
2-Jan et al. Present and future plans of the sunflower “Doubled Haploid” project, USDA project