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Questions related to Animal Genetics
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I am planning on inducing a young cohort of mice with tamoxifen between the age range of P21 to P28 (3-4 weeks). I was planning on using the calculations that I have used for adult mice (>8 weeks). Those calculations being tamoxifen dissolved in corn oil at a concentration of 20mg/mL and then injecting at a dose of 75mg (tamoxifen)/kg (bodyweight). These being the suggested calculations from Jackson Labs. Will I be okay to administer to the same concentration and dose at this age range?
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Yes, as long as you adjust for their body weight, it should be fine. I inject with hydroxytamoxifen at 6 weeks, but weigh the mice first and adjust accordingly.
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is there any ways that i can find genome similarity of an organism without whole genome sequencing ,like using maths formulas or experimental progress ?
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Prior to the era of whole genome sequencing, people were estimating similarity using DNA-DNA hybridization.
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Maybe impossible to discern yet, an Egyptian plover can maybe clean a Crocodile's mouth without getting eaten.
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Of the living birds, the birds of the infraclass Palaeognathae are the closest to alligators: Ostriches, Rheas, Tinamous etc....
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Please talk about the topics you are familiar with or things which makes sense (recommendation) on this site as this is not a general social media.
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I am relatively new to the genetics field and am curious if their is an established way of representing BAC transgenic mouse models. I know that a homozygous knockout trangenic model is expressed -/- etc. I was just curious if there is a correct notation for the addition of a BAC in a mouse model. Thank you.
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One effective way to represent BAC transgenic mice in a figure is to create a simplified schematic diagram. This diagram should include a depiction of a mouse with labeled components such as the BAC transgene and any relevant promoter regions, along with arrows or annotations indicating gene expression patterns or other key features. This approach provides a clear and concise visual representation of the transgenic mouse model and its essential elements
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Would you please let me to know about the methods for measurement of medullation and Kemp % on animal? My problem is that the wool sampling and sending to laboratory is not possible. So I would like to verify the possibility of a method to measure Kemp/medullation % in wool rapidly on the animal. I know "Benzene test" (attached file) for distinguishing of Kemp fibers, but Benzene is a risky material. Furthermore the use of portable OFDA in our situation is not possible.
Is there safe substance similar to benzene that has the similar optical refractive index ? Which safe liquid can be found that has a light refractive index similar to wool? (1.54). Sincerely,
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Response to my question by CHATGPT:
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How we can measure Kemp % in wool without using of benzene?
ChatGPT
Measuring the Kemp percentage in wool typically involves microscopic examination, but it can be done without the use of benzene. Here's a general procedure using a microscope and without the use of benzene:
Materials Needed:
  1. Microscope: A microscope with sufficient magnification for detailed fiber examination.
  2. Prepared Wool Samples: Obtain representative wool samples for analysis.
  3. Slides and Coverslips: To prepare slides for microscopic examination.
  4. Light Source: Ensure proper lighting for clear visibility.
Procedure:
  1. Prepare Wool Samples:
    • Cut a small section of wool from the sample for analysis.
  2. Create Microscopic Slides:
    • Place a small amount of the wool sample on a microscope slide.
    • Add a coverslip to create a flat surface for examination.
  3. Microscopic Examination:
    • Examine the wool fibers under the microscope at sufficient magnification (typically 100x to 400x).
    • Identify kemp fibers, which are coarser, thicker, and often have a more translucent appearance compared to regular wool fibers.
  4. Count Kemp Fibers:
    • Count the number of kemp fibers in the sample.
    • For a more accurate measurement, consider counting kemp fibers in multiple fields of view and taking an average.
  5. Calculate Kemp Percentage:
    • Calculate the Kemp percentage using the formula:
Kemp Percentage=(Number of Kemp FibersTotal Number of Fibers)×100Kemp Percentage=(Total Number of FibersNumber of Kemp Fibers​)×100
Notes:
  • Quality of Microscope: Ensure that the microscope used provides clear and detailed visibility to distinguish between regular wool fibers and kemp fibers.
  • Sampling: For representative results, take multiple samples from different areas of the wool lot.
  • Observation Criteria: Define clear criteria for identifying kemp fibers to maintain consistency in your observations.
This method doesn't involve the use of benzene, but it's important to note that microscopic examination is still crucial. If you encounter challenges or limitations, you may want to explore advanced image analysis techniques or consider seeking assistance from a specialized laboratory equipped for fiber analysis. Always prioritize safety and ethical considerations in any testing procedures.
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But I need a quick and tool-free method without a microscope.
ChatGPT
I understand the need for a quick and tool-free method without a microscope. While a thorough analysis of Kemp fibers typically requires microscopic examination, you can try a more rudimentary visual inspection approach. Keep in mind that this method may not be as precise as microscopic examination but can provide a rough estimate. Here's a simplified method:
Visual Inspection Method:
  1. Prepare the Wool Sample:
    • Cut a small representative section of wool from your sample.
  2. Separation of Fibers:
    • Spread out the wool fibers and separate them as much as possible.
  3. Visual Inspection:
    • Examine the wool fibers visually for any noticeable differences.
    • Look for fibers that appear thicker, coarser, or have a more translucent quality compared to the majority of fibers.
  4. Count Kemp Fibers:
    • Count the number of fibers that exhibit characteristics of kemp fibers.
    • For a more accurate estimate, consider counting kemp fibers in multiple sections of the sample.
  5. Calculate Kemp Percentage:
    • Use the formula:
Kemp Percentage=(Number of Kemp FibersTotal Number of Fibers)×100Kemp Percentage=(Total Number of FibersNumber of Kemp Fibers​)×100
Considerations:
  • This method relies on visual inspection and is subject to individual judgment.
  • It provides a rough estimate and may not be as accurate as microscopic examination.
  • For a more precise measurement, consider sending samples to a laboratory equipped for detailed fiber analysis.
While this method does not involve a microscope or chemicals, it's important to note its limitations. For more accurate and reliable results, especially in commercial or research contexts, microscopic examination or professional laboratory analysis is recommended.
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Please explain this method with a photo
ChatGPT
I'm afraid I cannot provide images directly, but I can guide you on what to look for during a visual inspection for Kemp fibers. Please note that this method is a simplified approach and might not be as accurate as microscopic examination. For more precise analysis, consulting a professional laboratory is recommended.
Visual Inspection Steps:
  1. Prepare the Wool Sample:
    • Cut a small, representative section of wool from your sample.
  2. Separation of Fibers:
    • Spread out the wool fibers on a clean surface and separate them as much as possible.
  3. Visual Inspection:
    • Look for fibers that exhibit characteristics of Kemp fibers. Key features to observe include:
      • Thickness: Kemp fibers are often thicker and coarser than regular wool fibers.
      • Translucency: Kemp fibers may appear more translucent than regular wool fibers.
      • Color: Kemp fibers might have a different color or shading compared to the rest of the wool.
  4. Count Kemp Fibers:
    • Count the number of fibers that display these characteristics.
  5. Calculate Kemp Percentage:
    • Use the formula: Kemp Percentage=(Number of Kemp FibersTotal Number of Fibers)×100Kemp Percentage=(Total Number of FibersNumber of Kemp Fibers​)×100
Visual Reference (Not an Actual Photo):
In the visual reference above (not an actual photo), you can imagine identifying thicker and coarser fibers with a more translucent appearance as potential Kemp fibers.
Remember, this visual inspection method is a basic approach and may not capture all Kemp fibers. For more accurate results, especially for commercial or research purposes, microscopic examination or professional laboratory analysis is recommended.
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Please explain this method with a photo. Or find an internet link with a photo please.
ChatGPT
I'm unable to provide images directly or browse the internet for specific photos. However, I can guide you on what to look for during a visual inspection for Kemp fibers, and you can use a search engine to find images as references.
Visual Inspection for Kemp Fibers:
  1. Thickness and Coarseness:
    • Kemp fibers are often thicker and coarser than regular wool fibers. Look for fibers with a visibly larger diameter.
  2. Translucency:
    • Kemp fibers may appear more translucent or have a lighter color than regular wool fibers. Hold them up to the light to observe any differences in transparency.
  3. Color Variation:
    • Kemp fibers might have a different color or shading compared to the rest of the wool. Look for fibers with noticeable color differences.
  4. Comparative Analysis:
    • Place a regular wool fiber next to a potential Kemp fiber for a side-by-side comparison. This can help highlight any differences in thickness, translucency, or color.
To find images for reference, you can use a search engine and look for terms such as "Kemp fibers in wool" or "Kemp wool vs regular wool." Ensure that the sources are reputable or from educational institutions, as accurate identification may require expertise.
Remember, while visual inspection can provide a rough estimate, microscopic examination remains the gold standard for precise analysis. If you have concerns about the accuracy of your visual inspection, consider seeking professional assistance from a laboratory equipped for fiber analysis.
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Who agrees with me that maybe technically I am over 100 Western European? How? Why? “I am over 100% Western European when all the max possible Western European blood percentages of my ethnicity estimate are added together and the highest possibilities of the other ethnicities are subtracted then I become over 100% Western European. Factors contributing to that genetic paradox are that I have a high mutational load(exemplified by my autism). And that the Southeast Asian Ethnicity is more Neanderthal than the European one”(Ohnemus 2023).
Supporting Sources:
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Check out your DNA - your certainty may well be rocky - many Scandinavians arrived in boats into today's Europe...
Christine
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Outcome depends on the type of food it takes right ? So if a cow consumes Genetically modified grass rather than normal will the quality of milk increase? And can we observe any changes in the behaviour ?
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One of the elements influencing the sensory qualities of milk and meat products is the kind of forages consumed by ruminants. The impact of the type of forages (corn silage, grass-based forages), the conservation strategy (hay versus silage), and the botanical composition of the grass on the sensory qualities of cheeses (colour, texture, flavour) are discussed for dairy products. There is no scientific evidence that genetically modified feed has an effect on milk output or composition. It is crucial to remember that cows consuming GM food do not modify an animal's (or a person's) DNA. Cow's milk has no GMOs. A contrast may be made to diabetics who use insulin; the individual does not become GMO. A dairy contrast is that a cow given chocolate does not produce the milk that comes from that animal.
Sravya Jasthi Hope this answer is relevant to your query.
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Dear experts: are all substrains of Bown Norway (BN) derived from the same strain? The most readily available strain is BN/Crl, but the reference genome is built on BN/NHsdMcwi. I was wondering if it's possible that those 2 strains were separately derived from the wild but both happened to be "brown norway".
Thank you!!
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No
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" In stark contrast to classical theory, the total heritable variance in a trait can be larger than the phenotypic variance in the trait, Var(TBV) > Var(P)..... In that case, a population contains a heritable variance which is greater than the observed phenotypic variance. Social interactions, therefore, result in hidden heritable variation ".( In book : Julius van der Werf et al. 2009 Adaptation and Fitness in Animal Populations - Page 116 )
Can Piter Bijama's sentence in the book be interpreted in this way: If in the formula heritability, genetic variance is greater than phenotypic variance, the heritability would be greater than one.!
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I agree with Rafat's view. I may add absence of sex linked effects, additive x additive interactions,epistasis and highly uniform prevalence of environmental interactions this minimising total phenotypic variance in the denominator ratio. Small SAMPLE SIZEstudied and unreliable standard error of h2 value are the major reasons for this situation to happen
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Can we arrive at true breeding values (TBVs) from average progeny performances, or would they still be estimated breeding values (EBVs)? Can true breeding values be found at all from retrospective phenotypic data (no genotypic data) of the animal?
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"The development and validation of a medium density SNP genotyping assay in Shrimp" is a research proposal I'm currently working on. Given the restricted budget allotted (9,600 USD) to the project, I'd like to know ahead of time how much it might probably cost me.
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sorry
outside my area of expertise
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Strictly going by the amount of research that has been done in the diapause phase (dauer) of C. elegans, which aspect (recovery, maintenance, entry) has received maximum attention.
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Hi, Pranjal Garg so first I would say you could search on Google Scholar. You should see, if the search is reduced to a minimum the question of citations. You could then do a search on Scopus and PubMed always getting the number of citations.
Trivially, if you also search on our ResearchGate portal you can find information on citations and various metrics such as interest related to that topic.
I hope I was helpful, if you need a hand in C. Elegans feel free to contact me.
Keep in touch.
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In Europe (in France and Germany at least), there is a new cultural-political position suggesting there were no human races … Not really … only as a delusion… as a constructed deception originating from the early modern times of beginning colonialism. – So not whites, no blacks (in former times: “negros” – sorry, I apologize for this), no yellow or Mongolian race, no Eskimos and so on.
The traditionalists in Europe still oppose this position and complain about a new ideological war with the progressive activists, who try for instance to make jobs dependent on compliance to the no-race-concept.
I would be especially interested in the opinions of coloured people and of non-Westerners. (But this is not meant as an exclusion … So all are invited (independent of any external traits) …).
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I do find this article belong to this research question.
The way that the media reports Black civil-rights protests has contributed to the long delay in reckoning with anti-Black racism, argues media researcher Danielle Kilgo. Kilgo and her colleagues used linguistic analysis to quantify narratives from newspapers, websites and television, mainly in the United States. The results reveal that civil-rights protesters are the least likely to have their concerns and demands presented substantively, compared with protestors focusing on other issues, such as women’s rights or gun control. “Less space is given to protesters’ quotes; more space to official sources,” she writes. “The dominant narrative accentuates trivial, disruptive and combative actions.”
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I have a database of snp genotypes analyzed with an Affimetryx platform I want to analyze with a reference genome, however I find obvious differences between Btau8 / UMD3.1.1 or ARS-UCD1.2, I must work with the latter that has been updated or keep me with UMD3.1.1?
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I would choose the last updated one, ARS-UCD1.2. There are quite important differences sometimes with previous assemblies, e.g. position of DGAT1 in ARS-UCD1.2 and in UMD3.1.1. If I would be the Reviewer I would ask for the most accurate/recent reference genome
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The application of conventional approaches in animal breeding ( selection and mating systems ) achieved very good results to improve the production traits of animals in the past and still working, far of the applications of molecular in the laboratories, what the molecular economic achievements in animal production.
Thank you for sharing your ideas
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In addition to the above, tools such as marker-assisted selection, genomic selection, post-genomic selection, and genome editing have yielded interesting results for animal breeding.
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I am a little bit confused about how to calculate reliability for EBV of each animal using the BLUPF90 program; taking into account repeated measures data, contemporary groups, and removing parent average effects. I think some programs of BLUPF90 family, such as ACCF90 and BLUPF90test, can compute the reliability directly through a few commands. How could I get them? May someone suggest me some ideas in order to create a script for that kind of analysis?
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Using Computer Programs JAA by Ignacy Misztal
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Cross-species sequence comparison is doing normally in sequence analysing. However, is it necessary or effective of doing corrections of the query sequence with the subject sequence when identifying an unknown species?
What is the underlying basis of correcting nucleotide mismatches of a query sequence?
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As a general rule, you should not correct ambiguities without referring to the chromatogram, unless you have multiple reads and can create a consensus.
Using an existing sequence as a template for correction is scientifically suspect as it can easily lead to confirmation bias. If an ambiguous sequence leads to an ambiguous identification, then that is the right result.
You may find that you need to replace ambiguity codes with 'N' in order to get comparison to work properly. Some programs, e.g. BLAST, treat the ambiguity codes as if they were nucleotides and search for a perfect character-for-character match.
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As mentioned before, i am interested to write a research paper in the field of poultry/broiler chicks, respectively in major of Animal Genetics and Reproduction, so i will be highly appreciated if someone come up with a great title for me.
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I following the best answer.
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I have tried to calculate genetic parameters using only Microsoft Excel ..
please tell me about an easy to understand application for calculating genetic parameters if I want to publish scopus articles at least Q3?
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For estimation of genetic parameter may software packages and algorithms are developed by different scientists. Harvay (1990) and wombat use sire and animal modal, respectively for estimations of parameters. Transcript for estimation of these parameters can b also written in R package. Thanks.
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I am thinking to investigate the roles of a specific gene during the embryonic development stages in a crab species. I was just wondering to ask about the possibility of gene knock-down or over-expression before hatching in aquatic animals.
Dose any have some experience regarding the drug/chemical/RNAi delivery into eggs in any aquatic animals?
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One problem you may face is that you do not have a genome or transcriptome. In that case you would need to sequence the part of the genome so that you can design the morpholino or CRISPR in order to perform knockdown (morpholino) or knockout (CRISPR). Unfortunately with CRISPR even if you do that you will not know what other sites in the genome the sgRNA has targetted - so maybe try both morpholino and CRISPR showing that both give the same phenotype.
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Hi Everyone,
I have a list of 2000 SNPs (chicken)and require to find close genes to all these 2000 SNPs.
I used to do that one by one in a small set of SNPs by using org.Gg.eg.DB, BiocManager, Entrezquery, and chicken database in R, but that way is most time-consuming.
It is appreciative, if anyone suggests to me a reasonable and practical way to do so.
Frankly, I have a hitch here and I need your constructive comments or suggestions.
Thanks in advance
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Hi,
As my friend Mr. Ghoreishifar and also Dr. Duy said, you can use R biomaRt package for this. You also can use the plink "--gene-report" command.
However, Here is a chunk of R code that helps you to find adjacent genes for your SNPs.
### Preparing Gallus Gallus Genes
library(biomaRt)
Gallus_Dataset = useMart(biomart = "ENSEMBL_MART_ENSEMBL", dataset = "ggallus_gene_ensembl",host = "www.ensembl.org")
genes = getBM(attributes = c("chromosome_name","external_gene_name", "ensembl_gene_id", "start_position", "end_position") ,mart = Gallus_Dataset)
genes$chromosome_name <- as.numeric(genes$chromosome_name) # please Ignore warning message
genes <- genes[!is.na(genes$chromosome_name),]
genes <- genes[order(genes$chromosome_name, genes$start_position),]
#################################
# your SNP list - you just need SNP, Chr, and position columns, and please use these colnames: SNP, Chr, position.
SNP_list <- read.table("your_SNPlist", header = T)
################################# loop
plusi=0; plusf=0 # if you need add an interval (e.g. 10000 for 10kb)
snp_ID = character()
chr_num = numeric()
SNP_Location = numeric()
Ens_Gene_Name = character ()
Gene_name <- character()
m = 1
for(k in 1:max(unique(genes$chromosome_name)))
{ cat("chromosome_Number:",k,"\n")
SNP = subset(SNP_list, SNP_list$Chr == k)
gene = subset(genes, genes$chromosome_name == k)
for(i in 1:length(SNP$Chr))
{
for(j in 1:length(gene$chromosome_name))
{
if((gene$start_position[j] - plusi) <= SNP$position[i] & SNP$position[i] <= (gene$end_position[j] + plusf))
{
snp_ID[m] = as.character(SNP$SNP[i])
chr_num[m] = SNP$Chromosome[i]
SNP_Location[m] = SNP$Location[i]
Ens_Gene_Name[m] = gene$ensembl_gene_id[j]
Gene_name[m] = gene$external_gene_name[j]
m = m + 1
}
}
}
}
My_Genes = data.frame(snp_ID,chr_num,SNP_Location, Ens_Gene_Name, Gene_name)
write.csv(My_Genes, file = "Genes.csv")
I didn't run the loop, please let me know if you have any problem.
Regards.
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Normally dN/dS ratios are calculated and interpreted as below one negative selection, above 1 is positive selection and 1 means neutral selection. How to interpret dS/dN ratios? Programs like SNAP provides dS/dN graphs and ratios.
For example:   
Averages of all pairwise comparisons: ds = 0.1678, dn = 0.4090, ds/dn = 0.4072, ps/pn = 0.4707
Please see image as well.
Can somebody explains it in simple words as I am not much familiar with this?
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Can anyone interpret the dN/dS=.099, which is defined as defualt in PAML when dS=0 or both dN=dS=0?
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A while ago the website of Qvotek went offline, and their supplies haven't been open for ordering.
We were using their custom 5 micron micropipettes/needles/tips for microinjections in zebra fish larvae. Is there any good alternative available?
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I can make these for you at Sutter!
Sincerely, Adair
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For context, our lab is working with a ROSA-tomato reporter line (strain B6.Cg-Gt(ROSA)26Sor<tm14(CAG-tdTomato)Hze>/ J) that we have crossed to several Cre mice for the purpose of identifying specific neuronal populations. While crossing these reporter mice into Cre lines appears to present no apparent problems for them, when we have attempted to cross them into additional lines (i.e. knockout or flox lines) in order to identify specific cells with the reporter (that say have receptor X knocked out as well) we've started to notice that over time the mice begin to develop bright pink pigmentation in their skin (i.e. bright pink paws, tails, feet, ears, etc). When we go to collect brains from these animals for physiological or histological experiments, we also notice that their brains are also bright pink! This has become problematic, as trying to identify specific cells in slices from these animals brains has been hampered by the presence of the reporter (to a lesser extent) in all the surrounding cells in the neural tissue.
I was wondering if anyone has ever experienced a similar problem if they have worked with this reporter strain in the past, and if they have any suggestions or details on how they tackled this issue when breeding up mice within this reporter line.
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For this reason we always use Cre positive males and never Cre positive females for breeding.
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I am working on a project involving parthenogenesis in crested geckos (Correlophus ciliatus), and I plan on comparing genes- particularly STRs- in samples from the eggs, the potential parents, and previous records (via GenBank, etc), to each other. However, I do not know how to successfully isolate DNA from a very early embryo in a shelled reptile egg. I will likely have to do this, because all the previous parthenogenic eggs from my geckos have failed long before complete development. Please excuse my phrasing, this is not a subject I have much experience in yet.
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I'm studying the polymorphism of a microsatellite related productive performance in 4 goat breeds and I would like to represent the distances between them according to its polymorphism (alleles and genotypes), which method is the most appropriate: PCoA, dendrogram,...? . Thank you in advance
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For me both are fine. As you want to show distance based on polymorphism, so you must show results in both graphs. It would be very nice presentation.
But I will prefer PCA over dendrogram, if you want to choose one of them.
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What do you think is the best genetic marker to define species?
In our genetic marker's world, what do you think is the best one to describe species, 12S, 16S, 18S, 28S, COI, COII, COIII, ITS1, ITS2 or Cytb?
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Sorry, i have no idea about COI and CytB.
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Hello,
I have some small secreted proteins which have the ability to move from plant to fungi. As they can move between plant and fungi, I assume these small secreted proteins have some domains responsible for their movement such as export and import domains. I am planning to generate a series of deletion constructs to identify domains that are responsible for protein movement. What might be the good experimental strategy to identify the domains? Is there any good system or experimental strategy that I can use for quick testing of my deletion constructs?
Thanks in advance
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Indeed the kind of experiment you use is too specific for general domain predicting tools (unless you know that there is a particular protein domain already observed to play a role in this process).
Despite that, testing deletions in silico is not so simples, especially if you want to make several deletions. One way I can think of is only possible if you have your protein PDB available. You can use Cytoscape [https://cytoscape.org/], and the RIN Analyzer plug-in [https://rinalyzer.de/]. RIN Analyzer created an interaction network between residues, allowing you to observe your protein as a network of nodes and edges. You need to read about the plug-in because it has tons of features and works with different other tools.
Then, you can use Interference [https://apps.cytoscape.org/apps/interference]. Interference allows you to create virtual knockouts, which reflects on a given set of topological parameters (You might need to send an e-mail to get it from the developers).
Please, check the version of Cytoscape to use both plug-ins because Interference is old. I also highlight that the use of these tools is an old protocol I tested, which provided some good results in a Protein-Protein Network, but I didn't test it in a Residue-Residue network. I don't know how it holds nowadays or if the developers still provide access to Interference. Nevertheless, this is a method I know, which is fast after you understand the tools.
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When working with eDNA we sometimes face some contamination, and it may lead to false-positive or negative, and I think if some of these cases, it creates a problem, or it may be interpreted as a grown on robustness, cause if we are using universal approach, we should be capable of finding any DNA sequences, like human DNA contamination, so what do you think about it?
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Abhijeet Singh I have some other questions on my page and a discussion where there is something that I think your opinion could really help me.
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I am completing my Master's in Biology on small mammal research (Sorex shrews) in Washington State. I am looking for a reliable lab in the US to send tail clips/liver samples to, to sequence the mitochondrial cytochrome b gene. I am hoping to use this to verify species and analyze relatedness between populations. Any advice is greatly appreciated!
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I have no opinion on the center M. cooper recommended but in case it does not work out I would suggest a visit to your MolBio department. DNA extraction and PCR amplification from such samples is usually rather straight forward using a kit such as:
OR
Good luck
Yoram
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If the virus is detected in serological and molecular tests is it interpreted as potentially zoonotic?
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If I have data of performance of chickens, biochemical analysis, egg production traits How calculate genetic correlation and phenotypic correlation?
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can i use GENSTAT to calculate the same
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Dear my professors and colleagues,
I prepare a review about use biotechnology and molecular marker at poultry breeding.
I want your help.
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Hello Dr. Esteftah
I recommend for you the following chapter
"Selection Methods in Poultry Breeding: From Genetics to Genomics"
Good Luck
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need help on finding biomarker for F1 hybrid and backcross of a fish species
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can you tell us how you overcame this problem?
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How to calculate PIC Polymorphism information content?
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You can also use GenAlex, an excel based software, for PIC estimations.
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How to calculate heterozygosity ?
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What happened to this pigeon's wing feathers?
Is it a genetically problem? Or a dietary deficiency?
What is your suggestion for treatment?
-It's sisters and brothers show this appearance too.
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Check for Ragged condition, which is genetical.
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Scientists rush to treat diseases with Gene Therapy: It must be good for Humanity, surely?
Eg: Cystic Fibrosis
But creating a method of delivery for genetic material may bring all the psychopaths out to play: could the delivery of genetic material be weaponised by errant regimes? Viral vectors may be an ideal weapon of mass destruction
Modern science demands that we publish all our methodology in great detail. But whose eyes are falling upon this research and should we not be thinking of a way to better control the flow of potentially catastrophic information?
Or is it too late? Pandora's Box...
' Most people were silent. I remembered the line from the Hindu scripture, the Bhagavad Gita; Vishnu is trying to persuade the Prince that he should do his duty and, to impress him, takes on his multi-armed form and says, 'Now I am become Death, the destroyer of worlds.'
J. Robert Oppenheimer - Wikipedia'
'Father of the Atom Bomb'
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Hi Fazleh, it is true that we are in this tight spot because any and all doctors can prescribe antibiotics to anybody ad libitum. Gene therapy is different because it has to be individualized.
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Research proposal in Animal Genetics and Breeding.
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Specially in the field of conservation of Indigenous breeds of livestock.
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Hello researchers
all of us know, that we need a special protocol to extract DNA from frozen blood other than protocol which used to extract DNA from fresh blood .
the question is : .what are the specific changes in blood properties that obligate us to use a special protocol to extract its DNA.
best regard
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I am aware that several genetic nomenclatures exist for specific groups of organisms. Unfortunatelly, such nomenclature is not available for my group (diatoms, microalgae, protists)and I did not find any general genetic nomenclature.
From what I read it seems there is a consensus among geneticists to distinguish between name formats of proteins (non-italicised) and corresponding genes (italicised; e.g. COI vs. COI). I have suspicion that this is often written incorrectly in taxonomy papers. Seems to me that most people write even protein-coding genes entirely non-italicised. Anyway, a letter coming for part of the gene/protein (lets call it sufix here for convenience) should be non-italicised (e.g. rbcL, psbA). Question is, shouldn’t „I“ sufix in „COI“ also be non-italicised because it also stays for the part of the gene/protein? Then when I refer to certain subregions of these genes and I define them as "COI-5P" and "rbcL-3P" (see postscript) then these „-5P“ and „-3P“ sufices should probably also be non-italicised, right? Following this logic it seems that these genes should be correctly written this way: COI-5P, rbcL-3P.
Yet another chapter are ribosomal genes which are written non-italicised as far as I have seen. It is true that it is easy to distinguish gene (LSU rDNA) and the product (LSU rRNA) if written in full. However, as short forms (just LSU or SSU) are often used in papers (also non-italicised) I guess it would be beneficial to distinguish product and the gene in the same way as in protein-coding genes. So I would prefer to write them this way to keep the same format as in protein-coding genes regardless of product type (protein vs. RNA): LSU rDNA and SSU rDNA, in short LSU and SSU (btw I would prefer to entirely avoid short forms here), and when speaking about products then LSU and SSU. I did not find anything in nomenclatures about genes encoding another product than proteins so I do not know. What is your opinion?
PS: Just to be sure what genes and their parts I am dealing with: COI = gene encoding Cytochrome c oxidase subunit I; COI-5P = 5' region of the mitochondrial gene encoding Cytochrome c oxidase subunit I (distinguished by specific primer pair in my manuscript); ITS rDNA, nuclear gene Internal Transcribed Spacer; LSU rDNA, nuclear gene encoding large-ribosomal subunit; psbA, plastid gene encoding Photosystem II protein D1; rbcL, plastid gene encoding large subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase; rbcL-3P, 3' region of rbcL; SSU rDNA, nuclear gene encoding small-ribosomal subunit; UPA, Universal Plastid Amplicon; V4 SSU rDNA, subregion of SSU rDNA.
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Dear Ziguo, Raffael, Ali and Gerald, thank you very much for your interesting contributions. The phycological journal I plan to submit to updated their list of abbreviations (that don't have to be written in full) just few days ago. They distinguish between the name formats (or symbol formats, to be more precise) of genes and proteins now. Surprisingly, however, they do it in an opposite way than recommended in gene nomenclatures. They italicize protein symbols, instead of genes. So it still seems to be pretty mess. I think I will still try to submit the manuscript with italicized gene symbols for that seems to be the correct way of writing them to me. If there is some discussion with the editor or referees on the topic, I will keep you informed here. All the best, Jan
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Cloning and transgenic animal
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an organism with different cells emerged from the same zygote is mosaic and an organism composed of different populations of genetically distinct cells originated from different zygotes is chimera
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I am doing a study and we looked at the tongue of Obese and Lean Zucker rats over a period of 3 months. The tongue is known to have increased fat as the rats gain weight/age. I did a microarray of the tongues from baseline, one month, two month, and three month. There are a number of genes associated with Collagen that signficantly decrease over time, including Col1a1, Col3a1, Col1a2, etc. Does anyone know why this is? I thought that there would be increased in these genes over time.
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Thanks you for the response Evripidis. Do you have any idea why stearyl-Coa desaturase 1 and CD36 would have decreased over time, but no differences in the groups? 
I have been using this paper ( https://www.ncbi.nlm.nih.gov/pubmed/16284748as ) reference and from my interpretation I should have expected scd1 to be continually over expressed over time, not decreased.
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Hi, I am asking about the maximum period of time which the blood sample still fresh and can be used for the RNA extraction, from the collection to the analysis procedure?
Thank you
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mr hussain & Al-sa'aidi, thanks for your comments
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Which universal/ housekeeping genes I can use to find presence of any animal origin (as contaminant) in animal feed samples (by PCR/Real Time PCR)? Kindly suggest its the primer probe sequences.
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I want to look at the level of gene flow / migration between fish populations sampled at 10 km intervals within a river system to see if there is a link between genetic and morphological variation between the populations. I'm using microsatellite loci and the fish have only been present in the system for 40-60 generations.
I was intending on using BayesAss as its meant for contemporary migration, but fear that it will only look at <5 generations.
Which program should I use - Migrate, IMA, BayesAss? Any advice would be appreciated.
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Hi, 
See the attached PDF file.
Good Luck.
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I have breed seven Rat, all of them has given birth but after 14th day I have observed that one female rat eating her own baby. What is the reason behind this kind of cannibalism? Is it possible can we read this behavior through any kind of molecular analysis?
Any suggestions? 
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See this "Rat breeding guide" at:
Maternal Infanticide
The term infanticide is defined as the killing of an infant. It is hard to determine, unless you actually witness it, whether or not a female has committed infanticide or if the pup has died naturally. It is not typical for mother to kill their own offspring. Mother rats may kill the offspring of other females and virgin females will often kill babies (suggesting that hormones play an active role in determining female behavior to offspring). Yet there certainly are scenarios when mothers kill their own.Some hairless mothers who are unable to lactate may kill their entire litter. Hairless females with diminished lactation may cull their own litter one by one until they reach the number of babies that they can provide nourishment for.
Typically infanticide is committed during the first few days of life and the killing of an individual pup is more likely than the killing of an entire litter. Some factors that may lead to maternal infanticide include: hormonal imbalances, environmental stress, hunger, protein deficiencies, vitamin deficiencies, and obesity.
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Dear all,
I'm currently working on mammal genomes. I had received Illumina NGS data and decided to use QDD (on Windows) to fish out microsatellites for PCR primer design. I've encountered some problems and hopefully someone can help me up here.
1. By following the instructions in http://net.imbe.fr/~emeglecz/qdd_installation.html, I've downloaded Active Perl, BLAST+, ClustalW and Primer3. For Primer3, should I downloaded version 2.3.7 (the C code), version 4.0.0 (Web Interfaces - Primer3 Web) or 2.3.6 (Web Interfaces - Primer3Plus)?
2. Can I use the raw data from NGS (paired ends reads, 1GB) as the input file for Pipe1 in QDD?
3. I've tried the above and my laptop is still working on Pipe2 after 12 hours. How long will Pipe2 and Pipe 3 take for a sample size 1GB?
4. Anyone has a detail workflow for using QDD on Windows to design PCR primers?
Thank you in advance for helping.
Great Day
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Running on a linux server can solve your problem. You should look for a linux server and run on it using multi threads. 
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I am looking for a reference in which a single gene mutant having weak phenotype when combined with another single gene mutant having strong phenotype of the relative trait, result in a weaker phenotype.
For example, a single mutant plant with extremely dawarf phenotype when combined with another single mutant with slightly dawarf phenotype, gave a slight dawarf double mutant phenotype. Please share if you know any reference in plants or animals. Thanks
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As per Mendelian laws of inkeritance, dwarf phenotype is expresses by recessive alleles. The double mutant ab in your example  will be dwarf. "Extremely" dwarf or "slightly" dwarf  observed appears due to quantitative effect of alleles expressing dwarf phenotype.
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Hi every body
I am going to optimize the Cas9 gene in Grainthat is why, looking for the right tool for this purpose
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Just for your reference. I don't know whether you need it:
Some people have also modified Cas9 gene by adding a Nucleus Localization Signal (NLS) to increase its efficiency. Below is one example from a commercial company (see the link below):
"EnGen Cas9 NLS, S. pyogenes contains Simian virus 40 (SV40) T antigen nuclear localization sequence (NLS) on the N- and C- termini of the protein."
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How can i access data sets for cattle genetic diversity studies using molecular microsatellite markers, especially for cattle breeds in Sub-Saharan Africa. I need to compare with my own results that i found using ISAG/FAO recommended markers
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There are very few animals with polyploidy like salamanders. Why is it that polyploidy is so uncommon in animals? On the other hand, there are numerous examples of polyploid plants. If it is something to do with the gene dosage, how does it not affect plants?
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I'm looking for additional information (frequency, distribution, etc) about a congenital Abnormality in goat's udder callled weeping teats. 
Regards,
Stefano
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Dear Pierre, 
Could you provide me the papers you was talking about?
Best
Stefano
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I'm trying to evaluate the cost-benefit of working with this model in the lab.
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In Europe (and I assume America) Zebra finches are cheap to buy, easy to keep and breed, and are cheerful undemanding creatures. They do not fight (much) unlike many species of small pet birds. They do very well in cages or small aviaries. You could have a big colony quite easily but if you only have two or three years you may need to be doing research rather than breeding finches. Housing would be cheap to provide and they are happy to be hot.
Seed alone is a calcium, methionine and lysine deficient diet. Unproductive Zebra finches can manage on seed alone BUT your stock will be bigger and healthier (as Stefan says) if you give them a source of calcium, which could be the eggshells crushed and protein from the eggs (hardboiled). However, indoor birds will need some vitamin D and I would suggest whatever you feed, the birds need a good quality powdered vitamin and mineral supplement on their seed each day as well as some small sized grit (suitable for canaries is OK). Initially they were desert birds but they do need access to water.
I only say all this because I have spent 40 years trying to rectify chronic ill health in badly fed captive birds
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i want to search some gene associated with plumage colour and shank colour of native chicken. its happy to receive answers. 
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The question is too wide. Hunting behavior in dogs is a complex of different traits.
Each trait is controled by different sets of genes.There are also different patterns of hunting behavior in different breeds of dogs (different hounds, pointers, shepherds etc.). To answer your question it is necessary to know in what trait exactly you are interested in. In other case the answer will be - almost all genes somehow could influence hunting behavior.
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I am researching the SNPs simple and cheap protocols, methods to apply on animal genetic resources?
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You can also use the BLUPF90 family of program by Misztal, which are open access and allows you perform analysis such as genome-wide association. You can access the manual at http://nce.ads.uga.edu/wiki/lib/exe/fetch.php?media=blupf90_all2.pdf.
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We did a study on a free-ranging population of this species, in which we tested whether spatial associations (2 adult deer within 25 m of each other) varied with several factors such as season, home range overlap, genetic relatedness, and sex, age and disease status of pairs of deer.  
Relatedness was not a good predictor of spatial associations. 
Pairwise relatedness measures were estimated in SPAGeDi version 1.4 (Hardy & Vekemans 2002) using the estimator by Queller & Goodnight (1989).
Relatedness was on average -0.003 ± 0.005 (±SE, SD = 0.15, range -0.4 to 0.6). 
I would like to compare these values with others generated in other mule deer populations, but I cannot find any reference!
Any guidance will be appreciated. 
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By spatial association, do you mean social association (existing in the same group at the same time) or general spatial proximity (existing in a similar place)? What exactly did you do for your analysis for for "association strength?" I can think of a number of different metrics that I could call "association strength" and some would be weaker than others. And there are some statistical approaches that make more sense than others, as well.
So, if I've done my math right, you have n = 32 adult deer (assuming the 982 is a typo for 992, because 992 would give a half matrix of 32 individuals)? What's this in context of your overall population density? If we sampled Toronto for 30 people, we'd get very few individuals that are related to each other by chance. However, in a village of 300, for the same average family size, obviously there's going to be more per-capita relatives. My first suspicion is that given a mere 6 individuals have high relatedness, your sampling density was low (unless mortality is high and you have a stationary or declining population density). However, this assumes you sampled your deer at random. If your sampling protocol involved exhaustively sampling all animals that had contact with a group of focal individuals, and you were comparing them to random non-contacted controls from the same population, then suddenly you're looking at a decent number. It all depends on your sampling design.
A word of caution on the contact rate stuff: 0 < r < 0.125 puts you in a foxy place. Since you're thinking about mechanistic action (the animals makes decision x based on characteristic y), you need to think how that factor is going to be assayed in nature. You can make some argument based on odour cues and imprinting for close relatives, but once you get past 2nd degree kindred you need to consider whether the animal might reliably distinguish anything further than a cousin. You might consider using "cousin level or greater" as a binary predictive factor. Also, I'm assuming that you've stripped known parent/offspring-at-heel pairs out, since it wouldn't be very surprising to see that mom pays a lot of attention to her still-young fawns. If you don't strip that, you run the risk that your effect is entirely does with fawns or yearlings at heel; while technically, that's relatedness predicting contact rate, it's a very specific type of relatedness.
The group membership thing is most interesting. There was a recent paper (Biosa et al 2015 in J. Zool.) that found that their spatial segregation had a temporal component to it, with opposite sex relatives negatively associated during breeding periods. Without knowing much more about your study and study system, I'd wonder if you considered what the deer are 'trying to do' life-history-wise the time of year you observed/sampled them.
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Osteopetrosis is an ophthalmic disease, the scientists think two gene are implicate in the expression. We actually find a case so extreme to this anomaly, but we haven't a possibility to analyse it by molecular tools, who can help us?
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I would be happy to help.
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I would like to know whether any individual belonging to any extinct or extant bird species is conserved in any museum or other place worldwide. Would like to know about genetic studies on this material.
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Thanks a lot Andrey, I would manage to do that
Regards
Carlos
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Is the chance that donor vector was integrated into genome randomly high or rare?
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Hi Yang. Random integration using CRISPR in mice seems to be rare. GeneCopoeia provides CRISPR transgenic mouse services, and in our hands 1) The frequency of correct donor insertion is about 3-5%, and 2) We almost never see random integration. This makes sense. If CRISPR is working, the frequency of integration will be stimulated by several orders of magnitude, so if you are screening about 100-200 mice, then the ffrequency of random integration will be below the levele of detection. This is opposed to cell lines, in which a selectable marker is placed on a donor plasmid. In that case, you are selecting for cells that are drug resistant, and the only way they can survive is to integrate the plasmid, whether randomly or correctly. That is why people can still detect drug resistant cells in control transfections of donor but no CRISPR. If you want to know more, visit us at http://www.genecopoeia.com/resource/technical-and-application-notes/, where we have technical literature on genome editing topics.
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Hi everybody, 
If a phylogenetic tree is reconstructed by maximum likelihood (ML) method, how the DNA sequences for one gene or genetic marker must overlap after alignment step ? There is a treshold to have a good phylogenetic reconstruction to respect ? If yes, can you indicate me with reference to read and learn.
Thanks you and best wishes
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Dating analyses always have a branch length prior, because the tree is ultrametric (all the tips were collected 0 Ma ago), and a molecular clock prior. A sequence with many autapomorphies is expected to coalesce more deeply in the tree than a sequence with few autapomorphies.
ITS1 and ITS2 are the ribosomal internal transcribed spacers 1 and 2.
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I used hypred package in R and constructed my base population then reference population that consists of 50 sires and 50 dams and my offspring are half sibs and full sibs. I used GBLUP method for measuring accuracy.
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I really appreciate your help. Thanks
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Will spending some months for going from 94% black 6 to 97-98% black 6 be worthwhile? And also will there be substantial difference in the glucose homeostasis then?
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 Dear Beatrice,
Thank you so much for your inputs. I will go through these and then i will see what can be done.
Thanks again.
Best regards,
Abhijit
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Do any one know the chromesome number of Lumbricus earthworms, except L. castaneus, L. festivus, L. frendi, L. rubellus and L. terrestris? Are there any species currently places in Lumbricus that has another chromosome number then 2n=36?
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Up to my best knowledge there are now poliploid speciemens in the genus Lumbricus found so far. (Please note that L. eiseni reported frequently  under this name does not belong to the genus Lumbricus but to Allolobophoridella !!!)
                  Regards,
                                        csaba
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Hi everybody 
I want to make simulated gastric and intestinal fluid which mimic real poultry stomach and small intestine condition.
In literature the  pH values of SGF and SIF are 1.5 and 7.4, respectively.
But in poultry, pH of proventriculus and small intestine is  4.5 and 6.5, respectively.
So, pH for my SGF will be 1.5 or 4.5? how about for SIF?
with thanks
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Thanks for your answer.
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Hi there,
I'm planning some immunofluorescence where I want to dual label either BDNF or TRKB with caspase-3.  However, for the species of tissue I'm using, I need to use an antibody that hasn't been raised in rabbit, as the caspase ab we have is anti-rabbit and validated for our species.  As most antibodies for BDNF are anti-rabbit, I was wondering if measuring TRKB expression is as good an indicator of neurogenesis as BDNF, or is this only when the case when BDNF is liganding with TRKB.
Having said that, I have sourced an anti-sheep polyclonal BDNF ab but I need to validate it first but would like some advice on using TRKB from people with more expertise than myself!
Thanks in advance.
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You could also use other markers for neurogenesis as doublecortine and BRDu. Maybe in this cases the combination of secondary antibodies will suit better your experiment.
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Considering the threat of extinction from interbreeding, inbreeding, cross breeding as well as the introduction of genetically and productively superior animals in line with the low input production systems in the developing world.
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It is true that uncontrolled introduction of exotic breeds and indiscriminate crossbreeding with local breeds may jeopardize the adaptability trait of the local breeds. Other significant risks and dangers facing conservation of local breeds can be signified by climate risk factors such as droughts and desertification that lead to shrinkage of pasture and overgrazing. Conservation for indigenous livestock breeds can be achieved through in-situ efforts exemplified by breeding stations which represent the focal points for conservation and sustainable use for so many gene pools from the national herd of any country. But the most important effort in this type of conservation is usually achieved by traditional communities who have conserved their genetic resource over centuries by traditional means. Ex-situ conservation is another type encompasses gene banks and public and private institutions.
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To describe the impact of liver, gizzard, heart, spleen, pancreas in broilers meat production.My experimental broilers were reared for 35 days. After slaughtering  offal's & glands were separately measured, but how can i compare the groups.
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Dear Torun
The answer depend on the hypothesis and the goals of your study, you can give more details about treatments and genetic groups, I hope the attached paper may be useful for you.
Good Luck
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what are the best microsatellite markers in camel for parentage verification? and How many marker should i use to confirm relationship.
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I'm not a "camel person" either, but ISAG has a recommend panel for parentage testing.   I have attached the notes from the ISAG 2014 meeting. I have also attached a couple of fairly recent papers which might be helpful.  Good luck!
Melissa
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We are creating a Thy1-EGFP colony from a breeding pair (male hemizygous for Thy1-EGFP and wild-type female). My question is related to the mating for the second generation. Shall I cross one of the females positive for GFP with her father (which is hemizygous for GFP) so we can increase the proportion of homozygous mice for GFP?. Or is it better not to cross the male with its daughters?. How would it be for the third generation?
Thanks!!!
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Is your Thy1-EGFP a knock-in (in the mouse chromosome 9) or another type of transgene? I am asking this because you say you have a hemizygous male (instead of a heterozygous male, which would be expected for a knock-in in an autosome). Does your Thy1-EGFP allele preserve the Thy1 function or does it disrupt it? Are you interested in studying the Thy1-EGFP allele while preserving its function or not? A detailed answer will depend on those questions, but if your Thy1-EGFP allele is a knock-in and the function of Thy1 is preserved, then there is no problem in backcrossing the male's F2 daughters with the F1 male (their father) to generate homozygous mice in the F3, which could be intercrossed to generate more homozygous mice. Please, be also aware of the heterozygous and/or wild-type mice you might need as controls.
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What genes are most responsible for the growth of ruminants such as goats?
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Dear Suhendra
Growth is quantitative trait represented polygenic trait and affected by many genes, we can imagine the number of enzymes ( genes ) and hormones ( genes ) shared in the growth process including food intake, digestion and metabolism, besides the effect of non-genetic factors and the interaction between G×E
Good Luck
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I am looking for rates to calibrate my analyses, but have not found any so far. Does anyone know of any research done in this area? There appears to be plenty on mtDNA markers, microsatellites and some nuclear genes, but none on neutral nuclear markers. Any help would be much appreciated!
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Hello Ashley,
It depends on the loci you are using and the group you are examining (hard to generalize across all fish). I have examined several markers in Centrachidae in the southeast US and Catosomidae in the southwest US and here are some insights that I have found.
Both of these groups have very differing substitution rates. Centrachidae has substitution rates similar to that of the average mammal rates, reflecting and more stable history with relatively large populations consent throughout time. Catosomidae, like most western fishes, have had an unstable history driven by volcanism and continental expansion and as such has presumable had periods of bottlenecks and expansions over and over again leading to a quicker substitution rate (almost an order of magnitude), this was found in Chen and Mayden 2012 and is consistent with the work I have in review. So history is very important and other factors including introgression, genome architecture, and genome duplication can also be very important.
Also, as you mention mutation rates vary across the genome. Even 'neutral markers' are not completely neutral but instead nearly-neutral and many of the markers that we call neutral are not. The general rule of thumb for eukaryotes (although these may be more basis to mammals) is an average of 2.2 x 10^-9. Below is a general list for various regions of the genome:
Protein-coding exons - 10^-9
Introns - 10^-8
Ribosomal proteins (like S7 that Derek mentioned) - 10^-6 to 10^-7
Microsatellites (and many other short tandem repeats) - 10^-4 to 10^-6
Mitochondria - 10^-5 to 10^-6
There are also ultra-conservative regions that have a much slow mutation rate and have become popular in the NGS world. Also, when people refer to neutral markers they often are referring to either ribosomal proteins or EPIC markers (exon primed intron coding) that often contain both exons and introns and when you sequence these markers you can often see the rate heterogeneity.
With all that said, applying a standard rate is possible and many researchers do using the standard eukaryote mutation rate of 2.2 x 10^-9 (can not think of the citation right now), but you should be careful and only use it on EPIC markers and not other markers like ribosomal proteins (i.e. S7 and 18S). Also this should be avoided if your organism has had a history of bottlenecks and expansions. The far better thing to do in my opinion is to fossil calibrate your marker as long as you have the calibration points. For examples in fishes see Near et al., 2012 in PNAS for all ray-finned fishes or Unmack et al., 2014 in PloS for Catosomus.
Hope this helps. There is definitely literature out there, they can just be hard to find and typically easier to find if you look more at the family level then in all of fishes.
Best Regards
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Hi,
I have around nine traits, which I would like to use in the animal model (estimate heritabilities and genetic, phenotypic correlations). Haven't worked with these models before, I found out that increasing number of traits in the model results in convergence problems.
Is there a way to improve the convergence (I use vce), or what would be the best design for my study, should I split the traits into several models? Perhaps if someone could give me some information on the main pitfalls when working with animal models that would be great.
Thank you.
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Dear Julija,
Unfortunately, there is no unique solution for your problem. Indeed, a multi-trait analysis can be problematic as the number of traits analyzed increase.
To begin with, you would have to have lots of data to make sure you can estimate all variance components in a 9x9 variance-covariance matrix, which are 9 + (9*(9-1)/2) = 45 parameters.
Another problem is about using "wrong" starting values for these parameters. It is good to use reasonable starting values (e.g. based on single and two-trait analyses, or based on other datasets, etc..) when estimating genetic parameters.
Another issue could be the use of one trait as a explanatory variable of another trait. For example, when calculating genetic correlations between average daily gain (ADG) and Residual Feed Intake (RFI), we usually have problems because ADG is the trait in one model (ADG) and one of the explanatory for another model (RFI).
So, one suggestion is for you to start slow and estimate genetic parameters for each trait. Then you start doing two traits at a time, and so on... get a feeling for the data first!
Nick
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Hello, I am currently volunteering with an association which studies fin whales in the western Mediterranean sea. Specifically, we are willing to collect fin whale's faeces to perform genetic and hormonal analyses. The faeces are a loose aggregation of particles that get attached to the holes of the net and contaminate future samples if we use it more than once (it is almost impossible to clean!). We thought of creating some sort of device that allows us to change the net everytime we collect faeces.
Does anybody know a way to avoid the faeces getting stuck on the net or have created a new one ("home-made" net) to collect faeces? Thank you! :)
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Answer
Try adding one or two layers of coffee filters in your hand-held net (assuming that is what you use to scoop the whale poop). You then take the filters with the faeces out and add new layers for the next sampling. Try it out first with a VERY ripe tomato that you squeeze in a bath tub, to mimic the whale poop floating in the sea...