chadn737

Could be many things. I would sequence some of the products to see what you are getting. Depending on the population or individuals you are working on, you could be seeing natural variation.

Eva Jablonka is part of that group, so it is guaranteed that they propose an overemphasis on epigenetics. However most epigenomic differences are not epigenetic, but due to genetic differences. Jablonka has long ignored the fact that there are just very few examples of true epigenetic phenomena with any long-term effects. In short term this may play a role, but in describing the breadth of evolution, it will not.

I'm not sure what you mean by "phenotype influenced" as the phenotype is in part a product of the genotype and in this case the phenotype would be "leadership". I think you have confused "phenotype" as being the same as "environment". The genotype and environment interact to produce the phenotype, which is the physical/mental/behavioral characteristic. As for additive vs non-additive. Additive genetics is the idea that each gene contributes some proportion towards a trait and that variation in these genes can be added/subtracted directly to come up with the contribution of each gene. For instance, gene A contributes to 5% of the phenotype and gene B contributes to 10%, then gene A and gene B contribute 15% of the phenotypic variance. Non-additive genetics comes into play when you have gene interactions that do not allow for such simple 5 + 10 math. This is typically due to epistasis. Say that gene A has two variants: variant 1 and variant 2. If you have variant 1, then the interaction of this variant with gene B masks any effect of gene B, but if you have variant 2, then you see the effects of gene B. So you only see the 10% phenotypic contribution of gene B if you have variant 2 of gene A, otherwise, gene B has no effect if you have variant 1. Therefore the relative contribution of each gene is not a simple gene A + gene B addition as the contribution of gene B is dependent upon gene A. Thus the genetics of this is "non-additive".

Major in anything related to molecular biology or genetics. The exact title doesn't matter. It would be easy to go into genetic engineering with a Biology, Microbiology, Molecular Biology, Genetics, Biochemistry, etc degree.

It sounds like he is describing the difference between "amount" of protein versus "activity" of the protein. Many proteins have different activity levels depending upon modifications made to them. For instance, the addition of a phosphate group (called phosphorylation) to a protein may activate, deactivate, or increase/decrease its activity. Secondly, changes in gene expression do not automatically result in increased protein production. Many genes are regulated as much, if not more at the level of translation than they are at the level of gene expression.

Context?

GWAS does not find causative SNPs, it finds associated SNPs. If a non-causative SNP is in tight linkage with a causative one, it will show up as significant in a GWAS study. Typically, in GWAS, one uses common SNPs, not rare SNPs. It is often suspected that rare SNPs are causative, rather than common SNPs. The point of GWAS is to identify regions and hopefully even genes that are associated with a trait, not necessarily the SNP itself.

Promoters are put in with the gene, typically a promoter not native to the gene being inserted.

Excel.....do not use excel. Export your data in a tab delimited or comma separated text file and use command line tools to handle this. Its the only way to reliably handle large data sets like this and not go crazy. The information you are seeking could be quickly determined if you learn to use the command line and the great tools available. I highly recommend that you export to a tab-delimited format and try to convert in some way to a BED format. http://genome.ucsc.edu/FAQ/FAQformat.html This will enable you to use BED tools https://code.google.com/p/bedtools/ to find those sites that intersect with coding regions. Not only that, but once it is in BED format, you will be easily able to upload it or convert it into formats uploadable to a browser for visualization. If you do not know how to work from the terminal and have time, learn how to. UNIX and basic scripting should be a standard part of any education in genetics at the graduate level anymore. If you don't have the time, try to find somebody with a computer science/bioinformatics background to help you.

I would avoid a browser for working with so many SNPs. What format is your data in? If you happen to have it in a BED file or something similar, this task could be extremely simple and fast.

Depends in part on the type of mutation. SNP vs INDEL vs Transposition vs CNV... Based on more resent whole genome sequencing it appears to be on the order of ~50-100 mutations per individual. There are probably around that many differences new mutations in you, in me, in each of your parents, and so on.

I'm not interested in whether one considers "homosexuality" an "error" or not. The morality of it is not something that particularly interests me. I don't think homosexuality is more or less moral whether it is genetic or environmental or more likely some mix of the two. I am not homosexual, so the morality as it pertains to me personally is something I consider irrelevant. Beyond that, if it does not cause others harm, then I consider the morality of it to be none of the business of anyone not participating in the act. I'm pretty simple like that. My interest in it extends to the biology only, in particular the genetics, because I love genetics. The use of terminology like "biological error" is meaningless to me. We are all "mutants" and the products of "mutants" and so to me defining things as "error" becomes rather meaningless. If homosexuality has the effect of improving the survival of relatives, as some have suggested as an evolutionary explanation, then low levels of homosexuality can actually be seen as advantageous. I don't particularly agree with this because I think the evidence for it is very weak, but that is the only reason I do not agree with it. Otherwise....I don't care. Again, I'm pretty simple in usually only caring about what the biology says as long as it doesn't cause harm to others. I say all this in case you think I have some agenda in this argument, I don't. I disagree with your arguments purely based on evidence, not morals, religion, or any other non-scientific reason. I'll address your arguments later, I just wanted to clarify that because you seem to think that I might be arguing from a non-scientific standpoint.

I read that paper when it first came out. Good old PR propaganda and bad science reporting led to a lot of misconceptions. That paper is not a "study", at least not in the traditional sense. They don't produce any data, they don't even conduct an actual meta-study. Rather its more a review, where they make an argument based on actual research against genetic causes and then propose a model for how epigenomic features (epigenomic is different than epigenetic) could be the cause of homosexuality. Quite frankly I don't buy it because epigenomic marks are rarely inherited in mammals and actually proving that epigenomic marks are the cause rather than genetic variants is extremely difficult and has only been done in a limited number of circumstances. Their argument simply boils down to that there is variation between monozygotic twins and as of yet no actual genes have been linked to homosexuality. Neither of which rules out a genetic component. While several studies have been done to measure the heritability of homosexuality, very few studies have actually tried to map the trait and none with the statistical power to detect highly quantitative traits that contribute only a small portion of the heritability. Then there is also the fact that homosexuality seems to carry a high environmental factor, making it even more difficult to find linked or associated genes if it is caused by many common variants with small contributions to an overall genetic component.

They simply asked for orientation, which we all know is a really bad measure of sexual preference. A penile plethysmograph might provide better data. It looks like they compensated for this, but I can't see what the results were after the correction. Why is asking someone for their orientation a bad measure of sexual preference? As far as twin studies go, one of the most extensive and best to date used data from all twin-pairs in Sweden, including thousands of individuals. This is what I base my previous figures on. They did not base their assessment on self-reported sexual attraction, but rather on lifetime number of same-sex and opposite-sex partners that a person had ever "sexually" been with, deliberately avoiding using an actual description of sexual intercourse. Bailey and Pillard came up with estimates of ~0.31-0.74 based on that data. While more significant than the .34-.39 figure of the Swedish twin study, the population size was much smaller. Even if we take this upper limit, genetics does not fully account for ones sexual orientation. The fact that there is a higher rate of homosexuality amongst adopted siblings than the general population also suggests a major environmental factor. Why are you critical about how to interpret these findings? If there is a scientific reason for such criticism, then that is valid and I would love to hear it. Otherwise, one should be careful that one's criticism is not based simply on biases. I said quite the opposite in fact. I specifically said that "epigenetic" does not mean environmentally induced. Only that it has to be heritable and independent of genetic variation. Most true epigenetic variants appear to be simply due to random gain/loss of methylation, not environment.

No, it does not pose any unique challenge to twin studies. Twin studies are meant to measure heredity and the combination of genetic components, not specific genes. Furthermore, if homosexuality is a quantitative trait caused by multiple recessive alleles, then it is unsurprising that the parents would be heterosexual. I really do not like to throw around the term "epigenetic" lightly because "epigenetic" is typically misused by nearly everyone, including many scientists. The proper definition of "epigenetic" is "hertitable differences that are not caused by differences in underlying sequences". "Epigenetics" is not the environment. We have a term for that....the "environment" and when the environment interacts with our genes its called "gene by environment interactions" or as is often stated "GxE". "Epigenetics" was coined by Waddington in the 1950s for a very specific idea, while the fact that GxE interactions has been known since Fisher or earlier in the early 1910s. Epigenetics is also not synonymous with DNA methylation or histone modifications. Most of these variants are actually "genetic" because they are caused by neighboring or underlying genetic variation and thus are not truly "epigenetic". Furthermore, if homosexuality were truly "epigenetic" then it would be heritable and indistinguishable from the genetic component of homosexuality as measured by the standard twin study. Not to say that environmental conditions or variants of DNA methylation cannot underly part or all of homosexuality, just that by a proper definition of epigenetics, its really not epigenetic. I know I am being quite the stickler on this, but I work in epigenetics and it is a pet peeve of mine to see the term thrown around as a catch all for anything and everything that doesn't resemble simple genetics. It makes the field of epigenetics meaningless. De novo mutations will either be shared by twins and thus show up as the genetic component or if not shared, will lead to an underestimation of the genetic component. Its unlikely to be largely due to de novo mutations, however, because you would have to have a very high frequency of similar de novo mutations to reach this sort of frequency in a population. This is especially true of the study populations of the size used in the best twin studies, that include thousands of individuals. There is clearly a quantitative genetic component to homosexuality, however, it really is only in the range of ~34-39% of the phenotypic variance for males and even less for females. It is clear that the largest source of variance in sexuality is the individual's "unique environment". Whether this occurs in the womb, in early childhood, or whatever, I don't know. While it is interesting why some people are homosexual, we should not let our understanding of the biology be predetermined by what we think "it should be" rather than what it is. Homosexuality is clearly a complex trait and like ALL complex traits, there are both genetic and environmental contributions. Human height is a complex trait that is determined by a combination of environment and genetics. So is intelligence. Of course there is going to be variance in the relative contribution of genetics and environment and we should just accept as fact what is fact and not presume that it must be one or the other.

Its a valid question and I do not understand this response. It is the job of science to explain questions like this. Mechanisms of evolution like Natural Selection typically eliminate diversity, so it is important to understand what creates it and what preserves it.

I mean all of it. You're basic hereditary study cannot distinguish between so specific environmental factors, except for the shared and unique environment of the individual. In some of the largest twin studies, genetics accounted for ~34-39% of the variance while the unique environment accounted for ~61-66%, and the shared nearly none. In women its ~18-19% genetic, ~16-17% shared environment, and 64-66% unique environment. I don't see why you should hope for anything, that leads to biased assessment of the data.

Diversity is caused by mutation, plain and simple. The spread and maintenance of diversity needs to be viewed as a game of chance (genetic drift) and of competition between alleles (natural selection). The interplay of these last two forces maintains or eliminates diversity.

Heredity studies indicate that female homosexuality is not very heritable at all and thus unlikely to be primarily due to genetics. Male homosexuality has varying degrees of heritability and so does have some genetic basis. However, it is clear from these studies that there is also a good deal of environmental factors at work.

Whether or not Natural Selection is the driving force is still a matter of debate. Kimura argued that it was Genetic Drift, not Natural Selection that explained evolution at a molecular level.....its important to note that Kimura was talking about molecular evolution, not necessarily phenotypic evolution. Masatoshi Nei, whom I'm a fan of and increasingly agree with argues that Mutation is actually the primary force as it is the ultimate source of new variety, whether for Natural Selection or Genetic Drift. In reality, these are all probably equally valid, depending on the context. If you are looking to explain phenotypic evolution at a whole organismal level, then you might be most interested in Natural Selection. If you are looking to understand Genomic evolution at the molecular level, Genetic Drift might be the major player, and if you are looking to understand evolution from a very deep long term level, then Mutation, the ultimate source of novelty may be the most appropriate.

Based on models of evolution we can make numerous predictions about how genomes and organisms evolve and then test those models against the actual data. These models are also used to guide modern plant and animal breeding, which is evolution in action.

All of them.

Its meaningless. For one, Africa is not homogenous. It has lots of varied environments with differing types of food. Secondly, man has evolved to be a generalist and omnivore.

Lactose tolerance is a fairly easy trait to identify since it is a single gene trait. Other adaptations are likely multigenic and more subtle.

The beauty of having evolved to be an omnivore is that we evolved to eat a wide variety of things, not something specific. Thats why there is no "best".