Non-mendelian genetics/ non-darwinian evolution

Your last question: As far as I know 'NO'. How does one begin to construct a model that equally represents every single homo sapien permutation, or do we go about the approval process like the FDA 'beneficial to at least 5-7% of the test population? doesn't kill you? ta-da you're approved'.My following points are made in the context of complex diseases.
1) Evolution scientists like to use 'Neutral DNA Model'...this is crazy for the rest of us, BUT right now there is not a workable alternative...neutral DNA?? So, in our group we plug away at epigenetics and functional genomics (NOT the computer versions), and wait.
2) Mendelian genetics is fine if you are trying to explain "easy" stuff, but with humans if you try to publish a paper in a reputable journal and you say 'major allele' you better qualify that with ethnicity/age/geographical location (possible reason why a consensus for DNA model for evolution can't be reached and is certainly not trivial).

Unfortunately, this is not the case. If it was then we would not need 50 million (at least, hehe) different medications for the same phenotype. Why? Say you have an individual who is homozygous at a certain position (just to make it easy). This genotype is then found to be in LD (linkage disequalibrium sp?) with 3 other positions in the same gene. However, each of these four have different associations with phenotype (there is some overlap). These phenotypic associations involve different genes. With just that do you think you could make a sweeping statement about the world popuation? I would hazard the answer is 'no' because one now needs to factor in ethnicity, yes it does matter, geographic location, and environment that these genes matured in. However, you should be able to if you were to think Mendelian Genetics can cover it all. At our center we have looked into how many different combinations one would have to consider if using mendelian genetics....the number gets very high. So, that's what I meant about "easy" versus what one gets in reality when studying complex diseases in humans. I certainly don't think Mendelian Genetics is defunct....quite the opposite...it's just not enough for us (our work). Therefore, in terms of what WK mentioned I think that the idea/scope of Mendelian Genetics needs to be overhauled. The whole idea of it referring to eye color/hair color/leaf size needs to be left in 2nd grade and more mature, realistic definitions of "traits" and concepts in high school and especially college need to be presented. Of course, weed out opinion from fact at your discretion.

Pink: 1) I do not argue with the fact that "mechanistically" the way in which a gene is inherited is Mendelian! (thought I had gotten that across the first post I made?)
2) However, the fallout expectation that many (which was one of the main points I felt WK was making in bringing this up) who are not neck deep in this stuff is a simple 'if you have this genotype then you have this phenotype'...because this is what people will remember from their science class if they took one. As you know the simple-ness of it all is what gets played on by creationists and others that are not in the field. So, I do think some re-vamping is in order.
3) The reality? You can put whatever gene you want there but epigenetics will weigh in on how the gene gets expressed, if it is, as well as ALL of the other factors I mentioned previously.
Ethnicity:To put this in context: My point was supposed to be that despite the Mendelian segregation of gene A which contains a SNP that is in LD with a couple of other SNPs and in Western European's it is not only highly associated with Asthma, but many other markers of the disease.....the association is gone when you look at an Asian population, for example. Despite Mendelian genetics "at work" you get two different phenotypes.
Anyway, I think it's moot as WK seems to be looking for non-Mendelian in the context of mechanistic not interpretation.

Yeah, I got the sense we were entering a round-about at the end of my last post. My take on the initial post was that WK was interested in getting a re-vamping as well, so I don't think I am alone in this "frustration".
1) Ok, drop the ethnicity thing...you, and maybe others, misunderstood my intent.
2) First of all, with the limited number of labs doing ACTUAL functional studies on SNPs (I work in one) you are overstretching your statement, because in fact you cannot say "SNPs are often NOT functional polymorphisms and rather just markers for them." at this point. Well, that seems to be what the majority do think. Btw, I'm sure you'll correct me if I'm wrong, I don't think Mendel EVER said anything about the role of environment on inheritance, so your implication that it's covered and simply someone else's misunderstanding of Mendelian genetics is inaccurate. And this is absolutely the reason why I am against looking at evolution based on a neutral DNA model. Because the underlying statement is that just because the gene is there or not means you get the exact same phenotype through time.Anyway, I think you and I have kicked this dead horse enough.-Cheers

Well, I second the vote for the resource Mammuthus recommended because I think it gives you the best flexibility in terms of setting your own parameters.

People do specifically discuss Mendelian Phenotypes which is misleading because it encourages a correlation to be drawn between your (which I agree with btw) Mendelian Genetics. Unfortunately, like I've already stated this does not hold when you are trying to describe complex diseases. So, for the last time when it comes to complex diseases just because you have gene X does not mean you will have disease X. Therefore, I think this needs to discussed in the coursework of students understanding genetics and the subsequent phenotypes.

Alright, imprint to me means epigenetics. So, I would ask you if you think it is parental OR species inheritance since I think the jury is still out on parental imprinting. In the case of parental imprinting (whether heritable or not) one would still need to consider environment whether it be uterine, nuclear, or ex vivo (antigens). So, in fact I would agree with Ook on this as being a non-Darwinian factor. On the other hand, I would say that it does not contradict mendelian genetics, but that it is supplemental.

Since you like to hear yourself I will answer you with your very own statements which simply re-state what I have been trying to say from the beginning, but apparently you won't stop until you have said everything, so here you go:Here's my statement in the form of your question: I would interject that traits is equivalent to phenotypes.Here's my answer in the form of your statement: Excuse you! Really? Are you trying to be clever? Remember this: Whew, there for a second I wasn't sure if you thought phenotype was independent of genotype or not especially since you were taking the liberty of telling me I am the one who is misleading. You're right, I guess some would equate complex diseases to the "highly polygenic trait" of height! Give me a break.

I have been known to not communicate well.
Let me make ONE MORE attempt, please remember the context.
1) Mendelian genetics, with the understanding that the general public and even many scientists, have is inadequate in promoting understanding and therefore appropriate (targeted approaches) that lead to the comprehensive characterization of complex diseases.....this in no way reflects Pink Sasquatch's level of understanding.
2) The above idea can be illustrated in the fact that a 'Neutral DNA model' is used by some evolutionary scientists to describe how genes have evolved in humans. The problem is that this involves assuming equal contribution by mere presence alone.
3) So, yes, I think that a 'Neutral DNA model' is an inadequate way to describe where we are today in terms of complex diseases. As I, probably unclearly, pointed out I think it is due in part to carrying the ideas of AaBBCcDD=you will be 6 feet tall to cover ALL heritable attributes from our ancestors. It is my opinon that this is flawed when it comes to complex diseases, and could be addressed by encouraging more expansive teaching that incorporates current research endeavors.For everything else you wrote:
Are you suggesting that the general public (WK's "concern" in the first post I thought) and even most scientists have the same level of understanding of genetics as someone with a degree in it? Because you must not have the same access I do to the number of people I can count that directly associate a phenotype with the genotype.....despite you repeating that they are independent.

1) Yes, in that it could be a species (I hope I have that right) effect. It has been suggested that imprinting is a possible epigenetic explanation for why we are "more evolved", or just plain different, than chimps while still sharing 99% sequence similiarity, as an example. 2) In my opinion, the species imprinting does not in any way preclude parental imprinting in the context you mention above.
3) In contrast, at this point I don't think we can separate the possible pattern of transgenerational heritability and effects on that pattern such as, again, what you suggest above such as maternal effect genes (and many others).I hope I did not parse your question too much.

I agree with this. My thoughts would be that
1) Species imprinting could contribute to differential expression of coding/non-coding between species that share significant nucleotide homology and explain the tolerated accrual of mutations one sees in the non-coding sections of human DNA by setting the stage for this differential methylation/acetylation you were suggesting as a species block...maybe. Where the focus is conservation of specific species. - Then the parental imprinting, much more plasticity involved, where the imprinting of heritability affected by environment (oocyte, in utero, nuclear, take your pick) but again not in a mendelian fashion, but in addition to mendelian genetics. I think that is what you were already saying though (right?). The focus would be conservation of organism function (whatever level that might be).So, a tri-level approach (species imprinting, parental imprinting, and mendelian genetics) to getting to the point that you and I are discussing this (of course that simple ). Maybe this was what you were suggesting as well? I hope I managed to make sense since my communication skills seem to wane at times.

You know what, lol, I'm calling a truce. I think somewhere the gist if what I had meant to say in the first post has gotten lost. We are not getting any further and we have digressed to picking at small things, and I do mean 'we', so have a great week .-Cheers