The point I was making about the high functionality argument from the DI is that they clearly thinking they are making a design argument. These are not those who support common descent. That others may think the amount of functionality is high is due to a different set of reasonings. (Poor reasoning, IMHO, but something we can determine).
I am sure they think it’s also significant in terms of design… but it’s also an argument against the current understanding of common descent.
There are good reasons based on evolution why more than 10% or 25% of the human genome should not have functional significance (depending on the paper you go by). So a higher amount of functionality will be significant.
OK. Thanks for that reference. I understand their calculations now and what they’re being referenced against.
Let me unpack this…
The numbers reported in the paper seem within expected ranges and at least comparable with most studies. The percent of the genome transcribed (ENCODE consortium results ~80%) is simply not holding up as indicative of specific biological functionality but as gratuitous transcription (i.e. noise). I would not agree that the percentage of the human genome considered functional “has been increasing over the years” as a general statement. Most reasoned estimates have been fairly consistent for a couple decades or more. There are outliers but you need to take those with a grain of salt.
I’m not sure about the common descent issue, as humans display sequence similarities in the upper 90’s% range with chimps. That’s about what we’d expect from common descent and accumulation of predominantly neutral variation. One might expect less variation if most of the genome is constrained.
As of now, common descent + neutral mutations gives a prediction that the major part of the human genome not be functional.(There was a paper capping that similarity at 25%, I haven’t read the paper, I will see if I can find it).
If it turns out to be wrong. Obviously scientists will have to look for an explanation.
Do you expect the majority of neutral mutations to be selected for or against? If not, the vast part of the genome will be non functional.
Especially in more recent species like human beings.
I don’t see why that would be wrong.
@Ashwin_s I very much appreciate your contributions, so do not take this the wrong way. I’m not sure why, when you hit the limits of your knowledge, you just fall back into doubting their is an answer, and that scientists are just lost. You have a long way to go before you can safely make that leap. If it doesn’t make sense to you, I’m usually seeing that you are using words in a poorly defined way (e.g. “function” here), neglecting the grey zone between the black and white, and usually do not know about alternate ways of have confirming claims.
When you get to the limits of your knowledge, that is okay. Just ask questions. Don’t make pronouncments like this:
False. It just doesn’t work this way.
A big issue here is the word “function”, which has a very large number of conflicting definitions. In neutral theory, we mean it in a very precise way, which does not correspond at all with ENCODE’s definition. I will also add that all the confusion about the word function, has encouraged some scientists to propose something called: “near neutral theory”.
Near neutral theory starts to explicitly account for things like pleiotropy (as you’ve pointed to before with omnigenomics), without challenging any of the fundamental findings of neutral theory. In my view, when I say “neutral theory”, I mean both neutral and near neutral theory. This is very similar to how Larry Moran talks about it too. The distinction without much of a difference.
In neutral theory, function is defined in connection to selection.
Let me ask you a question, how do you independently confirm a “function” will or will not be selected for or against? It’s something that is contingent.
At some point, you will have to look at function in real terms. If most of the genome turns out to have some function (I am using the word here as it is used in English), then you will at the least have to redefine the word function in neutral theory… or perhaps explain why some useful traits are selected for while others (perhaps the vast majority) are not selected for.
Do you predict a vast difference between functions that are selected for vis a vis functions(english word again) that are useful to the organism. If not, I don’t see why you are protesting.
Depends what precisely function we are talking about.
If you mean at the sequence level, there are a wide range of experiments and analysis to build the case for or against function and ways to define function too. Function is almost never defined as an end itself but as a way to translate between scales.
There are two main definitions of function that are used in discussions like these. The definition that most biologists use is “affects fitness in a meaningful way”. The other definition, the one that ENCODE used, is “does something”. Obviously, just because a stretch of DNA does something does not necessarily mean that it affects fitness. For example, a stretch of DNA that is only transcribed once a day in every 1,000 cells is probably not going to affect fitness in any real way, but that stretch of DNA is still doing something. If a stretch of DNA binds a transcription factor but doesn’t produce an RNA transcript or affect the transcription of other genes then it probably doesn’t affect fitness even though it is doing something.
So the real divide is between fitness and activity.
Not necessarily. Function connotes some activity useful to the organism. To what extent the parts of the genome involved in useful activity for the organism vis a vis those relevant in terms of fitness coincide is an important question. If the former is a much larger percentage than the latter, it would be something interesting to know.