JLT
Posts: 740
Joined: Jan. 2008
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WHY? Why did you make me read that drivel?
The most obvious blunder is that he equates "RNA transcripts present" with "has function". To be fair, this misconception was widespread in the press when the ENCODE articles were published. But it's wrong nonetheless.
Larry Moran wrote about some of the limitations of the study here.
Something not directly related to ENCODE but exactly to the point:
Larry Moran | Quote | There are a lot of studies suggesting that a substantial percentage of the genome is transcribed even though less than 5% is known to be functional. This leads to the idea that it encodes some unknown function. The argument is that these regions would not be transcribed unless they were doing something useful.
One objection to these studies is that the workers are looking at artifacts. The so-called transcripts are just noise from accidental transcription. This ties in with the idea that the EST database is full of examples of "transcripts" that don't make any biological sense.
There's another possibility. The regions of junk DNA could be transcribed regularly but the transcripts are rapidly degraded. They do not have a biological function. They are junk RNA.
Arthur Hunt has just posted an article on Panda's Thinb that supports this idea [Junk to the second power]. He describes the work of Wyers et al. (2005) in yeast cells. They show that there is a large class of junk RNA. The take-home lesson here is that you can't assume that some region of genomic DNA is functional just because it's transcribed. It's a lesson that many people need to keep in mind. |
And he's not alone with this view.
T. Ryan Gregory:
| Quote | - A large fraction of the sequences analyzed, both in introns and intergenic regions, appears to be transcribed. However, most of this DNA is not conserved and there is no clear indication of function. It could be that the transcripts themselves play a functional role or that the process of transcription but not the transcripts per se contributes an important effect. It could be that the regions they examined, which were typically gene-dense, included transcribed introns (no surprise) plus longer-than-expected regulatory regions such as promoters near but outside of genes (e.g., Cooper et al. 2007), but that on the whole the long stretches of non-coding DNA in between genes are not actually transcribed. Or, it could be that transcription in the human genome simply is very inefficient. For example, the data in this study suggest that 19% of pseudogenes in their sample are transcribed, even though by definition they cannot encode a protein and are unlikely to play a regulatory role. It also appears that in other groups, e.g., plants (Wong et al. 2000), there is lots of intergenic DNA that is not transcribed, which may indicate that this is a process unique to mammals and is not typical of eukaryotic genomes.
- Looking at a broader scale, we must bear in mind that about half the human genome consists of transposable elements. Some of these clearly do have functions (e.g., in gene regulation), but others persist as disease-causing mutagens. It could be that a large portion of these have taken on functions, but this remains to be shown. We are also left with the question of why a pufferfish would require only 10% as much non-coding DNA as a human whereas an average salamander needs 10 times more than we do. The well known patterns of genome size diversity make it difficult to explain the presence of all non-coding DNA in functional terms, even as there is growing evidence that a significant portion of non-coding DNA is indeed functionally important. |
Also interesting: Ultra-conserved non-coding regions must be functional ... right?
We KNOW that e. g. the human genome contains long stretches of non-functional DNA e. g. transposons, repetitive elements, pseudogenes etc. (Larry Moran again). So, the whole premise of the YEC article is bogus.
The next annoying thing was this:
| Quote | Let’s now put this information together with Haldane’s dilemma.17 Famous geneticist J.B.S. Haldane calculated that it would take about 300 generations for a favourable mutation to become fixed in a population (every member having a double copy of it). He calculated that in the approximately 6 million years since our supposed hominid ancestor split from the chimpanzee line, only about 1000 (<2000 according to ReMine18) such mutations could become fixed. This is certainly not nearly enough to turn an ape into a human. But most importantly, we now know that there are about 125 million single nucleotide differences between humans and chimps, resulting from about 40 million mutational events. This means that somewhere between 39,998,000 and 124,998,000 deleterious changes have occurred since the split with our common ancestor.
That means we have degenerated from chimps, which
makes a mockery of the whole mutation/selection theory
of origin. |
First of all, Haldane's dilemma doesn't exist anymore (in the stated form). Second, the author falsly equates "doesn't get fixed" with "is deleterious".
And the rest is also either wrong, stupid, or both.
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"Random mutations, if they are truly random, will affect, and potentially damage, any aspect of the organism, [...]
Thus, a realistic [computer] simulation [of evolution] would allow the program, OS, and hardware to be affected in a random fashion." GilDodgen, Frilly shirt owner
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