http://www.arn.org/blogs/index.php/literature/2007/06/16/encode_decodes_junk_dna
Maybe if evos spent half as much time listening to their critics instead of trying to silence dissent, they'd learn something. Obviously, other camps foresaw this finding and evos did not.
Why was that?
Answer: it
wasn't. Despite your claims that "evos" didn't see this coming while IDers did,
the paper linked at the very creationist website you linked to says
exactly the opposite.
The project found that nearly the entire genome may be represented in primary transcripts that extensively overlap and include many nonprotein-coding regions. The idea of a network of transcripts has been suggested before (e.g., Cheng et al. 2005; Carninci et al. 2006), but data from the ENCODE project provide firmer footing for further investigation of this challenge to the concept of lone transcription units (Denoeud et al. 2007; Emanuelsson et al. 2007; Rozowsky et al. 2007; Ruan et al. 2007; Trinklein et al. 2007). New transcription start sites (TSSs) were identified, and the arrangement of regulatory sequences (and binding of transcription factors) around TSSs was more broadly described to show the range of locations (Denoeud et al. 2007; Trinklein et al. 2007; Xi et al. 2007; Zhang et al. 2007). Some enhancers that previously mapped distal to the known TSSs were found by the ENCODE project to be near the newly described TSSs and transcripts, suggesting a role in regulating proximal expression. A richer view of the connections between chromatin structure, regulation of transcription, and replication has emerged from integrating these data sets. For example, earlier knowledge of the types of histone modifications that correlate with gene expression has been amplified to create a predictor of expression based on these modifications and chromatin accessibility (The ENCODE Project Consortium 2007; Koch et al. 2007; Thurman et al. 2007; Zhang et al. 2007), and correlations between the timing of replication and chromatin structure were also described (Karnani et al. 2007). Another result from integrating data sets shows that ∼60% of the bases found to be under evolutionary constraint in genome comparisons are correlated with functional sites identified by the project’s experimental approaches (Margulies et al. 2007). One anticipates this proportion will increase as binding sites for additional transcription factors and other elements are mapped.
So, far from being something that left evolutionary science totally gobsmacked and scrambling to explain it while IDers and other creationists smugly say "we told you so", what the ENCODE project found was actually
anticipated by biologists, and its findings actually confirm
other, previous findings, and even expand on those findings in a way that allows biologists to predict gene expression in ways they weren't able to before.
In fact, the ENCODE findings actually make the integration of your vaunted epigenetic heritability into the Synthetic Model even
less problematic than it was before, since it's easier to find and understand the noncoding genes that regulate epigenetic gene expression.
Evos will likely just say it was luck and continue to ignore the arguments of their critics and perhaps even deny their critics were the ones that were right all along in some detail like this.
Because, here in the real world of actual scientific evolutionary study, none of that is true.
Especially since, as Lukraak_Sisser pointed out to you, actual evolutionary theory long ago abandoned "junk DNA". It's only you IDers who cling to it.
I am not ignoring. Darwinism posits that gene accumulation can outweigh and did outweigh gene loss.
Where are the peer-reivewed studies to substantiate this claim? In other words, where do they compare rates of gene loss particularly through natural selection and isolation of subgroups with conceived rates of mutation rates of beneficial genes emerging?
I've asked this question for year and have never seen one single study and yet evos are confident they are doing real science assuming this untested claim has been verified.
Well,
here's a study about how additional genes created through genome duplication acquire novel functions at a rate almost equal to the rate at which those duplicated genes which serve no beneficial function are lost from the genome (a rate far
higher than previously expected - about 50% of all gene duplications will lead to functional divergence).
Here's a study that's less specifically about the
overall rate nonbeneficial gene loss vs. beneficial gene retention, but it does discuss both of those things in relation to the evolution of the eye in octopodes and humans. (Actually, there are a number of studies of individual genomes exploring the rate of gene addition [usually through duplication] and gene loss during that particular genome's evolutionary history. I can cite you a
lot of those, if you want)
[EDIT: There are also a number of papers written by Sergei Rodin about how your old friend epigenetics plays a role in increasing this retention factor even
further, via epigenetic silencing. But I can't find an open link to the papers that doesn't cost quite a bit of dosh that I can provide to you. Still, you can see a list of the papers I'm talking about
here.).