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Promoters

Loudmouth

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I love how evolutionists will turn on their own in an instant the second there is a hint that their darwinian religion may be threatened. You really get a feel for the objective, disinterested pursuit of scientific discovery.

The theory of evolution has never taken a firm stance on what percentage of a genome has selectable function, nor does it need to. For example, the bladderwort genome is probably over 80% functional.

The question that you need to answer is why 90% of the human genome can accumulate mutations at a rate consistent with neutral drift without losing function. How can a sequence of DNA stay functional no matter how much you change that DNA?

The fact is that nobody knows the full extent of the nature of the function of the genome. Molecular biologists are practically falling out of their chairs every day learning amazing unexpected new things about how these structures operate in the organism.

We do know that only 5-10% of the human genome shows evidence of negative selection.
 
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Loudmouth

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I don't know what paper you're referring to. I'm going by general statements I've read from the research.


Our results demonstrate that regulatory variation is pervasive throughout the genome, on average mildly deleterious, and individuals likely harbor more functionally important variants in noncoding compared with protein-coding DNA.

Personal and population genomics of human regulatory variation

Coding DNA makes up 2% of the genome. If functional non-coding DNA is double that of functional coding DNA, this would mean that 6% of the genome is functional with respect to fitness. This isn't too far away from most estimates.

[/I]Together, these observations suggest that the genome may, in fact, be extensively multiply encoded—i.e., that the same DNA element gives rise to different activities in different cell types. This possibility challenges our current notions of annotation, which are still rooted in a linear world, and cautions against formulating definitions of completeness based on older models such as the delineation of protein-coding genes.

This is part of their sleight of hand. Doing something different in different cell types does not mean that a sequence has function that affects fitness. "Doing something" is not the same as functional. If your trash can releases more odor molecules in the hot garage than the cooler kitchen, does that mean your trash has an important function in how your kitechen operates? No. When you throw out your trash, your kitchen continues to function just fine. No one expects junk DNA to be inert.

If it turns out that a substantial portion of that "junk" is functionally important to development of the organism then it presents the church of Darwinian mysticism with a major problem.

If it is functionally important, then why does this DNA show no evidence of negative selection?
 
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SLP

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The ENCODE Pilot Project raised a general alarm: Most elements defined by biochemical signatures lacked strong evolutionary conservation . Conversely, most highly conserved elements escaped annotation using biochemical or other functional assays ...


ENCODE's extrapolative "conclusions" have been their undoing - even members of the ENCODE project have written that they do not accept the claims of 80% function (see, for example, Max Libbrecht on ENCODE’s results regarding junk DNA. « Genomicron ).

If it turns out that a substantial portion of that "junk" is functionally important to development of the organism then it presents the church of Darwinian mysticism with a major problem. It will suddenly be the case that different types of animals are far, far more dissimilar than previously assumed (as genetic similarity up to this point has been primitively based on only a tiny fraction of protein coding genes)...

This is simply totally false. I know - I did molecular phylogenetic analyses in graduate school and we, in fact, NEVER used coding regions. Further, whole genome comparisons have been done between many species and the relationships are the same.
and along these same lines is the problem of how that much beneficial genomic diversity was selected for in the allotted evolutionary timespans. (i.e. Haldane's Dilemma on steroids.)

I see that you are completely unfamiliar with Haldane's model as well. This is what happens when one relies on creation 'scientists' for their information on science.
 
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whois

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They have.
here are a couple of sources that say they haven't

The Paradox of the “Ancient” Bacterium Which Contains “Modern” Protein-Coding Genes.htm


Discovery of Bacteria That Hasn't Evolved in 2 Billion Years Is New Validation of Darwin's Theory - ABC News.htm

i have both of these on my hard drive.
 
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Loudmouth

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here are a couple of sources that say they haven't

The Paradox of the “Ancient” Bacterium Which Contains “Modern” Protein-Coding Genes.htm

How do they determine if a bacterium is ancient?

Discovery of Bacteria That Hasn't Evolved in 2 Billion Years Is New Validation of Darwin's Theory - ABC News.htm

i have both of these on my hard drive.

How did they determine that it hadn't evolved? Where is the 2 billion year old genome to compare the modern genome to?
 
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whois

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How do they determine if a bacterium is ancient?



How did they determine that it hadn't evolved? Where is the 2 billion year old genome to compare the modern genome to?
you need to read the material to ascertain that.
the first source is a science paper, the second is a news source.
 
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Loudmouth

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you need to read the material to ascertain that.
the first source is a science paper, the second is a news source.

You need to read Mother Goose.

"Peter Piper picked a peck of pickled peppers;
A peck of pickled peppers Peter Piper picked;
If Peter Piper picked a peck of pickled peppers,
Where's the peck of pickled peppers Peter Piper picked?"

Please read the material.
 
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Resha Caner

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Promoters are where the RNA polymerases sit down on the DNA strand. Transcription of RNA starts downstream of the promoter, and it includes the transcription of a ribosome binding site (RBS). That is where the ribosome sits down on the mRNA, and translation starts at the ATG downstream of the RBS.

From my understanding, RNA polymerases are much more specific than viral integrases. Therefore, viral insertion occurs all over the genome while RNA polymerases only bind to certain portions of the genome.

Thanks. That was the information I needed. From here my mind wandered to wondering if variations in conditions could have an effect. For example, would a change in temperature make viral insertion more or less specific with respect to a promoter site. I found papers discussing the impacts of things like temperature and salinity on virus behavior, but I'm not sure they specifically relate to what I was asking.
 
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Loudmouth

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Thanks. That was the information I needed. From here my mind wandered to wondering if variations in conditions could have an effect. For example, would a change in temperature make viral insertion more or less specific with respect to a promoter site. I found papers discussing the impacts of things like temperature and salinity on virus behavior, but I'm not sure they specifically relate to what I was asking.

Different conditions such as temperature, pressure, salt content, pH, flow, mechanical stress, and external radiation can affect protein function. As an example, there are really cool protein interactions in muscle that can change gene expression in response to mechanical stress:

Sense and stretchability: the role of titin and titin-associated proteins in myocardial stress-sensing and mechanical dysfunction. - PubMed - NCBI

It isn't crazy at all to think that protein function can change with temperature or other conditions. The hard part is determining exactly what those changes are, if they exist.
 
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Resha Caner

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It isn't crazy at all to think that protein function can change with temperature or other conditions. The hard part is determining exactly what those changes are, if they exist.

Nuts. I broke my streak. I think this is the first time I've asked a question that isn't crazy.
 
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