Yes.
And also:
“If whenever you picked something of the ground and let go of it, it stayed suspended in the air and never fell back to the ground, gravity is wrong.”
So if you thought the Bible said gravity does not exist, you would be going thru the same song and dance routine to convince us that rocks stay suspended in the air when you let them go.
Not a good look, Salvador.
Why is that more of a problem for evolution than a problem for reproduction? Haven’t you just shown that the human population is rapidly decreasing toward extinction? Incidentally, what’s your position on whether bumblebees can fly?
That’s an interesting point. As uncharacteristic as that would be, it appears Graur may have been overly cautious and circumspect in saying “If ENCODE is right, evolution is wrong.” He could have said, “If ENCODE is right, everything we know about human inheritance and reproduction is wrong.”
It’s even more restricted than that. If ENCODE is right, then population genetic models of the deleterious rate of mutation are wrong.
ENCODE hypothetically being right doesn’t somehow erase the evidence for the long and shared evolutionary history of all life. That’s what creationists like Sal want Graur to be saying, but that wouldn’t actually follow.
Consilience of independent phylogenies, the temporal distribution of fossils, and nesting hierarchical structure in the data, doesn’t magically stop being evidence for common descent, just because some models could theoretically be wrong about the deleterious load of mutations.
Ironically if ENCODE is right, then GE is doubly wrong, because that would imply natural selection has been extremely effective at weeding out deleterious mutations over life’s incredibly long history.
Interesting. Yet another point for Sal to try his best to handwave away.
Mature female cod produce around a million offspring. That would seem sufficient to overcome genetic entropy.
No it isn’t - that statement neither supports nor refutes Sanford’s thesis. It is perfectly possible for ENCODE to be right, evolution to be wrong and Sanford’s genetic entropy theory to still be a load of foetid dingo’s kidneys.
Not if the entire cod genome is functional, based on the formula Sal has latched onto.
Maybe, but not overfishing, sadly:
The cod genome would need to be fully functional and the same size as the human genome.
I wonder how many offspring puffer fish produce?
That isn’t necessary. It’s the quantity of functional sequence that needs to be considered.
Now that’s an interesting question. A little google finds that puffer fish in general lay only small numbers of eggs; one source says 3 to 7. Based on Sal’s formula, puffers should have been extinct within a few generations of their creation. So, if our estimate of the functional genome size of fugu is correct, there can be no such thing as fugu. Or perhaps Sal’s model of selection is wrong.
Again, you are ignoring sequence conservation. Are microRNA sequences conserved? In the vast majority of cases, yes they are.
Let’s also look the numbers. You are claiming that there are about 2,400 functional elements in introns. How many introns are there? About 207,000. This means that just 1% of introns have these functions, and that’s if we count the entire length of the intron which certainly isn’t needed. What percentage of the human genome is made up of introns? About 30%. This means that you have found function in just 0.3% of the genome. How does that change our conclusion that the vast majority, around 90% of the human genome, does not contain sequence specific function?
I am also confused as to your problem with miRNA in general. Why couldn’t miRNA regulation evolve? A mutation in the 3’ UTR of a gene produces a new binding site for an existing miRNA. If downregulation of that gene’s translation is beneficial in conditions that also upregulate expression of the miRNA then the mutation is kept. Mutations in the promoter region of the miRNA or its host gene can also have beneficial, deleterious, or neutral effects that can be seen by natural selection. You could also have duplication of an miRNA which is then free to mutate and find new targets in currently unused portions of a 3’ UTR. Where exactly do you see a problem?
It’s revealing what @stcordova chooses to omit. Let’s lend a hand (note that I will use very round numbers here and may toggle between nts and bp - this is to make the post easy to write and read):
From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5199132/:
The total number of introns in protein-coding genes = 134,497 (non-redundant)
total intron length = 9.4x10^8 bp (non-redundant)
In long-non-coding RNAs, the total number of introns = 21,297
Intron length in these = 2.1x10^8 bp
Thus, total intron length = 1.1x10^9 bp (approximately)
Every intron has a core of some 20 nts that is needed for splicing. This adds up to 3x10^6 bp of function.
If every intron has an enhancer that binds 5 transcription factors, and if every TF binds a 10 nt sequence, this gives us about 8x10^6 bp of functionality.
If every intron binds five splicing regulators, and each of these binds 10 nts of RNA, then we have another 8x10^6 bp of functionality.
Sternberg mentions 1664 microRNAs and 717 stable RNAs (snRNAs, snoRNAs). Generously, there will be 10^7 bp of functionality in these two groups (combined). (This is a wild overestimate – in reality, these classes of RNA contribute less than 0.1% of all intronic sequences).
Sternberg mentions 78,147 intron-derived non-coding RNAs. The paper he cites is old and draws from EST sequences, so it is not clear how many of these are “real”. However, the authors of the study note that:
“An overlapping tissue expression signature was detected for both species, comprising 198 transcripts; among these, 22 RNAs map to intronic regions with evidence of evolutionary conservation in humans and mice.”
So most of these may not be authentic. However, let’s say that all 78,000 or so have some function, mediated by binding to proteins. If each one binds 10 proteins (a very generous assumption), and each protein binds to a 10 nt motif, then each RNA would have 100 nts of functionality. This gives us 8x10^7 bp of functionality.
Adding these things up, then we come up with an estimate of some 10^8 bp of functionality. I would point out that I have made assumptions that are tremendously favorable to @stcordova – all introns don’t have enhancers, and all introns won’t bind splicing regulators, and intronic RNAs won’t all have function or bind so many proteins. Even when granting all of these things, we can see that less than 10% of all intronic sequences might be functional.
It’s pretty hard to see how one gets from this to the claims by IDists (like Sternberg and Wells) that 80% or more of intronic sequences are functional.
Or at this point we have identified 10% of known function inside introns. I think part of what maybe missing is what is required during embryo development.
And, right there, you have the entire science vs ID debate in a nutshell. @Art spells out the evidence clearly and in detail in a manner than no objective person could fail to understand
Then Bill just up and writes some nonsense he made up with nothing to support it, and figures he’s battled to a draw.
You are entitled to believe in the privacy of your own head, whatever makes you comfortable. Just don’t confuse your imaginations with empirical facts.
Empirical facts Rum 
An empirical fact is that in pubmed under introns in embryo development has produced 800 papers in the last 38 years and 100 over the last 6 years. "Functional introns" has produced 12 papers since January 1 of this year.
There is a hair bit of new information coming out about functional introns.
Infinitely better than disembodied mind magic POOF. 
Based on the low sequence conservation seen in introns (zoom into this browser track for an example), this expectation would lead one to conclude that animals that proceed through an embryonic stage cannot exist. At least, if I am understanding @colewd correctly in suggesting that the 90% of intronic sequences function in embryo development.
I think that the sequence integrity may have less to do with function then the length of the sequence which can help control expression timing during embryo development.
