Larry Moran, Dan Graur and other garbologists (promoters of the junkDNA perspective), have argued SINES and ALU elements are non-functional junk. That claim may have been a quasi-defensible position a decade ago, but real science marches forward. Dan Graur can only whine and complain about the hundreds of millions of dollars spent at the NIH and elsewhere that now strengthens his unwitting claim in 2013, “If ENCODE is right, Evolution is wrong.”
Larry said in Junk in Your Genome: SINES
In humans, the largest family of SINEs is called Alu elements after the fact that the sequence is cleaved by the restriction endonuclease Alu. These SINEs are also derived from 7SL RNA but the rearrangement is different from that in mouse. (They have a common ancestor.) There are about one million Alu elements in the human genome.
SINEs make up about 13% of the human genome. The largest proportion, by far, is Alu elements but there are small numbers of SINEs derived from other cellular RNAs such as the U RNAs required for splicing and snoRNAs (Garcia-Perez et al. 2007).
SINEs are parasites (selfish DNA). They are not essential for human survival and reproduction, especially the huge majority of SINEs that are defective. Thus, at least 13% of the human genome is clearly junk. The total amount of junk DNA contributed by all transposable elements is 44% of the genome (Kidwell 2005).
Thursday, February 07, 2008
Where to begin? First off, Larry’s claim was made over 8 years ago. Larry ran the risk of becoming the butt of jokes since a scientific discovery here and there could overturn his precarious claims.
Below is a video associated with a 2015 paper from National Academy of Sciences, a mere 7 years after Larry’s claim was made. One important aspect of SINES are the CTFC binding site motifs often found in SINEs. The motifs can’t be randomly located, otherwise they would not properly create functional chromatin extrusion loops. Further, these CTFC binding site motifs must be coordinated to “point” in the right direction many base pairs away in order for these extrusion loops to form. See this amazing video of extrusion loops and CTFC binding sites (which are often found in SINES):
CTCF-binding locations represent regulatory sequences that are highly constrained over the course of evolution [sic]. To gain insight into how these DNA elements are conserved and spread through the genome, we defined the full spectrum of CTCF-binding sites, including a 33/34-mer motif, and identified over five thousand highly conserved, robust, and tissue-independent CTCF-binding locations by comparing ChIP-seq data from six mammals. Our data indicate that activation of retroelements has produced species-specific expansions of CTCF binding in rodents, dogs, and opossum, which often functionally serve as chromatin and transcriptional insulators.
…
We therefore searched for an alternative mechanism for the de novo creation in a common mammalian ancestor of the thousands of CTCF-binding events now found throughout mammals. Despite the generally high conservation of CTCF motif-word usage, we noted that specific sets of motif-words were overrepresented in rodents (mouse and rat), dog, and opossum (Figure 4A). We found that the vast majority of these overrepresented motif-words are embedded within SINE transposons (Figures 4B and andS4S4).
The following 2015 paper lists many roles of ALU elements, about 7 years after Larry’s claims about ALUs were vomited onto the internet. Will he feel as confident now about his claims or will retractions be forthcoming?
The role of Alu elements in the cis-regulation of RNA processing
Alu elements are an important engine for functional diversity within the primate transcriptome. As building blocks of extra genetic material, retroelements are used to invent new ways to vary mRNA. The almost 300 nt long Alu element is an ideal player for several reasons: (1) Alus are frequently inserted into non-coding regions of pre-mRNAs, (2) when transcribed, they easily form stable secondary structures that seed a number of different RNA processing events, and (3) small changes to their sequence make them targets for a number of RNA-binding proteins that regulate gene expression. Depending on its location and specific sequence, the Alu element can induce different RNA processing events (Fig. 5). If two inverted Alus reside on each side of an exon, they can form a double-stranded RNA structure that may induce back-splicing and the formation of circular RNA. An intronic Alu with a mutated or edited sequence can induce alternative splicing or Alu exonization. Inverted repeat elements can also contribute to transcript variations in a more fine-tuned manner by inducing A-to-I editing within coding sequence. Also, Alus in introns and 3′UTRs can provide both miRNAs and their target sequences. In this review, we have only highlighted a few examples of how Alu elements may contribute to transcriptome variation in primates. These effects certainly combine with the better explored genomic variations that Alus create. Future studies will most likely reveal additional mechanisms on how these elements modulate our genetics.
Here is an example from that paper:
Possible Alu-induced RNA processing events. a Inverted Alus on each side of an exon that form a dsRNA structure may induce exonic RNA circularization. b An intronic Alu with a mutated or edited sequence can induce alternative splicing and/or Alu exonization. c Inverted Alu elements forming a dsRNA structure frequently induce A-to-I editing at nearby sites. d Within introns Alus can contribute to maturation of miRNAs. eAlu elements in 3′UTRs may act as miRNA targets
Dazz, Petrushka,
I was referring to the genetic components of myopia and allergies. Petrushka was right to point out the environmental factors, and that was an oversight on my part for not being more rigorous.
For Myopia, here is one balanced viewpoint that suggests genetic factors:
http://www.the-medical-dictionary.com/myopia_article_6.htm
The view is many allergic tendencies are heritable:
http://kidshealth.org/en/parents/allergy.html
Of course, this all raises the philosophical question what does it mean to be healthy, dare I say physically “fit”. The medical notions of fitness are different than those of population geneticists.
I suppose Octomom would be considered “fit” by population geneticists since she has a strong desire to make so many babies and has passed on many copies of her genes. I think Dr. Phil and most of the USA think Octomom is unfit.
Sal Cordova says,
Every newborn baby has about 100 new mutations. If 10% of the genome is functional then this means about 10 mutations per generation in functional regions. Some of these mutations will be beneficial, some neutral, and some deleterious. If we just consider mutations in coding regions then there will be only one of two of these and many will be relatively neutral. The best estimates suggest that one third of mutations in coding regions are significantly deleterious enough to affect fitness.
The other parts of the functional genome might be even less susceptible to bad mutations so it’s reasonable to expect that every generation accumulates only one or two deleterious mutations. Most of them are recessive so they have no immediate effect on the survival of the individual. However, their accumulation in the population does cause a problem.
Dominant lethals will be eliminated right away.
There’s considerable controversy over the average number of deleterious mutations that can theoretically be tolerated in the human population. It’s almost certainly less than three (3). It’s probably more than one (1).
So it looks like having a genome that’s 10% functional is okay although Michael Lynch thinks we are headed for mutational meltdown.
You could create an entire ‘universe’ in the 1980s in 48Kb.
https://www.theguardian.com/books/2003/oct/18/features.weekend
My gravitar image represents 10% of that 48Kb.
How much would seem like enough information Sal?
Thanks for you comments Dr. Moran.
It is worth pointing out the medical community and the population genetics community have different notions of what defines fit and therefore what constitutes functional. Sometimes they coincidentally agree on what constitutes good and bad mutations like say a mutation that is lethal, but sometimes the definitions are incompatible.
There was an interesting experiment with Drosophilla, fruit flies. They were exposed to radiation and even though their organs and body functions were being obviously compromised, the isolated lab population was deemed fit! This was owing to the fact the flies kept making babies about the same rate as before, even with all the birth defects.
This shows how the S-coefficients which measure relative fitness just sort of float in the air, it is a concept that lacks the desirable characteristics of physical properties that tend to be more persistent like say mass or electron charge.
We may not actually go into reproductive mutational meltdown, we may just become sicker and dumber all the while making more babies. That apparently has been the case since the world became industrialized and are now 7 billion people.
If we just use the notion of functional in the medical sense and then assume most function compromising mutations will be selected against, but not more than the selection load a population can tolerate, we can still predict genomic deterioration. Whether that leads to population contraction (mutational meltdown) remains to be seen because there are so many environmental factors to consider.
I personally don’t like the notion of physiological function being related to reproductive success. Even Lewontin and Andreas Wagner pointed out this is a difficult way to judge what is and is not functional or what defines functional systems.
Wagner himself said:
which sounds a lot like Behe!
John Harshman,
It’s very popular in the pretentiosphere.
stcordova,
I’ll ask again: how does the enormous number of deleterious mutations you think have happened become fixed in a population the size of humanity’s in 6000 years?
Larry Moran,
I really struggle to see how, in a population with our characteristics.
[eta: ie huge and growing]
You can read his argument here: http://www.genetics.org/content/202/3/869
Sorry I missed your question. Brief answer, “I don’t know”.
Rhetorical question: If a deleterious mutation gets fixed (due to drift), what happens to the S coefficient of that trait? After a few generations we might just make that the new normal and set S = 1.
S is deleterious relative to some ideal in the population. When it becomes fixed in the population such that there are no variants for that trait (like say winglessness in beetles), it’s the new normal. It may stop being a drag on fitness of the population once it becomes fixed. That may sound absurd, but that’s why I take population genetic concepts with a grain of salt since it allows such absurdities. S is relative fitness in a competitive environment. It has little to say about absolute fitness of the population when the competition is removed — case example, the lab isolated drosophila population that was blasted by radiation. Other case examples are reductive evolution scenarios. It’s really hard to say what the impact of fixing bad traits (like missing organs in tapeworms) is on absolute fitness of a population or an entire species line.
How does anyone know something is deleterious or not unless one is measuring from some known ideal. I don’t know how many deleterious mutations have been fixed in the human population. If a lot of them hit around the time of Noah’s flood, then that’s a population bottle neck, it’s pretty easy to fix traits that way.
How much of the genome do you think is deleterious? That’s pretty hard to put a figure on.
So to answer your question, “I don’t know.”
I said I think there could be junk, but I also think 82.5 megabytes is an awfully small instruction base to build something like a human brain. Could we build an Artificial Intelligent system in 82.5 megabytes that can do the things a human brain can do like coordinate someone dancing and singing and learning and seeing and remembering, etc not to mention handling the process of self-assembling and self-healing?
I see little harm in adopting the 80% functional figure as working hypothesis for the medical community. It gets the job done and gets research funded. I certainly don’t see what’s coming out of this research as bad data. The HOTAIR lincRNA is a great example of a class RNAs once thought to be junk now thought to be functional, on top of that HOTAIR was the first known example of trans acting RNA regulation of DNA. There are many more candidates of such lincRNAs. Now we have the possibility of pseudogenes participating in miRNA regulation via sponging, CTFC SINES involved in chromatin extrusion, and ALU involved with regulation of circRNAs and then involved in neural development through A-to-I editing. I don’t see much need to try to settle the question of junk or functionality anytime soon. There are so many experiments that need to be done first….
As an aside, I think humans lost an awful amount of memory and brain capacity. Those few people that seem to remember almost everything — that may have been more the norm with the first humans, now it is the exception. If those people with such powerful minds could donate some of their cells or tissues, that might be helpful to us identifying what is and is not junk in our genome or whatever.
And presumably those first humans, like Noah, also lived for 900+ years?
stcordova,
Real answer: If a deleterious mutation gets fixed by drift, that is not the end of the matter. If an allele was deleterious and fixes, the selective landscape remains in place – it does not disappear on fixation; it’s just that (at that hypothetical moment) there is no allele around to exploit it. But the back-mutation, other mutations with similar or better advantage at the locus, and mutations at all other loci, are all being produced. A drift-fixed deleterious allele is (in all but the smallest populations) of shaky tenure, by comparison with any variant beneficial to an equivalent degree.
Over-extention of intuitions on single mutations being fixed by drift, with nothing else going on … it’s a bit of an oversimplification in my book. Makes the math easier, but does not address the probably highly dynamic reality.
But the problem I was probing at, for a YEC, is how a huge number of deleterious alleles can become fixed in the human population when it is expanding at a colossal rate, going from Noah to now (to say nothing of the required mutation rate). Most alleles fixing now must date back substantially further than 6000 years, and in a population of our size, vast numbers of mildly deleterious alleles will not be drifting to fixation, because the bigger the population, the less drift and the longer it takes. I wonder if Remine has anything to say on the deleterious substitution rate? He should, if consistent, be arguing against you and Sanford. If there ain’t time for evolution by NS, there certainly ain’t for extensive evolution by drift.
Dave Carlson,
Hmmm. Deleterious with respect to what? Human judgement? Benefit is conditional on the selective environment alleles find themselves in. If selection against deleterious alleles is removed, they are no longer deleterious. I don’t see the social/medical concerns as ‘genetic meltdown’ in Muller’s sense, an actual threat to the long term survival of the species.
We might not be able to sustain the selective environment indefinitely, for cost reasons, but that’s a different issue. We aren’t sustaining the actual environment very well either.
With the size and distribution of the global population NOTHING is going to get fixed either by drift or selection. If we assume a lot of deleterious are near neutral:
Time to fixation:
Ne ~= 1 billion
generation time ~= 20 years
4Ne = 4 x 1 x 20 = 80 billion years
But that’s a bit absurd since in that length of time, given accepted mutation rate, every nucleotide position will be mutated, so it’s pointless to invoke that approximation on those timescales — among other absurdities.
There are no alleles fixing now and maybe few any over the last few thousand years given the time to fixation equation. If we assume for the sake of argument humans were around for 200,000 years, an 4Ne x years ~= 200,000 implies and Ne of 2,500
since
4 x Ne x 20 years = 4 x 2500 x 20 years = 200,000 years
So I don’t know when anything was fixing since a few generations after Noah, if at all.
Function breaking mutations can be widespread in the population and cause damage without reaching fixation. It’s just that every individual has a different set of defects than any other individual. That was the problem I highlighted here, it’s not the rate of fixation of the bad, it’s what I call the breaking rate problem, which is essentially Muller mutational load problem:
Yes, when God cursed humanity.
Sal, I assume you aren’t going to address Larry’s numbers in any detail. Which of them are wrong, and why?
stcordova,
Therefore the population is NOT in mutational meltdown.
That’s not mutational meltdown. If smaller demes get different sets of detrimental alleles, that is hardly going to be a problem for the entire species. The non-detrimental alleles still exist in vast numbers.
That petulant, short-sighted asshole! “I’ve made a fruit, don’t eat it, you ate it, now you’re for it. And your descendants” But still, the earth is only 6000 years old or so, sez you. So I don’t know what you are agreeing with there.
stcordova,
Human Ne is nothing like 1 billion.
stcordova,
The principal absurdities are in your analysis. The fact, it fact if were, that every nucleotide position may be mutated in a given time period has no bearing on fixations. You have probably explored a substantial amount of nucleotide space in your gonads. Things actually have to get into multiple descendants to be of evolutionary significance. And there are only so many spaces available in a population at a given time.
This is reminiscent of Behe’s daft argument on Plasmodium‘s exploration of genetic space.
stcordova,
That’s absurd. You think Ne can be derived from population age and generation length?
Uh, Allan, world population today size is 7 billion, Ne of about a billion today is not far fetched. You’re looking at your evolutionary theories again and not actual physical facts.
What’s six orders of magnitude between friends?
Sal, can you provide some examples of estimates of effective population size that don’t use evolutionary theory (i.e., population genetics) in any way?
I don’t have strong opinions on Lynch’s thesis, but the paper is well written and interesting. I would recommend reading it in full (if you have already, my apologies!).
stcordova,
Uh, Sal, You Are Wrong. Again. There’s no point plugging a value for ‘Sal-Ne’ into Kimura’s equations, which are based upon evolutionary Ne. The two bear very little relation to each other, except they are both numbers.
You should try and understand what Ne represents if you want to do ‘rithmetic with it. You are basically saying that the modern human population has the variation that would be expected of an ‘ideal’ steady-state panmictic population of 1 billion. That’s nonsense. Or, don’t use the term ‘Ne’ when you mean something else.
Dave Carlson,
It’s been a while but I have read it. My post was an imagined discussion with Lynch!
You want to stand by a silly claim that the world’s present Ne must only be tens of thousands, go ahead. By you criticizing my value of 1 billion, that’s pretty much what you’re doing because that Ne ~= 1 billion figure was in reference to the present day, not in the past (where I referenced Noah, and my presumption of Ne ~= 8 for Noah’s time).
Besides, this is way off topic. The topic was function of SINES and ALUs.
Thanks any way for the conversation even if it was way off topic.
From this paper:
http://www.ncbi.nlm.nih.gov/pubmed/26803450
So much for the suggestion ALUs are junk, at least in primate brains. 🙂
In light of the data on ALUs, are there commenters out there who want to insist absolutely that ALUs are junk, or is there at least a spectre of possibility ALUs (a subset of SINES) have important function, at least in human brains?
From Bio Numbers:
http://bionumbers.hms.harvard.edu/bionumber.aspx?id=111915
So, is 10% of the genome formerly junk now possibly functional? Any objections?
Did God curse humanity as Salvador claims?
Here is what one site says:
I bet it would be interesting to see what the various young earth creationists and biblical literalists (like the atheists here at TSZ represented by the likes of keiths and Richardthughes) have to say about this.
No doubt there is an algorithm for that.
I just love all the comments which address the person not the idea. Can we stop pretending that “the moderators” here at TSZ are not just a bunch of atheist stooges?
This kind of BS makes me want to puke. Salvador is not a Young Earth Creationist, he is a Young Life creationist.
He realizes that the earth is more than 6000 years old, and that the universe is more than 6000 years old, but clings to the hope that life itself is recent.
Which of you is more than 6000 years old? No one? QED.
stcordova,
I want to stand by the claim of what Ne means. And in those terms, yes it is of the order of thousands. It is evidently not what you think it is, but God forbid you should learn anything. You took an evolutionary parameter (Ne) then plugged a random value into it that does not represent what Ne means in evolutionary equations. There is no way, beyond hypermutation, that you could have an Ne of a billion by growth of a population that was 2 6000 years ago with 20 year generations. Nor one that only hit a census size of a billion 250 years ago.
If Sal-Ne is nothing to do with evolution, stop using it in an evolutionary computation.
Well might you say ‘oh, this is off topic. ALUs are RAM.’.
Mung,
Sal self-describes as a YEC.
Sal, glad to see that, when prompted, you were able to figure out that the text you bolded in the OP is specifically NOT talking about Alus. Your OP was a mite misleading there, and site rules require me to assume that you didn’t understand the difference between SINES and Alus when you wrote the OP.
[Cue Sal petulantly pointing out that Alus are a subset of SINES, and that he has demonstrated that he knows this. Heh.]
I object.
What proportion of those one million Alus are in genes? In exons?
For what proportion of those one million Alus has the RNA-editing been shown to be functional?
Perhaps 0.1% of the genome formerly “junk” is now functional? Any objections, Sal?
Similarly, 5,000 CTCF-binding sites represent 0.01% of the genome.
Care to ever actually, y’know, do the math?
Right on que.
I said way back here:
Do you not have issues reading that phrase. Oh yeah you’re the same guy I had problems with phrases “somtatic and/or transgenerational” that I had to draw up venn diagrams that are appropriate for 2nd graders to help you with comprehension.
The structure of the OP is based on Larry Moran’s comment that inspired the OP:
Take that! The distinction was made in the OP through quotation of Dr. Moran. Did you miss it? You’re misrepresentation and veiled insult has been called.
The first part of the OP described CTFC-binding-motif-bearing-SINES involved in chromatin extrusion before the OP went into the second part which turned out to be more substantive, namely ALU SINES.
I merely argued for possibility, not the absolute demonstration of every nucleotide. I already said I think there is junk in the genome, but I’m not willing to write off entire classes of DNA like ALU merely on evolutionary whims that have ZERO experimental evidence like some of those here at TSZ and elsewhere.
In contrast, there is experimental evidence supporting the hypothesis of ALU having function.
From the biostars citation and this paper:
http://www.ncbi.nlm.nih.gov/pubmed/26803450
“editing is predicted to occur at over a hundred million sites, with the vast majority positioned in primate-specific inverted repetitive elements of non-coding Alu sequences:”
100 million is about 3% of the genome. So what is the vast majority (51%-99%), so that is about 1.5-2.9%. So you’ve understated the figures by a factor of about 15 to 29.
But then the ALU itself being repetitive means it is a motif and likely used to provide some sort of binding address for molecular machines, so maybe the whole ALU is functional as a whole since the whole ALU is apparently needed to from ALU-derived dsRNAs.
I just did, apparently you didn’t.
And from this paper:
http://genome.cshlp.org/content/early/2013/12/17/gr.164749.113.full.pdf+html
We’ve been over the radiometric argument with Sal. He’s a YEC.
LOL, Sal.
My questions were based on the idea that you had read (and understood) the paper you were quoting from.
I should have known better. 😉
Still no response re the proportion of RNA-editing that is functional, I see.
I am curious, though: when you wrote the OP, did you realize that the text you chose to bold was specifically NOT about Alus?
Yes, can’t you read. I introduced what the first paper I was referring to:
So I was talking about SINES containing CTFC binding sites.
Sheesh. Your ability to misread is breath taking.
I then addressed ALU SINES in particular after addressing SINES containing CTFC binding sites.
Grasping at straws now since you can’t refute the substance of the claims, you have to misread what is written in order to make semblance of a rebuttal.
You yourself don’t show too much understanding by this comment:
Why be concerned with the few ALUs in exons? A large fraction of ALUs are in introns which are part of genes, which when paired, create dsRNAs which apparently participate in determining whether there will be constitutive vs. alternative splicing.
The paired ALUs that form dsRNA are about 3/4 the 1 million ALUs.
and
Take that!
Any more straws to grasp at?
I also just refuted you erroneous calculation of 0.1%. Are you going to even acknowledge you didn’t comprehend the biostar numbers provided earlier from which, if you had bothered to read, would have saved you making yet another stupid set of remarks.
Take that, DNA_jock, your getting outshined by the real RNA world of the transcriptome and the editosome. RNA rocks.
But anyway, thanks for the conversation, I’ll rephrase things differently in the future so you won’t have such worthless quibbles on that topic again. But now that you’re math has been corrected, what do you think about the possibility of ALU functionality? Possible or not possible. Worth exploring or not worth exploring?
stcordova,
Sal, you might (I only say might 🙂 ) get better treatment here if you could rein in your tendency for triumphalism, hyperbole and cherry-picking.
FYI it’s Alu, in honor of Arthrobacter luteus, not ALU.
Still no estimate as to the proportion that are functional, nor evidence to support any estimate.
So, no math then.
I’ll take that.
🙂
I believe Sal was, at least at one point, toying with “old earth, young life”, which is if anything sillier than YEC.
Hey, the second good thing you said, I was in error to capitalize the last two letters. What a pal.
The first good thing you said was what an interesting paper I presented on chromatin extrusion.
ProbablY a holdoveR from ALU in thE computeR worlD:
https://en.wikipedia.org/wiki/Arithmetic_logic_unit
petrushka,
There is no point too small for Mung to score. Had I said ‘life’ instead of ‘the planet’, not one iota of my intent would have been lost. So we can consider it so amended. I’d hate to make anyone puke.
Actually ALUs are Arithmetic Logic Units, and Alus are the most dominant class of SINES. See, dnA_JOck taught me how to use lower case “l” and lower case “u”. 🙂 Things I learned today….
You seem more interested in talking about my YEC views than an interesting biochemistry and molecular biology topic like CTFC SINES’ role in chromatin extrusion and newly discovered potential function of Alus:
You give the impression to me anyway you’re disappointed to hear about these amazing discoveries. You’d rather talk about me and my l’ole YEC views than these experimental results.
You don’t seem at all excited about the possibility we have discovered new amazing biological machinery like A-to-I editing’s role in brain function. Has your interest in this sort of science waned? I find it pretty exciting personally to think what a truly amazing device the human brain is and what a clever way Alus (once thought to definitely be junk) may be recruited to make the human brain more special than any brain in the animal kingdom (or all life for that matter). You don’t seem to share my enthusiasm for these recent scientific discoveries. You prefer to talk about my YEC views than science. Well, I’m flattered, but now’s your chance to talk about some new science discoveries rather than my YEC ideas, so I suggest you seize the opportunity to talk about Alus in this wonderful exploration of new found possibilities of function in the human genome.
stcordova,
Well, I’m glad at least to see that you realize your YEC ideas aren’t science. I will admit in turn that I’m less interested in your fuzzy-minded notions of physiology than in any justifications or explications of YEC. Perhaps it’s because I’m a systematist.
stcordova,
Yeah, thing is, I was paraphrasing you, so nice try but no banana.
stcordova,
The subject came up, and is relevant to debates on junk, so I pursued it. It’s also relevant to your oft-pursued thesis that the human genome is degrading in some way. Which you now seem disinterested in.
I’m quite interested in YEC, but the OP didn’t mention YEC, and none of the papers I cited in the OP were related to YEC, and the issue of A-to-I editing and functionality of Alu’s and other SINES is independent of YEC. So it should have been clear the topics in the OP are what I was hoping the discussion would focus on.
You could talk about whether you agree with the inferences like those made in the PNAS and Cold Spring Harbor papers (both publications are from highly reputable institutions) regarding Alus. Do you think Alus are important to primate brain development, or do you at least accept the strong possibility.
And if you want to talk about chromatin extrusion and the pairing of CTFC SINES, that’s fine as well.
I love Sal.
All these things he mentions support Young Earth Life.
But we know that the earth is not 6000 years old and that life on earth is not 6000 years old.
Young Earth Life Creationism is Dead.
stcordova,
You’re a fine one to grumble about derails, Sal Cordova! It came up in comments. Perhaps you should have a look at the second part of your OP title.
(I paraphrase) “Alus Have Function And Evolutionists Are Talking Crap”.
“… hey, how come no-one wants to talk about Alu function?”.
Population genetic considerations are relevant to junk DNA, and whether ‘garbologists’ are wrong, and generations, population size and fixation times come into that. If you’re arguing for a population genetic mechanism that is inconsistent with the time you think available, it’s worth a mention I feel.