Some evidence ALUs and SINES aren’t junk and garbologists are wrong

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):

Waves of Retrotransposon Expansion Remodel Genome Organization and CTCF Binding in Multiple Mammalian Lineages

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:
alu example figure 5

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

129 thoughts on “Some evidence ALUs and SINES aren’t junk and garbologists are wrong

  1. stcordova: Well, I’m flattered, but now’s your chance to talk about some new science discoveries rather than my YEC ideas

    Why would anyone want to seriously ‘talk science’ with you when you’ve shown exactly what you think of ‘science’ over the years?

  2. Something to note in a forgotten article by evolutionary biologist Richard Sternberg. It will take two comments to show his point. So this comment is the first part…

    This figure below is from this freely available paper:
    http://www.nature.com/nature/journal/v428/n6982/full/nature02426.html#f12

    The fortunes of these SINEs during mouse and rat evolution have been different (Fig. 12). B4 probably became extinct before the mouse–rat speciation, while B2 has remained productive in both lineages, scattering >100,000 copies in each genome after this time. Interestingly, the fate of the B1 and ID SINEs has been opposite in rat and mouse. While B1 is still active in mouse, having left over 200,000 mouse-specific copies in its trail, the youngest of the 40,000 rat-specific B1 copies are 6–7% diverged from their source, indicating a relatively early extinction in the rat lineage. On the other hand, after the mouse–rat split only a few hundred ID copies may have inserted in mouse, whereas this previously minor SINE (approx 60,000 copies predate the speciation) increased its activity in rat to produce 160,000 ID copies.

    The figure shows the sequence divergence of various classes of SINES:

  3. Part 2 of the comment stream started previously. Sternberg references the diagram below.

    http://www.evolutionnews.org/2010/03/beginning_to_decipher_the_sine032981.html

    That Strange SINE Signal…Again
    The almost one-to-one correspondence of mouse-specific and rat-specific SINE insertion events along homologous regions of the two genomes is almost as remarkable as the matching geographical distributions of the monoliths in the analogy of the two moons. Remember the graph (from Figure 9c of Ref. 1):

    We have two genomes that went their separate ways 22 million years ago. We have two lineages that have been subjected to different historical events. Yet, when we compare the chromosome locations of mouse B1s/B2s/B4s with those of rat IDs, they look almost the same. Where the ID SINEs rise in density, so do the B1s/B2s/B4s SINEs; where the ID SINE levels decrease, so also do the B1s/B2s/B4s SINE levels. Independent mutational events have generated equivalent genomic patterns. How can we causally account for this striking pattern?

    In the paper written by Francis Collins and his colleagues, under the heading Co-localization of SINEs in rat and mouse1, we read:

    “The cause of the unusual distribution patterns of SINEs…is apparently a conserved feature, independent of the primary sequence of the SINE…” (Italics mine.)

    Let’s unpack this part of the sentence. We have:

    1) A cause of some sort.

    2) A cause that is conserved between the mouse and rat.

    3) A cause that is independent of SINE primary DNA sequences.

    That’s all very well and good, but the specific cause is never mentioned. Where, then, can we find it?

    Thinking Like a Darwinian
    Experts such as John Avise, Francisco Ayala, Francis Collins, and Darrel Falk tell us that we must think like Darwinians before we can begin to make sense of the data, since nothing else is scientific, or indeed even reasonable. So let’s play along and think like Darwinians, limiting ourselves to what Collins and his colleagues have authoritatively provided. Recall that they are:

    •Chance mutations continually degrade genomes that are largely junk

    •SINEs are for the most part nonsensical junk

    •Natural selection is the sole creative force in evolution

    •Except when genetic drift (neutral evolution) is also a factor

    We can call this conceptual scheme the “BioLogos box.”

    We’ll start, then, with chance mutations. We know that the enzymes encoded by the L1 retrotransposon copy and paste SINEs into mammalian genomes. So perhaps this is the causative agent that acts independently of primary DNA sequence? And since L1 is present in all mammalian genomes, we may just be on the trail of the “conserved cause.”

    But wait. L1 also mobilizes itself. This is a problem, for when we compare LINE and SINE distributions along chromosomes, it is clear that in the regions where the former is abundant the latter is not, and vice versa. Remember the graph (from Figure 9d of Ref. 1):

    But we have no plausible mechanistic explanation for why the mouse L1 machinery would have pasted B1s/B2s/B4s–over twenty-two million years, no less–into the same general locations and at much the same densities, as the rat L1 machinery pasted ID elements over the same period of time.

    Not to fear. We still have to consider that worker of miracles, natural selection. This mechanism eliminates harmful features while preserving those that enhance survival. So let’s construct a hypothesis: Mouse and rat SINE distributions reflect the differential removal of these DNA repeats from regions where their presence would be harmful. In other words, we predict that sequences where mouse B1s/B2s/B4s and rat IDs peak in density are segments of the genome that are largely junk; conversely, in the sections where these SINEs taper off, functional coding regions are to be found.

    Does this hypothesis point in the right causal direction? I don’t think so. Here is why. Remember the statement made by Falk in defense of Ayala contra Meyer:

    He [Ayala] does say that on average there are about 40 copies of Alu sequences between every two genes, but this is simply a fact.

    Well, both Falk and Ayala are correct–and that is the problem with the selection hypothesis. Protein-coding genes make up only ~1.5% of the mammalian genome. Where do the peaks of B1s/B2s/B4s and IDs occur along the mouse and rat chromosomes, respectively? In and around the ~1.5% of the genome that is protein-coding. Remember the following statement in the sentence of the Nature paper quoted above1:

    The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature, independent of the primary sequence of the SINE… (Italics mine.)

    Whatever the mystery cause is, it plucked out the species-specific SINEs from the junkety-junk LINE regions, and piled them high around the “twenty-five thousand genes” of the mouse and rat. Or it directed the SINEs to rain down on the gene-rich regions and in much lesser amounts elsewhere. This contradicts our selection hypothesis, unless the SINEs are doing something important in and around those protein-coding regions. But since so much ink has been spilled arguing that nothing of the sort is the case–these are junk elements, even harmful–we must turn to some other factor.

    Reaching into the BioLogos box, we now pull out “genetic drift.” Neutral evolution means that a mutation–regardless of whether it is beneficial, neutral, or negative–can become fixed or lost in a lineage solely by chance. With respect to a SINE insertion, its persistence in a lineage would have to be a genetic coin toss: If heads, the SINE stays in a site; if tails, it is lost. So for a pure neutralist model to account for the graphs we have seen, ~300,000 random mutation events in the mouse have to match, somehow, the ~300,000 random mutation events in the rat.

    What are the odds of that?

  4. DNA_jock:

    I object.
    What proportion of those one million Alus are in genes? In exons?

    From this paper, at around 3/4 are in genes in the introns, and introns are part of genes.

    , 730,622 Alu elements that reside within introns
    and 185,534 introns were extracted.

    https://www.researchgate.net/publication/23281933_Intronic_Alus_Influence_Alternative_Splicing

    and

    In exons?

    Introns aren’t exons, DNA_Jock. 🙄

    Additionally, from:
    http://rnajournal.cshlp.org/content/19/5/591.abstract

    It seems that the AS genes, and specifically, the AS RNA processing genes, contain more Alu repeats and more organized secondary structures and therefore more editing sites than any other genes. Higher numbers of reverse-oriented Alu repeats and secondary structures increase the probability of both editing and AS.

    In human, RNA editing was also shown to be frequent in the central nervous system (Levanon et al. 2004). Improper RNA editing was found in neurological disorders including depression, epilepsy, amyotrophic lateral sclerosis, and schizophrenia (Maas et al. 2006; Grohmann et al. 2010). Lower levels of editing were found in glioblastoma multiforme (GBM) and have been associated with epileptic seizures (Maas et al. 2001; Paz et al. 2007). The wide extent of RNA editing in the CNS and the relation between ADAR activity and AS, as globally examined and demonstrated in the present study, highlight the importance of ADAR in the acquisition of higher functions in primate evolution.

    Shazam!

    Despite this:

    DNA_Jock says:

    Still no estimate as to the proportion that are functional, nor evidence to support any estimate.

    Don’t equate plugging your ears and closing your eyes as the same thing as absence of evidence. I cited several papers providing reasonable evidence of function. The fact that doesn’t count as evidence for you doesn’t mean it should not count as evidence for everyone else.

  5. stcordova,

    SINEs may differentially accumulate in gene rich regions because they are the regions most accessible to their mode of action. It’s harder to transpose into heterochromatin. But no, evolutionary theories, mechanistic constraints, loadabollocks, lalalalala.

    Introns part of genes? Hmmmm. Depends, really.

  6. Oh, Sal,
    My “exons” question was a test, to see if you actually read and understand the papers that you cite. You failed.
    But you are getting there, Sal, albeit very slowly.
    Here’s an easier question:
    Of the million Alus, how many intronic inverted pairs are there?

  7. There’s a guy in Australia who picked up a multi-pound chunk of nearly pure gold.

    Proof that not all the earth’s surface is devoid of large chunks of gold.

  8. My “exons” question was a test, to see if you actually read and understand the papers that you cite. You failed.

    Kind of funny hearing that from the guy who could not comprehend that 100 million editiable sites implies more potentially functional genomic sites than the pathetic 0.1% you said were potentially functional in Alus.

    DNA_jock’s math:

    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?

    http://theskepticalzone.com/wp/some-evidence-alus-and-sines-arent-junk-and-garbologists-are-wrong/comment-page-2/#comment-138136

    The lack of understanding is yours since a large fraction Alus, around 3/4, is in the introns, not exons. Cold spring harbor reports 100 million editable sites mostly in Alus generated RNA transcripts. I cited the report here:
    http://theskepticalzone.com/wp/some-evidence-alus-and-sines-arent-junk-and-garbologists-are-wrong/comment-page-2/#comment-138138

    I knew about the Cold Spring Harbor paper, because I looked up some of the references in the papers cited in the OP. Pretty sharp of me, eh?

    Here is a math lesson for you DNA_jock.

    There are around 3.3 gigabase pairs in the genome, or 6.6 gigabases (counting both strands). If 100 million DNA sites transcribe to 100 million RNA sites that are editable, that implies 100 million RNA editable sites that can be generated by 100 million DNA sites. (since A is editable, but T on the other strand is not, 100 million DNA base pair positions transcribe to only 100 million A-to-I editable RNA positions, not 200 million A-to-I editable RNA positions).

    100 million / 6.6 giga bases ~= 1.5%.

    Do you need lessons on how to use a calculator, because 1.5% is a lot bigger than your 0.1% figure. I derived the 1.5% figure by taking the figures in the papers I cited, you asserted the 0.1% figure because you were obsessed with Alus in exons rather than realizing Alus could be functional while residing outside of exons.. In other words you got caught pulling figures out of your fuzzy misunderstandings, just like you argue chromatin is a fuzzy concept.

    After being caught, and offer a retraction and say, “Sal was right”, you spin spin spin.

    Here’s a suggestion, before you pretend you actually are in a position to look down your nose at me, you might want to try comprehending

    100 million/ 6.6 giga bases ~= 1.5%, not 0.1%.

    Maybe you should change your handle to DNA_howler. Hahaha!

  9. LMAO
    I objected to your claim

    So, is 10% of the genome formerly junk now possibly functional? Any objections?

    Asking you the question:

    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?

    which question you have yet to even attempt to answer.
    To make it easier for you, Sal, I asked you:

    Of the million Alus, how many intronic inverted pairs are there?

    because those are the ones that your sources claim might be involved in RNA editing. And the number is available in the sentence following the one you quoted as your source of the 3/4 in introns number.
    From Sal’s reference:

    Overall, 730,622 Alu elements that reside within introns
    and 185,534 introns were extracted. This analysis showed that
    there are 85,126 introns that contain at least one Alu element; of
    these, 5009 introns contained at least two Alu elements in opposite
    orientation.

    5009 x 300 x 2 (generously assuming that the entirety of both Alus is required, but not counting redundant pairs) = 3 million.
    3 million / 3.3 billion = 0.1%
    Your misplaced triumphalism makes me smile.
    But these numbers are meaningless, until you can produce and defend an estimate for what proportion are in fact functional…
    ETA: The CSHL count of “editable sites” is meaningless; by this standard, every base pair is potentially functional.

  10. because those are the ones [Alus in exons] that your sources claim might be involved in RNA editing.

    No, and that’s howler. You say that right after I cited a paper on intronic Alus, which refers to Alus within introns, not Alus within exons. Too funny. Here is it is.

    https://www.researchgate.net/publication/23281933_Intronic_Alus_Influence_Alternative_Splicing

    Intronic Alus Influence Alternative Splicing

    Author Summary The human genome is crowded with over one million copies of primate-specific retrotransposed elements, termed Alu. A large fraction of Alu elements are located within intronic sequences.

    Gee, DNA_jock, did you not notice intron is spelled “INTRON” not “EXON”.

    The papers I cited involved lots of intronic Alus not exonic ones — you know, the ones that are called “Intronic Alus” right there in the title of the paper you refuse to acknowledge. Boy talk about stubborn determination to remain in denial right when it is spelled out in the title of a paper I cited.

    DNA_Jock with his usual LMAO to hide the fact he got caught:

    3 million / 3.3 billion = 0.1%

    Contrast DNA_Jocks claim, with cold spring harbor laboratories (a respected organization):. He just embarrasses himself with his calculations.

    http://genome.cshlp.org/content/early/2013/12/17/gr.164749.113.full.pdf+html

    Taking into account expression of both strands, this brings the total number of editable genomic sites in the set of editable Alus to 105.7 Mbp, representing 1.5% of the entire bases in the human genome. It should be noted that additional Alu elements not belonging to the ‘editable Alu’ set are also heavily edited

    The calculation is basically:

    105.7 million / 6.6 billion = 1.5 %

    DNA_jock just pulled his numbers out of his one non-reading.

    The CSHL count of “editable sites” is meaningless; by this standard, every base pair is potentially functional.

    You have a problem with that? But the bases that are described as editable are those that are ADAR mediated edits not any possible edit, specifically edits on A’s. C,G, and T aren’t ADAR mediated A-to-I editable. You’d think someone with the handle “DNA_Jock” would understand A-to-I editable doesn’t mean C, G or T are A-to-I editable. Howler. That’s even more funny than you’re “chromatin is wonderfully fuzzy concept” claim.

    Sure there could be other ways to edit the other bases, but those aren’t A-to-I edits. The most common RNA edit known so far is A-to-I edits.

    Furthermore, other researchers actually did sequencing to specifically find that the Alu generated RNAs showed actual editing (not just potential editing) in ways they believed quite meaningful to brain function:

    http://www.cell.com/trends/genetics/abstract/S0168-9525(04)00332-4?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0168952504003324%3Fshowall%3Dtrue

    To check whether the detected differences are primate- or rodent-specific, we repeated the two analyses (single and multi mismatch counts in RNAs relative to genome) on the genomes of rat (10 999 RNA sequences), chicken (19 218 RNA sequences) and fly (14 632 RNA sequences). These genomes showed editing patterns similar to the mouse genome (Figure 1), suggesting that the differences seen between human and mouse stem from unique primate- (or human-) specific factors.

    Editing levels vary between different tissues 13 and 22. Thus, differences between the tissue distributions of available human and mouse RNA sequences could lead to a bias in our results. To rule out this possibility, we repeated the human–mouse comparison for RNA sequences of the same homogeneous tissue origin. We used three different tissues that have a significant and similar number of sequences for both organisms: brain, thymus and testis. We found that the level of editing in human is significant in all three tissues (at least 3% of sequences are edited), whereas in mouse the editing is undetectable

    So there is detectible actual A-to-I editing, not just potential editing (as you insinuate). Furthermore, as pointed out in another paper:

    http://www.ncbi.nlm.nih.gov/pubmed/20566853

    Binary use of A or I in millions of sites in the neural cell transcriptome can be considered equivalent to the 0’s and 1’s used for information storage and processing by computers. It is tempting to speculate that the more abundant RNA editing found in the human brain may contribute to the more advanced human capabilities such as memory, learning, and cognition. This suggestion is consistent with the hypothesis that the advantage of complex organisms lies in the development of a digital programming system based on noncoding RNA signaling (46, 56). The combinatorial posttranscriptional RNA editing of noncoding sequences may therefore contribute to higher brain functions

    You don’t want to accept the opinions and findings that Alus are actually edited and therefore potentially functional, that’s up to you, but these authors have more credibility with me because they apparently know

    105.7 million/ 6.6 giga bases ~= 1.5%, not 0.1%

  11. stcordova: because those are the ones [Alus in exons] that your sources claim might be involved in RNA editing.

    Sal, you need to pay attention. That was worse than a quote mine. That was explicit contradiction of the actual words. Let’s go back to the source:

    To make it easier for you, Sal, I asked you:

    Of the million Alus, how many intronic inverted pairs are there?

    because those are the ones that your sources claim might be involved in RNA editing.

    You should be able to see that he’s referring to intronic inverted pairs, not exons. The misplaced triumphalism is getting old.

  12. Sal, you need to pay attention. That was worse than a quote mine. That was explicit contradiction of the actual words
    ….
    You should be able to see that he’s referring to intronic inverted pairs, not exons. The misplaced triumphalism is getting old.

    The figure of 5009 used by DNA_jock for his miscalculation is for an ALU pair within the same intron, hence that’s why he gets a figure of 0.1% not 1.5%. He went into the usual incomprehensible mode so that when his opponent can’t understand his gibberish, he assumes his opponent knows nothing. Well, I know 1.5% isn’t equal to 0.1%. 🙂

    When he got called on this discrepancy between his 0.1% and the Cold Spring Harbor figure of 1.5%, he finally revealed where he was pulling his numbers. Dumb! dsRNAs are not restricted to forming from the same intron, in fact some dsRNAs involve an ALU in an intron and one in and exon such as described in this paper:

    http://www.nature.com/nbt/journal/v22/n8/full/nbt996.html

    The gene contains two Alu repeats with opposite orientations, one of which
    overlaps with an exon.

    In fact the diagram this refers to shows :

    (intronic ALU) + exon + intron + (inverted exonic ALU)

    so that clearly is more than a pair of ALU inside an intron.

    But the bottom line is DNA_jock ignored the 1.5% number right there in the paper.

    So in regards to your comment:

    The misplaced triumphalism is getting old.

    Oh, you should be referring to DNA_jock, because I at least know 1.5% isn’t the same as 0.1%, which is more than I can say for DNA_jock.

    If he kept getting 0.1% with his calculations, and cold spring harbor reported 1.5%, he was wrong in his understanding, and worse it was beneath him to acknowledge he couldn’t reconcile the problem.

    105.7 million/ 6.6 giga bases ~= 1.5%, not 0.1%

    You’re obviously missing something and so is DNA_jock.

    Sal, you need to pay attention.

    Speak to yourself.

    1.5% does not equal 0.1%.

  13. DNA_Jock and John Harshman have some obsolete understanding of Alus.

    From Lehninger Principels of Biochemistry sixth edition (as in like the last few years):

    gene. The ADAR-promoted A-to-I editing is particularly common in transcripts derived from the genes of primates. Perhaps 90% or more of the editing occurs in Alu elements, a subset of the eukaryotic transposons called short interspersed elements (SINEs), that are particularly common in mammalian genomes. There are over a million of the 300 bp Alu elements in human DNA, making up about 10% of the genome. These are concentrated near protein-encoding genes, often appearing in introns and untranslated regions at the 39 and 59 ends of transcripts. When it is first synthesized (prior to processing), the average human mRNA includes 10 to 20 Alu elements. The ADAR enzymes bind to and promote A-to-I editing only in duplex regions of RNA. The abundant Alu elements offer many opportunities for intramolecular base pairing within the transcripts, providing the duplex targets required by the ADARs. Some of the editing affects the coding sequences of genes. Defects in ADAR function have been associated with a variety of human neurological conditions, including amyotrophic lateral sclerosis (ALS), epilepsy, and major depression.

    The genomes of all vertebrates are replete with SINEs, but many different types of SINES are present in most of these organisms. The Alu elements predominate only in the primates. Careful screening of genes and transcripts indicates that A-to-I editing is 30 to 40 times more prevalent in humans than in mice, largely due to the presence of many Alu elements. Large-scale A-to-I editing and an increased level of alternative splicing (see Fig. 26–21) are two features that set primate genomes apart from those of other mammals. It is not yet clear whether these reactions are incidental or whether they played key roles in the evolution of primates and, ultimately, humans.

    Nelson, David L.; Cox, Michael M.. Lehninger Principles of Biochemistry (Page 1113). W.H. Freeman. Kindle Edition.

    Besides, I know 1.5% isn’t the same as 0.1% I learned that even before high school!

    DNA_Jock, try to learn some textbook stuff from textbooks that are more recent, and learn some basic math too, like the fact 1.5% doesn’t equal 0.1%. 🙂

  14. Nothing of what you brainlessly quoted goes even one iota towards demonstrating that DNA_Jock or John Harshman have “an obsolete understanding of Alus”. And it doesn’t call the reality of common descent into question. At all.

  15. Rumraket,

    Well, I certainly know better than Francisco Ayala about Alus:

    http://biologos.org/blogs/archive/on-reading-the-cells-signature/

    The human genome includes about twenty-five thousand genes and lots of other (mostly short) switch sequences, which turn on and off genes in different tissues and at different times and play other functional roles. There are also lots and lots of DNA sequences that are nonsensical. For example, there are about one million virtually identical Alu sequences that are each three-hundred letters (nucleotides) long and are spread throughout the human genome. Think about it: there are in the human genome about twenty-five thousand genes, but one million interspersed Alu sequences; forty times more Alu sequences than genes. It is as if the editor of Signature of the Cell would have inserted between every two pages of Meyer’s book, forty additional pages, each containing the same three hundred letters. Likely, Meyer would not think of his editor as being “intelligent.” Would a function ever be found for these one million nearly identical Alu sequences? It seems most unlikely. In fact, we know how these sequences come about: one new Alu sequence appears in the genome for every ten newborns, generation after generation. The Designer at work? Unlikely: many of these sequences damage the genome causing abortion of the fetus during the early weeks of life.

    Perhaps one could attribute the obnoxious presence of the Alu sequences to degenerative biological processes that are not the result of ID. But was the Designer incompetent or malevolent in not avoiding the eventuality of this degeneration? Come to think of it: why is it that most species become extinct? More than two million species of organisms now live on Earth. But the fossil record shows that more than ninety-nine percent of all species that ever lived became extinct. That is more than one billion extinct species. How come? Is this dreadful waste an outcome intended by the Designer? Or is extinction an outcome of degeneration of genetic information and biological processes? If so, was the Designer not intelligent enough or benevolent enough to avoid the enormity of this waste?

    Ayala needs to read up on the latest. Has he retracted his un-informed article? Nope.

  16. Oh really?

    Yes really. If Ayala, Ken Miller and Dennis Venema show up here I’ll set ’em straight on some of their errors.

  17. Sal,

    Yes really. If Ayala, Ken Miller and Dennis Venema show up here I’ll set ’em straight on some of their errors.

    Why not publish a paper and set their errors in stone for all eternity?

  18. Mung: But warranted arrogance is very Christian.

    Does that actually mean something, or is the network of in-jokes that makes it a multi level sneer only available to you, Mung?

  19. Oh Sal,

    My apologies for upsetting you again, but you really shouldn’t re-visit this thread, where you put on such a stellar display of wilful ignorance, and flagrant misunderstanding (introns/exons, anyone? LOL).
    It’s really simple: a rather goofy paper from CSHL reckons that there are 100 million “editable” nucleotides in Alus. Cool story bro.
    The question has always been (remember, the topic is junk DNA) what proportion of these editable sites have function.
    So, until you come up with some evidence regarding this proportion, showing that it is above 6.7%, I’ll stick with my original ballpark estimate.

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