I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.
Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.
If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.
One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.
Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.
That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).
Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.
The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”
So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.
So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.
The hybridization demonstrates that the DNA double strand is dynamic. What makes you think that missing the point makes your ignorance look any better?
When doing an experiment with DNA hybridization, intelligent humans only introduce the molecule. It would not hybridize of the DNA needed a magical being to separate it so that the molecule could hybridize.
Yeah. It happens all the time. DNA strands separate, then they hybridize together again. What part about the word dynamic is so hard for you to understand?
No Mung, that’s your fantasy, not mine. It’s your fantasy that they need help to separate. It’s your fantasy that they cannot separate otherwise.
And not just short stretches. Any length at all.
https://en.wikipedia.org/wiki/Nucleic_acid_hybridization
So when a section of DNA or RNA folds on itself that is a case of hybridization. If not why not?
So now you’re admitting that this is dynamic!
stcordova,
I’m not missing the point. It’s not about guarantees, It’s about accidents that may or may not happen. Why do you think some people have less repeats than other people? If a number of repeats is necessary, as you say, then how do those people lose some? Why is there variation in copy number? Because there’s no guarantee Sal. It happens because it can happen. That’s why.
Entorpy,
I found a paper that answers my quesitons and puts your errant speculations to rest. The replications were confirmed to be independent of RecA-mediated homologous recombination, thus confirming it is slippage not homologous recombination.
Your explanation was faulty. The following paper gave me a satisfactory explanation and also discounts your explanation because it showed the events being independent of RecA-mediated homologous recombination as well as a mechanism that specifically targets the tandem repeat.
Sorry, no offense intended. I saw a flaw in your explanation quite readily, and this paper confirms my intuition. I’m not as naïve as you believe I am since I obviously smelled the flaw in your explanation as confirmed by the citation.
Thanks anyway:
PS
In light of what I found DNA_jock should maybe reconsider changing his handle to dna_JOKE! Hahaha!
The Theory of Accidental Evolution.
Moved some posts to guano
No, not any length at all, at least not in DNA, which is normally double-stranded. Only short bits come unzipped spontaneously, though much longer bits are separated by enzymes at various times. RNA is of course usually single-stranded, and stems are often fairly short and so are more likely to separate. Where are you trying to go with this?
By the way, have you now figured out the pyramid analogy?
Interesting
Sal asks how D4Z4 repeats (which are 3300 bases long) arise, and both Corneel and Entropy respond “unequal cross-over”, with a description of the process for good measure.
Sal asks “Does this happen for non-coding DNA? How does it recognize a discrete unit like an long repeat (say over 200 bases) over some arbitrary unit?” and opines “For a repeat to be actually nicely copied, somehow the repeated unit needs to have a means of identifying the start and stop of the repeat.”
Well that’s a stupid thing to write. I mean really stupid. Any high school biology student would recognize that there is no need to recognize the ends of the repeat.
When called on it, he goes to his huffy credentialist defense: “ I was top of my class in biochemistry.” and “I have a friend who’s a biology professor from [??] Vanderbilt.”
I point out the stupidity, so Sal does a quick Wikipedia search and discovers Slipped Strand Mispairing. Sal goes on the offensive: “As far as your claims against my credentialism, I have high school diploma, and I figured out slip strand misparing isn’t the same as homolgous recombination, which is more than I can say for you.”
Not a mistake I have made, nor would make, Sal… [see sardonic resort to credentialism below]. And it is very naughty of you to claim that I did.
I point out that SSM is the source of 2-, 3- and 4- base repeats, and is NOT the cause of the D4Z4 repeats which are the result of unequal cross-over.
Sal doubles down:
ROFLMAO
So much wrong here, so little time. Firstly, the logic fail. Even if SSM were widespread and the mechanism by which D4Z4 arose, that wouldn’t make Sal’s original claims any less stupid. Secondly, the nature of the evidence: Sal’s citation discusses SSM and its role in bacterial genome evolution. So it has zero relevance to D4Z4 and similar long repeats in eukaryotes. Didn’t you notice the bit about “recA-independent”. That’s the bacterial strand invasion protein, Sal. Yikes!
And, as I noted, almost all SSM leads to very short repeats. Rarely long ones. D4Z4 is still the result of unequal cross-over.
Finally, Sal, you gave me a blast-from-the-past thrill equal to the one you gave me when you cited the October 18th 1982 announcement of Aaron Klug’s Nobel Prize: I knew Sue Lovett, Sue Lovett was drinking buddy of mine. I still remember standing behind her at the 1984 Cold Spring Harbor Symposium “Recombination at the DNA Level” (I was there as an invited speaker). I was standing next to Jim Watson, and he spent the entire session checking out her ass. I mean full on Harvey Weinstein. Rick Fishel and I told her what happened later over drinks and pool in Huntingdon.
We were not talking about bacteria, but about eukaryotes, more specifically about a case of copy number variation in the human genome, where tandem duplications are sites where non-allelic homologous recombination can occur and result in variations in the number of repeats.
As DNA_jock explained, slippage more often refers to smallish duplications. Look at the very article you quoted. Figure1 shows repetitive sequences, like “GGGGGGG,” not complete duplicated regions like those you were originally talking about. When complete regions, gene size for example, duplicate, then it’s not normally called slippage. It’s normally called recombination.
Same reference, Figure 2, shows a case of non-homologous recombination, and Figure 3 shows a case of homologous recombination (even though the authors called it slippage too). The homologous recombination, in this case, occurring during DNA replication, not RecA mediated. The kind of recombination is called homologous because it involves large regions of DNA, thus homologous regions of DNA. It doesn’t matter if it involves RecA or not.
Anyway, the basic idea is the very same for Figure 3 as in my explanations. There’s a duplicate, it aligns to the incorrect region by complementarity, which is exactly what I said, and thus a duplicate is formed.
You are only confirming what I said. Complementarity aligns the incorrect repeats thus resulting in variation in tandem repeats.
What’s offensive is your insistence that I got it wrong for explaining you one mechanism that clearly works, and for explaining you that complementarity is how these copies recognize each other thus resulting in copy number variation. That there’s other mechanisms, also involving complementarity, doesn’t mean that I was wrong, it means that I didn’t explain other ways in which these things can happen, but I gave you the basic ingredient: the complementarity between long repeats.
Also, check and you’ll understand that even when it happens during replication, it does not guarantee anything. It happens because it can happen.
Yeah. But Sal feels some kind of need to save face, and ends up confirming that he might not understand these concepts very well.
Sal, check tthe second paragraph under “mechanism” here.
You’re welcome.
Whistling past the graveyard
You’re understanding of this is terrible which I’ll explain. But first, I was mentioning the tandem repeats in terms of satellite DNA or something like D4Z4, not entire whole genome repeats or large segment repeats.
Look at this paper:
http://mmbr.asm.org/content/72/4/686/F1.expansion.html
Note the legend:
and you can get the paper here:
And something you didn’t point out in your link:
The thing your referenced with homologous recombination dealt with LCR (low copy number) repeats where the copied segment is more than several thousand bases, not really satellite repeats (the focus of my discussion on Tandem Repeats).
Yeah, if you do a whole segment or whole genome duplication which also happens to contains a tandem repeat, you create a huge repeat, but that wasn’t what I was talking about.
I was specifically talking about tandem repeats which are orderly repeats like the satelites found centromeres and then the repeats in telomere. I wasn’t talking Segmental repeats or Whole Genome repeats. Do you not understand the difference?
Can you read the diagram below? What is the mechanism for creating tandem repeats? Uh, er, its not homologous recombination, it’s slippage and gene conversion.
The is a specific problem in creating many repeating elements in a tandem repeat. Your reasoning was totally incoherent as it was describing a random duplication event, not duplications like tandem repeats that are very orderly where many many copies are involved.
This is the second paper I cited, and you and DNA jock can’t seem to digest it. You complained the first paper deal with a prokaryote, but it was the same paper cited by Eukaryotic paper studying tandem repeats. Now I cited a specific Eukaryotic paper that describes exactly what I was talking about with a diagram below. Don’t extend a “you’re welcome” for feeding me and other readers junk like you just did.
My intuition said your explanation was incoherent, and now I just provided a second paper confirming you were wrong.
Click for larger image:
http://mmbr.asm.org/content/72/4/686/F1.large.jpg
Yup. I just buried the guy with the diagram below. 🙂
http://mmbr.asm.org/content/72/4/686/F1.large.jpg
For the reader’s benefit, Entropy was talking about unequal crossover homologous recombination, not gene conversions homologous recombinations.
Construction of a 100 unit tandem repeat needs to identify the unit of the repeat to have a good chance of making such a long tandem repeat, other wise the copies of the units could be interrupted and instead of a tandem repeat one creates dispersed repeats! Entropy didn’t address that issue, but he seemed to keep focusing on rote complementarity instead of the real issue. He just ignored it or didn’t even realize it was an issue. He presumed I was critical of his explanations because I didn’t understand. I was critical of his explanations because he didn’t understand what the real problem was, namely, the continuity of the tandem repeat.
And one other thing, since I specifically highlighted the tandem repeats in the centromeric regions, cross overs are kind of hard to come by in that region. He didn’t account for that, yet he kept showing diagrams of cross overs! Sheesh!
Mung,
I got “we use cookies to improve your experience with the site”. Perhaps I might try that as an incentive.
Mung,
A clade can be formed by a single bacterium and its descendants; the ‘apomorphies’ being simply mutations that arise on the way. If one takes aliquots of culture from time to time, founding separate lineages, then tries to reconstruct the phylogeny, there is absolutely no requirement to explain the mutations. It is enough that they occur.
stcordova,
What exactly appears to be the problem? Entropy and DNA_jock are correct to point out that copy numbers of D4Z4 cannot expand by replication slippage, because it is too long. Hence unequal crossing over is a perfectly reasonable explanation. It was the first one that came to my mind, because it is a known to be the main driver for gene duplications. This is all very basic genetics.
Why do you oppose that explanation?
Yeah I don’t get the problem either. Different size repeats have different mechanistic explanations for their origin.
Oh, Sal, when you are in a hole, stop digging. You should type slower, too.
You were talking about tandem repeats, like D4Z4, and you made a really, really dumb statement, to wit: “For a repeat to be actually nicely copied, somehow the repeated unit needs to have a means of identifying the start and stop of the repeat.”
In fact, for a repeat to be “nicely” copied, (“precisely” copied, even) all that has to happen is that somewhere in the middle of the repeat ‘recognizes’ the corresponding spot in a different repeat. This process is homology-driven, and leads to either gene conversion or cross-over, depending on how the resulting Holliday is resolved.
Nobody said anything that could ever apply to Whole Genome Repeats. You only mention them in an attempt to muddy the waters. We are used to your behavior.
Okay, that’s really funny. First off “you and DNA jock can’t seem to digest it” seems a tad premature, given that this comment is the first time you cite Richard, 2009. Really, Sal, it has come to this?
Secondly, this is a 30 page review article about the origin of micro- and mini-satellites — 2-, 3-, 4- (I forgot 5-, they’re important too) base repeats, the type that generally grow via SSM, and the subject of the author’s research career. (But beware grasshopper, they can also expand by unequal cross-over: Entropy’s answer to your question was correct). Of those 30 pages, the author devotes just one page to the kind of larger tandem repeats that you originally asked about. What does he say:
Ooops.
This is what happens when you cite papers that you probably did not read and certainly did not understand.
Would you like some Maalox for that indigestion, Sal?
Nope. I told you a billion times already. As long as there’s a sufficiently long complementary sequence, recombination can happen anywhere without “identifying” the “unit” of the repeat. The recombination could involve complementary pairing between many strand sizes that could cover only half of a “unit” (anywhere within the “unit”), only one quarter, a complete unit, two units, a unit and a third, etc. No “identification of the unit of the repeat” required other than the tendency for complementary strands to pair with each other.
Your examples with other mechanisms still involve complementarity. Had you really understood, you would not make such a big deal out of whether it’s unequal crossing over (aka non-allelic homologous recombination) or “slippage.”
Now for that review that “proves me wrong”:
This would have been trivial for anybody who understood the most basic genetics, and the most basic of DNA structure. You could have said, “thanks, I found that slippage could also work,” and we would not be discussing trivialities-made-into-big-deals-by-you out of your need to save face, only to end up showing that you have poor understanding and reading skills of the very material that you bring as proof that I’m so terribly wrong.
P.S. Thanks for there review. It’s a bit old, but I think I can use it for the courses I teach.
DNA_Jock,
Ha! We cited the very same paragraph!
Well, it was the only relevant paragraph in the whole review…
LOL
ETA: for moar lulz we should have highlighted ‘minisatellite’ in that paragraph…
It’s a tandem repeat, I guess.
Done.
Corneel,
And great teaching example, to boot.
Hey Sal, try this:
Copy and paste this page into a text editing program, into two windows.
Align the two homologous 313 character stretches. Recombine the texts — the cross-over can be ANYWHERE within the aligned 313 character region. There’s no need to ‘recognize’ the ends.
Now you have a “nice” 1692 character duplication.
Align the two homologous 1692 character stretches. Recombine the texts again — the cross-over can be ANYWHERE within the aligned 1692 character region.
Now you have two “nice” 1692 character duplications in tandem.
Repeat ad nauseam
Literally.
For rDNA repeats, there’s a goodly dose of mitotic recombination too. At least there is in S. cerevisiae. It happened to me once. Quite the most embarrassing paper I ever published.
DNA_Jock,
😀
Yes of course, D4Z4 is too long for slippage, but the issue isn’t homologous recombination, it’s the identification of the repeat unit.
Sp100-rs in Mus Musculus can have 2000 repeats. Why that gene and not others. It’s not like other genes can’t be subject to homologous recombination too! Why is one unit singled out for repeat like Sp100-rs and not others.
That was the issue. Entropy didn’t answer the question being posed. He and DNA_jock still don’t understand things like Sp100-rs don’t look exactly like random duplications. There is a mechanism that causes preference.
This paper is discussion of the gene that has 60-2000 copies in Mus Musculus:
https://www.ncbi.nlm.nih.gov/pubmed/11534816
Entropy failed to explain why one repeat is favored over another. It’s not like there aren’t other genes that can be duplicated. So why that one! That’s the problem. And why the non-coding D4Z4?
stcordova,
Stop it already Sal. Read what we wrote for you above. All you do each and every time is confirm that you really don’t understand. You don’t understand the very articles you quote at us. Sheesh.
So Entropy, why Sp100-rs in Mus Musculus has 60 to 2000 repeats? It’s not like there aren’t other genes that can’t be subject to repeat. That’s the problem.
I’ve just begun. Thanks to Corneel, I found a way to express the problem more cogently. You see, in that paper I cited, it said paralogous tandem of repeats of GENEs are RARE. The one notable exception was Sp100-rs. Why Sp100-rs, a chimera of fused genes? That was the question. Your “explanation” didn’t explain why one repeat unit over another.
So you read what I wrote. Explain why Sp100-rs over any other gene. When you can do that, that may or may not explain some other repeat. Of course you don’t have an explanation. That was my point.
All I have to do is repeat what I told you already:
Of course, then you move the goalposts by asking a different question (you never asked me why that gene and not other genes):
The reason some regions get tandem duplications and others don’t is just that shit happens, and that some duplications might be harmful enough that, if they happened, we wouldn’t get to see them.
If you understood the mechanism (any of the mechanisms), you’d understand that whether the region is coding or non-coding doesn’t matter at all. If you understood the other mechanisms you’ve insisted on portraying as proving me wrong, you’d understand that those don’t explain why one gene and not another either.
You keep embarrassing yourself. Why not try reading for understanding, or stopping it until you ave the time to, ahem, digest this stuff! Sheesh!
I insist, you didn’t ask that question Sal. Please check other answers above. You’re only embarrassing yourself and showing that you truly have no idea, or no capacity to read for comprehension. Either way, you’re doing the opposite of saving face.
P.S. I explained, though, in my very first explanation, that once you have some repeats within region, the opportunities for the region to suffer lots of copy number variation increase. Do you see the relevance in regards to your new question? Of course not. You don’t understand this at all, do you?
Corneel,
Thank you so much for pointing out my error. I would presume slippage can’t account for repeats larger than something like an Okazaki fragment.
In any case, visiting a Tri-nucleotide repeat, in somatic cells we have a mechanism possibly for one class of repeat:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2681094/
That is more what I was looking for. Another paper then links this to Excision Repair and Mismatch Repair.
http://www.pnas.org/content/107/52/22582.full?sid=04400978-3e57-4328-bca5-1307fb29d48e#ref-3
What I need to see is why tandem repeats specifically are targeted for duplication or anything else.
stcordova,
Sal! I specifically mentioned Huntington’s disease after you mentioned slippage for the first time!
Sheesh! read the comments and stop embarrassing yourself for once!
Yes, I did, but I couldn’t express it so cogently until I found Sp100-rs in Mus Musculus that has 60 to 2000 repeats.
So, not for me, explain for the readers why Sp100-rs is singled out. It’s not like other sections of DNA can’t be subject to homologous recombination. Spell it out. Don’t tell me to read more of your stuff, how about you explain why Sp100-rs is singled out for 2000 duplications and other genes aren’t? Show how homolgous recombination explains such preference for making a tandem repeat of one gene 2000 times more than another gene. Explain it for the readers if not for me. Show how complimentarity will favor The Sp100-rs gene after it became a chimera for homologous recombination crossover or DSB or whatever — show how this will favor Sp100-rs over any other gene.
Now you’re complaining I stop asking a question, right when it gets really really interesting.
For the millionth time, because tandem duplications abound in positions where non-allelic homologous recombination can occur!
You’re unreachable, aren’t you?
Check above. I think other readers would see that I have explained much more than you asked, and that you don’t seem to be able to understand any of it.
Oh so you admit the repeats involved in Huntington’s disease aren’t due to homologous recombination now that I cited a paper. But not for my sake, how about you explain to readers this:
Thanks Corneel for pointing out my mistake, and I stand corrected on D4Z4. But you also helped me point out the mistake Entropy was making. He was failing to explain why one unit is favored for repeat over another, like Sp100-rs.
So, I don’t know what causes D4Z4 to have a variable copy number. The problem is why that Unit of repeat over some other random section of DNA. Further D4Z4 needs to be about 100 repeats, otherwise muscular dystrophy sets it (at 11 or below). It seems it has to be in a goldilox zone of the number of repeats.
I’m complaining that you neither read, nor understand the answers. That you neither read, nor understand the very articles you cite at us. That’s what I’m complaining about, that instead of continuing embarrassing yourself, maybe it would be a good idea for you to try and read the answers for comprehension.
No my illiterate friend, I pointed that out
yesterday!
Yes I don’t understand how complimentarity and homologous recombination would favor Sp100-rs to repeat 2000 times more than other genes. So explain it for me again succinctly since I missed your explanation as to why one gene would be favored for duplication 2000 times more than another based on Unequal Crossover mechanisms and homologous recombination. 🙂
I’ll say he does.
Sal,
To answer your NEW question, “why one repeat is favored over another”:
ALL genes may be subject to unequal cross-over. (They need a repeated sequence on either side. You might be able to think of a couple of possible candidates…<ggg>). Why do we see some genes in tandem duplications, and not others?
1) Shit happens, like Entropy told you.
2) Once you’ve got a duplication or two, then the opportunity for more duplications is increased significantly, like Entropy told you.
3)The duplications may or may not be adaptive:
For the mammalian somatotropin genes for instance, they duplicated and then DIVERGED. It’s the most common source of new genes (what you call “poofing”).
For the rDNA genes (discussed in your citation [Richard 2009] in the paragraph following the one that Entropy and I both quoted), the increase in copy number is, in and of itself, adaptive.
For most other genes, not so much.
Sal, please cease with the desperate attempts to defend your wounded pride, and THINK for a minute.
ETA: Hox genes, too, I suspect…
Gee Entropy, I seem to recall other genes can be subject to recombination and thus tandem repeat duplication. Isn’t that right? So how again does homolgous recombination explain that Sp100-rs is duplicated 2000 more than a typical gene. It seems really really really special since there aren’t orthologs of this chimera found in other mammals.
That review paper I cited (the one with the diagram) points out:
So explain for the reader how homolgous re-combination simultaneously makes tandem repeats rare but also makes one tandem repeat have 60-2000 copies. I’m obviously too illerate and dense to understand your explanation.
So, if you can, not for my sake, but for interested readers sake, explain why one unit (like the Sp100-rs gene) is favored soooooooo much for repeat over other units (like say the unfused non-chimeric Sp100 in Mus Caroli). Explain the reasons for preferential copying based on homologous recombination and complimentarity. 🙂
I started composing an answer but I see I have been scooped. So I’ll just be repeating Entropy and DNA_Jock here:
1) Because the oportunity for imprecise homologous pairing during meiosis increases as the number of duplicates increases
2) Also, the copy number of many genes is constrained by dosage requirements. You of all people should have thought of that 🙂
stcordova,
Both DNA_jock and me have explained this to you at large. Why should we do it again if you won’t read the answers? Hell, for all you’ve shown you would not understand the answers anyway. You seem to lack the most minimal background.
If you do care, check above. There’s plenty that you missed out of your desperation to save face. Again, only to continue embarrassing yourself.
Corneel,
Let’s start out with the chimeric Sp100-rs gene when it was first created by accidental fusion of Sp100 and csprs. Are you saying it was by chance that Sp100-rs was singled out as the one that got amplified 2000 times over other genes? I mean, there are genes more “ancient” than Sp100-rs. Why didn’t they get subject to so much more tandem duplication?
And fwiw, can’t unequal crossover reduce copy number since one segment must lose for another to gain.