A Prediction Tested

Several themes have been doing the rounds lately. The origin of organelles, standards of evidence, common descent, the role of phylogenetic analysis, and the meaning of ‘prediction’ in science. Here’s a case study/rambling discourse that links a few themes.

Researching an answer to a separate question (I do try), I was struck by a thought about RecA. RecA (also going by the names RAD51, Dmc1 and RADA in different groups, for historical reasons) is a ubiquitous group of proteins involved in homologous DNA repair. That’s a process whereby a break in DNA can be ‘patched’ if a homologous sequence can be located. Matching sequence either side of the gap is aligned (by nothing more sophisticated than the binding energy of DNA complementarity) and then a DNA polymerase template-copies from the intact strand to the broken one between the two complementary sequences. Both accidental and deliberate breaks are repaired by this, hence it is involved both in maintaining DNA integrity and in the more ‘orchestrated’ process of crossover formation in meiosis.

Because this process relies on quite a high degree of complementarity, it works best on sister chromosomes – those recently replicated, within the current cell cycle, and hence clearly commonly descended. This is all a prokaryote has to work with, outside of instances of LGT. In eukaryotic diploids, the donor for repair can be the homologous diploid chromosome (that’s a terminological confusion: the chromosome pair with the greatest amount of homology is actually not the homologous pair, but the sister pair). But even in diploids, the sister is ‘preferred’ for repair – when not available, the normal repair pathway is ‘nonhomologous end joining’, which simply splices the break. An exception to this is during crossover of meiosis. Most crossovers form between homologues, not sisters.

So, thinks I, if chloroplasts and mitochondria evolved from bacteria, their RecA equivalents should be more like those of bacteria than archaea. To the internet!

It so happens that all these proteins are, in the modern eukaryote, held in nuclear DNA. So in a plant, you’ve got your RAD51s, plus Dmc1 specific to meiosis, but you’ve also got RecA proteins targeting, respectively, mitochondria and chloroplasts. RECA1 heads for chloroplasts, RECA3 for mitochondria. There’s also RECA2 which goes to both.

More specific and comprehensive phylogenetic analysis reveals quite a complex picture. Nonetheless, the Lin paper notes a ‘striking’ sequence similarity between the recA genes of plants and protists and those of the bacteria from which they are presumed to have come. There is a healthy 61% sequence match between RECA1 and the RecA of cyanobacteria. Sequence identity for RECA3/bacteria is not so high, but interestingly, Arabidopsis RECA3 can complement E. coli deficient in bacterial recA. E. coli are Gammaproteobacteria, not Alphaproteobacteria as is thought to be the group from which mitochondria came, but still not a million miles away. That’s not conclusive of a common origin, but is a noteworthy fact, consistent with structural conservation.

And that, really, is where I was headed. I started from the hypothesis that mitochondria and chloroplasts originated as bacteria. A prediction of that hypothesis is that organelle-targeted proteins would be expected in general to align more closely with bacterial than with archaeal or non-organellar eukaryote proteins. That prediction has been borne out. The hypothesis has been strengthened by that observation. How can that be? I did the same a few days ago with N-formyl methionine as translation initiator. Maybe I’m cherry-picking, but there are no searches I’m not mentioning that drew a blank. This is the sum total of my ‘research’: two things that it occurred to me to look for, and I found them both.

Also of interest to me, given the conviction explored in my ‘Evolution of Sex’ paper that meiosis is foundational to the modern eukaryote clade, is the finding that Dmc1 apparently evolved very early during what it pleases me to call ‘eukaryogenesis’. Whether it preceded or succeeded the mitochondrial endosymbiosis is not clear, which is one reason I don’t think of endosymbiosis as definitively the origin of the eukaryotic cell, whatever lols may accompany someone finding an author who does just that (Hi, Mung!).

Another point to ponder: homologous recombination relies upon a physical analogue of the algorithmic alignment performed during sequence comparison. It is only by anchoring matching sequences that ‘differences’ – in repair, the missing vs the intact sequence – can be located. Molecular differences between taxa are trumpeted by Creationists, but they are located in much the same way. The question remains: where does the alignment come from? In the case of sister chromosomes, it is non-controversially common descent – the sisters arise in the same cell cycle. In the case of diploid homologues, again not too controversial – the bases of the haploid chromosomes in gametes can reasonably be assumed to have a common origin in template-copies originating in an ancestral cell. But somehow, for the Creationist, this logic breaks down somewhere not clearly specified outside of the species. Alignment suddenly stops being common descent and becomes the completely indistinguishable ‘common design’. I don’t see why.

206 thoughts on “A Prediction Tested

  1. More predictions: pictures showing how rilly complex Homologous Repair is, and a challenge to evolve HR from scratch.

  2. Researching an answer to a separate question (I do try), I was struck by a thought about RecA. RecA (also going by the names RAD51, Dmc1 and RADA in different groups, for historical reasons) is a ubiquitous group of proteins involved in homologous DNA repair. That’s a process whereby a break in DNA can be ‘patched’ if a homologous sequence can be located.

    And by homologous you mean a similar sequence due to sharing a common ancestor? How do you suppose that the repair machinery detects whether the degree of identity is due to common ancestry?

  3. Mung: And by homologous you mean a similar sequence due to sharing a common ancestor? How do you suppose that the repair machinery detects whether the degree of identity is due to common ancestry?

    Made my day.

  4. Mung,

    I would like to know what Alan means by a process. Is it like a law of physics?

    Is it one of those things that we say just happens, without asking too many questions?

    How did life arise? “Well, it just did, why do you have to know everything?”

  5. phoodoo:
    Mung,

    I would like to know what Alan means by a process.Is it like a law of physics?

    Process :a series of actions that produce a change or development: the process of digestion. 2. a method of doing or producing something.

    Is it one of those things that we say just happens, without asking too many questions?

    You are confusing design with the theory of evolution

    How did life arise? “Well, it just did, why do you have to know everything?”

    Actually the answer is, it is unknown. Again you seem unaware that that is a more relevant complaint about ID than evolution. “Design just happened, do you have to know everything?”

  6. newton: You are confusing design with the theory of evolution

    That’s just silly. Evolution is supposed to be the designer. It’s supposed to be the process by which designs are achieved.

  7. Whether it preceded or succeeded the mitochondrial endosymbiosis is not clear, which is one reason I don’t think of endosymbiosis as definitively the origin of the eukaryotic cell, whatever lols may accompany someone finding an author who does just that (Hi, Mung!).

  8. So, thinks I, if chloroplasts and mitochondria evolved from bacteria, their RecA equivalents should be more like those of bacteria than archaea.

    So, thinks I, if chloroplasts and mitochondria were designed to have similarities to bacteria, their ReCA equivalents should be more like those of bacteria than archaea.

    So then how do you explain eukaryotic chromatin-like fibers in archaea yet eukaryotic RecA equivalents in bacteria but not in archaea! Are you arguing chromatin is more ancient than homologous repair?

  9. Also of interest to me, given the conviction explored in my ‘Evolution of Sex’

    Any chance you can explore the possibility of homosexuals evolving new reproductive organs..? What would it take? This could be a good way of falsifying evolution wouldn’t it? Adaptation…selective pressure…population genetics…whatever it takes…

    Since it is of interest to you…given the conviction…

  10. stcordova,

    He is clueless…as is the evolutionary committee…but everyone in the education system is going to be bullied into believing it is a scientific fact as I referred to it in my Mystery #6…

    How is it possible that a 2% minority bullies their beliefs on 98% majority? Any ideas?

  11. stcordova: So, thinks I, if chloroplasts and mitochondria were designed to have similarities to bacteria, their ReCA equivalents should be more like those of bacteria than archaea.

    Why would they be designed to have similarities to bacteria? Why so many similarities, even though some of those similarities are located in the nuclear genome? “They were just designed that way” isn’t an explanation. So again we have competing explanations, one that emerges inevitably from the hypothesis, and another that’s makes no predictions other than that things are the way they are. Which is a better scientific hypothesis?

    So then how do you explain eukaryotic chromatin-like fibers in archaea yet eukaryotic RecA equivalents in bacteria but not in archaea! Are you arguing chromatin is more ancient than homologous repair?

    Those aren’t “eukaryotic RecA equivalents”. They’re bacterial RecA, and the eukaryotic RecA comes from endosymbiosis, i.e. bacteria too. While the chromatin proteins come from the archaeal host cell. I don’t see why you are incapable of understanding the simplest phylogenetic hypothesis.

  12. And that, really, is where I was headed. I started from the hypothesis that mitochondria and chloroplasts originated as bacteria. A prediction of that hypothesis is that organelle-targeted proteins are be expected in general to align more closely with bacterial than with archaeal or non-organellar eukaryote proteins.

    Why is that though to be a prediction of the hypothesis?

  13. Mitochondria are to be found in both plant and animal cells, whereas chloroplasts are found only in plant cells.

    So chloroplasts were in the common ancestor of all eukaryotes but then got lost in the lineage that led to animals? Why wasn’t that predicted?

  14. Mung: So chloroplasts were in the common ancestor of all eukaryotes but then got lost in the lineage that led to animals? Why wasn’t that predicted?

    Magic, even so-called scientific, has many variants, just as genetic code keeps evolving despite prediction by Dawkins that any mutation in it would be lethal… lol

  15. They’re bacterial RecA, and the eukaryotic RecA comes from endosymbiosis, i.e. bacteria too. While the chromatin proteins come from the archaeal host cell. I don’t see why you are incapable of understanding the simplest phylogenetic hypothesis.

    Are you saying the origin of eukaryotic homologous repair in nuclear DNA comes from exchange of DNA with the mitochondria DNA. How did homologous repair happen prior to this?

  16. John Harshman: Why would they be designed to have similarities to bacteria? Why so many similarities, even though some of those similarities are located in the nuclear genome? “They were just designed that way” isn’t an explanation.

    Harshman doesn’t know why the designs are similar as his predictions would be that the designs of 10 billion species would have no similarities; everyone one of them would not be DNA based and would use a different genetic code…

    Wait a minute? Wasn’t that Dawkins prediction some 30 years ago? He was wrong about the code…so it evolved…

    I wonder what is going to happen when the 4th domain of life is found….

  17. John Harshaman:

    I don’t see why you are incapable of understanding the simplest phylogenetic hypothesis.

    That’s why God sent smart guys like you to me to set me straight. 🙂

    So when did spliceosomal introns arrive, before or after RecA got transferred from the mitochondria to the nuclear dna of the eukaryote.

    Do you have evidence a bacterial gene can splice itself up and insert appropriate splicesomal introns into a eukaryotic gene?

  18. stcordova: Are you saying the origin of eukaryotic homologous repair in nuclear DNAcomes from exchange of DNA with the mitochondria DNA.How did homologous repair happen prior to this?

    Sigh. The RecA being discussed here is the RecA that’s found in mitochondria and chloroplasts, not the RecA involved in nuclear DNA repair.

  19. stcordova: So when did spliceosomal introns arrive, before or after RecA got transferred from the mitochondria to the nuclear dna of the eukaryote.

    Do you have evidence a bacterial gene can splice itself up and insert appropriate splicesomal introns into a eukaryotic gene?

    Sigh. After. Genes don’t splice themselves up or insert introns. What are you trying to say?

  20. A speculation based on 1 Cor 1 :20-29.

    John Harshman and other asked why a Designer might make something look somewhat evolved when it’s not.

    First, as I pointed out, on balance there are enough anomalies that common descent requires miracles no different than special creation to make common descent work. Theobald’s analysis totally ignores the problems of cherry picking I pointed out. Didn’t Theobald fail to account for this little problem.

    Let X represent an exon in a Eukaryote or the ancestor segment of an the exon in the prokaryote. Let i represent a fraction of an intron that is about the size of an exon.

    For a prokaryote the gene looks like:

    XXXXXXXXXX

    for a eukaryote the gene looks like:

    iiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiii

    So don’t say God didn’t leave evidence of a serious gap for those willing to see the truth, otherwise, evolutionists are just falling for a gigantic prank. Evolutionists can’t complain they weren’t given clues of special creation, they only have themselves to blame for their blindness to the gaps such as the one I pointed out and a buzzillion more!

    To paraphrase Pslam 37:13 “God laughs at the evolutionists and phylogenists”.

    So why did the designer do all this? Partly to be entertained at the foolishness of scientists who think they are wiser than God!

  21. John Harshman: Sigh. The RecA being discussed here is the RecA that’s found in mitochondria and chloroplasts, not the RecA involved in nuclear DNA repair.

    So? The question still stands. How did it migrate from the original DNA to the nuclear DNA of the eukarytic cell.

    From the OP:

    It so happens that all these proteins are, in the modern eukaryote, held in nuclear DNA.

  22. stcordova: So why did the designer do all this? Partly to be entertained at the foolishness of scientists who think they are wiser than God!

    What Bibilical passage details the way to cure pancreatic cancer?

  23. Mung: So? The question still stands. How did it migrate from the original DNA to the nuclear DNA of the eukarytic cell.

    From the OP:

    The answer is obvious…lets see if anyone can figure it out … except Harshman who already denied his own beliefs more than once…

  24. stcordova,

    I like this one:

    1 Cor 3:19-20

    “For the wisdom of this world is foolishness in God’s sight. As it is written: “He catches the wise in their craftiness.” And again, “The Lord knows that the thoughts of the wise are futile.”

  25. stcordova:
    A speculation based on 1 Cor 1 :20-29.

    John Harshman and other asked why a Designer might make something look somewhat evolved when it’s not.

    First, as I pointed out, on balance there are enough anomalies that common descent requires miracles no different thanspecial creation to make common descent work.Theobald’s analysis totally ignores the problems of cherry picking I pointed out.Didn’t Theobald fail to account for this little problem.

    Let X represent an exon in a Eukaryote or the ancestor segment of an the exon in the prokaryote.Let i represent a fraction of an intron that is about the size of an exon.

    For a prokaryote the gene looks like:

    XXXXXXXXXX

    for a eukaryote the gene looks like:

    iiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiii

    So don’t say God didn’t leave evidence of a serious gap for those willing to see the truth, otherwise, evolutionists are just falling for a gigantic prank.Evolutionists can’t complain they weren’t given clues of special creation, they only have themselves to blame for their blindness to the gaps such as the one I pointed out and a buzzillion more!

    To paraphrase Pslam 37:13“God laughs at the evolutionists and phylogenists”.

    So why did the designer do all this?Partly to be entertained at the foolishness ofscientists who think they are wiser than God!

    This must be another mystery of evolution…

    Praise Jesus that you can see…

    https://www.youtube.com/watch?v=wSaR9nwtt78

  26. stcordova:
    A speculation based on 1 Cor 1 :20-29.

    John Harshman and other asked why a Designer might make something look somewhat evolved when it’s not.

    And yet you don’t address that question.

    First, as I pointed out, on balance there are enough anomalies that common descent requires miracles no different thanspecial creation to make common descent work. Theobald’s analysis totally ignores the problems of cherry picking I pointed out. Didn’t Theobald fail to account for this little problem.

    There is no cherry-picking. If you want to do phylogenetic analysis, you have to deal with homologs. No homolog, no analysis. And even if you grant that miracles are necessary (which I don’t), common descent with miracles would still explain the data, while separate creation with miracles would not.

    Let X represent an exon in a Eukaryote or the ancestor segment of an the exon in the prokaryote.Let i represent a fraction of an intron that is about the size of an exon.

    For a prokaryote the gene looks like:

    XXXXXXXXXX

    for a eukaryote the gene looks like:

    iiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiii

    So don’t say God didn’t leave evidence of a serious gap for those willing to see the truth, otherwise, evolutionists are just falling for a gigantic prank. Evolutionists can’t complain they weren’t given clues of special creation, they only have themselves to blame for their blindness to the gaps such as the one I pointed out and a buzzillion more!

    Once again, you have not addressed the question. These are not clues of special creation. They are at most clues of miraculous intervention at various points in the evolutionary tree.

    To paraphrase Pslam 37:13“God laughs at the evolutionists and phylogenists”.

    So why did the designer do all this? Partly to be entertained at the foolishness ofscientists who think they are wiser than God!

    Finally, you answer the question. But the answer is theologically problematic. You have posed a deceptive God. You’re saying that your God is a petty asshole who would jigger all of creation just to fool scientists. And by “wiser than God”, don’t you mean “wiser than a biblical literalist creationist”? Because I don’t recall God making any claims about evolution.

    Another implication of your claim is that science is impossible, because God might have messed with any phenomenon or data just to annoy us, and we can’t trust anything we see.

  27. John Harshman:

    No homolog, no analysis.

    Rather, no homolog, no common descent. You have a problem with that obviously.

  28. So… Allan … How do you think this acquisition and loss came about?

    … mitochondria and chloroplasts originated as bacteria, engulfed by what? Some unknown entity … [BH: bacterial host]

    And when it divided you had 1:1 offspring and when those divided you had 3:1. and when those divided you had 7:1. So I’m wondering where you think the first miracle took place. At what point did cell division result in BOTH daughter cells having the ingested bacteria inside them. Or do you think the one lineage with the internal bacteria had such a huge advantage that it was still able to leave more offspring by its lonesome than all the other bateria-less hosts combined.

    Because right now the numbers just don’t match up.

    Now presumably the BH had it’s own way of making ATP and converting “food” to energy. Was it the same as or different from that of the bacteria? What happened to the original genes and proteins, did they disappear later like the chloroplasts?

    Anyone familiar with software design can understand modularity and specialization. But this “it just happened, that’s all” theory of endosymbiosis, well, there must have been so many changes needed to pull that off. And all by accident. Pure blind dumb luck. Wow, it just so happened that this cobbling together of two organisms into one would work! Miraculous, really.

  29. J-Mac,

    If I can laugh at evolutionists eager to make monkeys of themselves through the theory of common descent, then surely God can laugh at them too! Psalm 37:13.

    “But then with me the horrid doubt always arises whether the convictions of man’s mind, which has been developed from the mind of the lower animals, are of any value or at all trustworthy. Would any one trust in the convictions of a monkey’s mind, if there are any convictions in such a mind?

    Charles Darwin

  30. GlenDavidson: In other words, you ignore the signal and glom onto the noise (so to speak).

    No, coming from you, it’s all noise. If I captured a terrorist and wanted to make him talk, I’d loudly play your posts over and over again and make him listen.

  31. stcordova: Rather, no homolog, no common descent. You have a problem with that obviously.

    You can’t do a likelihood analysis with non-homologous sequences. Is that not clear to you? Do you understand what Theobald was doing in that publication? Have you even read it? If you’re confused, ask somebody at NIH if you don’t believe me.

    Now, can you explain Theobald’s result? Do you have any idea what that result was?

  32. stcordova,

    Sal, what do you have against monkeys? Did one steal your banana, or what? Can you explain why humans, other apes, and other monkeys fit into such a clear phylogenetic tree?

  33. In addition to the problem of the splicesomal introns, there is the problem of the Shine Dalgarno sequence in bacteria and the lack (or very low frequency) of such a sequence in corresponding Eukaryotic genes. To the extent Shine Dalagarno or whatever sequence is involved in recruitment of transcription factors, there has to be a lot of machinery to make this feasible.

    https://en.wikipedia.org/wiki/Shine-Dalgarno_sequence

    Theobald’s analysis avoided this. What that because it would make his computer Barf trying to digest this problem?

  34. stcordova: So, thinks I, if chloroplasts and mitochondria were designed to have similarities to bacteria, their ReCA equivalents should be more like those of bacteria than archaea.

    Why not simply identical? Why even be different at all? Why not the exact same one down to the last atom? Copy-paste? Remember, they all work.

  35. Mung: And by homologous you mean a similar sequence due to sharing a common ancestor? How do you suppose that the repair machinery detects whether the degree of identity is due to common ancestry?

    They don’t, but he explained why the term homologous as opposed to merely similar, is used. The chromosomes are commonly descended:
    “Because this process relies on quite a high degree of complementarity, it works best on sister chromosomes – those recently replicated, within the current cell cycle, and hence clearly commonly descended.”

    Strictly speaking the enzyme can work on anything that is similar enough regardless of how they came to be similar, it’s just that when it comes to the chromosomes inside the cell, they usually descent from the same template. So for the most part, recombination is between actually homologous sequences.

  36. Rumraket: Why not simply identical? Why even be different at all?

    Exactly!

    One bacterium becomes a mitochondrion, another one became a chloroplast. And no one blinks. It’s evolution! Anything can happen! Not just one, but two miracles.

    See, I don’t take the miraculous nature of endosymbiosis to be evidence against endosymbiosis, I take the miraculous nature of endosymbiosis to be evidence for the miraculous nature of endosymbiosis.

    I can hardly rap my head around all the improbable things that must have taken place. Life is miraculous. Get over it.

    ETA: rapping my head. haha.

  37. phoodoo: I would like to know what Alan means by a process. Is it like a law of physics?

    It is a series of chemical reactions, and yes they are subject to the basic physical forces.

    Is it one of those things that we say just happens, without asking too many questions?

    No. It’s just that, when you ask “why” they happen, nobody knows how to actually demonstrate that their pet answer is correct.

    You could say God makes it happen. And another guy can say it’s his telepathic powers. And another guy can say it’s destiny, or fate. Lots of shit can be made up and nobody knows how to determine which of all the options is actually the case. Including you.

    We’d all like to know the answer. But we need a way to find out. Got one? Tell me.

    How did life arise? “Well, it just did, why do you have to know everything?”

    You do know the origin of life is actively being investigated right?

    Do you know how it arose? No you don’t.

  38. stcordova: So then how do you explain eukaryotic chromatin-like fibers in archaea

    They evolved in archaea and eukaryotes inherited them through vertical descent?

    yet eukaryotic RecA equivalents in bacteria but not in archaea!

    RecA was transferred to the nucleus from the mitochondrial endosymbiont.

    I think that’s how you’d explain it.

  39. Mung: Exactly!

    One bacterium becomes a mitochondrion, another one became a chloroplast. And no one blinks. It’s evolution! Anything can happen! Not just one, but two miracles.

    See, I don’t take the miraculous nature of endosymbiosis to be evidence against endosymbiosis, I take the miraculous nature of endosymbiosis to be evidence for the miraculous nature of endosymbiosis.

    I can hardly rap my head around all the improbable things that must have taken place. Life is miraculous. Get over it.

    ETA: rapping my head. haha.

    Please define a miracle for me. What does it take for something to be a miracle? What does it mean that it is a miracle? What does that imply? I’d like answers to all these questions please.

  40. J-Mac: Also of interest to me, given the conviction explored in my ‘Evolution of Sex’

    Any chance you can explore the possibility of homosexuals evolving new reproductive organs..? What would it take? This could be a good way of falsifying evolution wouldn’t it? Adaptation…selective pressure…population genetics…whatever it takes…

    Since it is of interest to you…given the conviction…

    This is fantastically dumb and nothing but trolling. Welcome to ignore..

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