E. coli and their evolution

_{idnet.com.au
December 5, 2007

Intelligent Design

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I have been thinking about E. coli and their evolution.

E. coli live in the gut. They are passed environmentally from parents to children.

When humans and baboons had their presumed common ancestor ~ 20 mill years ago, that should be the last time when E. coli in our bowel had a common ancestor with E. coli in the bowel of baboons in the wild.

The following study looked at Baboon and Human E. coli (1985).

“The biotype data indicate that the amount and distribution of genetic variation in the E. coli among free-ranging baboon troops are similar to those in isolates from humans. However, E. coli isolates from baboons are able to utilize a greater variety of sugars as their sole carbon source, possibly because of a greater variety of sugars in the baboon diet.”

If we sequence the E. coli from wild baboons and “wild” humans we should be able to see what evolution can achieve. We already know gene transfer plays a role in gut bacteria.

As an ID supporter I predict that there will be extra genes in baboon E. coli and extra genes in human E. coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E. coli genes as there have been about 3X10^9 generations of separate development. Of special interest would be the flagellar genes.

What do you think of my predictions? Can ID make predictions? Is ID testable? Will anyone do this experiment?

Comments

lars. You get it. First, I am a doctor. I know babies are born without bacteria. I know also where they come out and that the area is rife with E Coli and other bugs. You don't have to eat faeces to get E Coli. Has anyone ever had the runs? That was from part of someone's faeces ending up in your mouth. The quoted paper demonstrates that these populations of E Coli have been separated for a long time. If E Coli over 3 billion generations can engineer new systems from RM and NS then ID is unlikely to stand. Until we do the research, how will we know? It is not hard to determine which genes are from LGT.idnet.com.au_{December 6, 2007
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This is a bit off topic, but this molecular biologist says [his strawman version of] ID is dumb. http://www.humanevents.com/article.php?id=23404
AIDS was unknown just thirty years ago. HIV, the virus that causes AIDS, did not exist fifty years ago. It evolved from a relatively harmless virus of lower primates. A new species evolved within our own lifetimes, before our own eyes. We developed drugs to combat it. It then went on to evolve drug resistance, again while we actually watched it happen and documented the timelines and intermediate forms.
I haven't finished "The Edge of Evolution", so I haven't gotten to the HIV discussion (I think there is one). This guy implies he's observed macroevolution. What gives?russ_{December 6, 2007
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Nochange, Strictly speaking, you don't have to eat poop - just the E.coli that was in it. So how do you know you don't eat or drink E. coli? Do you subject everything you plan to swallow to microbiological testing beforehand? Ever watched a cooking show and seen those celebrity chefs using their bare hands to mix a salad or taste a sauce or test a steak for how well done it is? Does everybody working in food preparation always wash their hands properly after using the toilet? Obviously not or there wouldn't be outbreaks of Hep A. Ever eaten an apple before washing it thoroughly? I could go on but I think that's enough.Janice_{December 6, 2007
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Janice, So for those of us who *don't* eat poop, would that mean that we don't have E. coli? (I would expect E. coli to be more common among Darwinists than among IDists - how's that for a prediction?). I mean, I could understand if there are still some weird tribes that carry E. coli, but wouldn't E. coli have gotten wiped out in modern society if it's all gotten through eating poop? Either that, or there's another way to get it? In the womb?Nochange_{December 6, 2007
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OK, I think I'm getting it now... I believe idnet is predicting that (a) the different E. coli genomes will each have some functional genes unshared with the other genome, but that (b) these genes will be shown to have originated via gene transfer as opposed to RM+NS. How does the latter prediction arise from ID? IDnet explained above that ID says undirected RM+NS is not capable of much; so any new, functional genes must have arrived some other way. Hence, gene transfer (if we exclude new intelligent input ... so this prediction assumes not only ID, but also assumes that intelligent input stopped before baboons and humans diverged... which I guess is basically Common Descent, but goes farther than Behe, who argues for intelligent input throughout the evolutionary process). Be that as it may, it's not obvious to me how you would test this prediction -- how do you know if a gene came about by gene transfer? Do you check other genomes for similar genes? Whose genomes do you check - the hosts'?lars_{December 6, 2007
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AussieID, They don't so much get passed as get swallowed. Transmission is faecal/oral.Janice_{December 6, 2007
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Is it reasonable to predict that the e coli genes would still be the same?Q_{December 6, 2007
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I see two potential problems with these predictions, although they may simply stem from my ignorance. My knowledge of biology is quite limited. One of them is that, as pointed out by Bob O'H above, it isn't entirely clear how the predictions contradict those of the theory of evolution. If the two strains of bacteria live in reasonably stable and similar (albeit not identical) environments, they presumably don't face particularly strong evolutionary pressures. The second problem concerns the verification of the prediction about horizontal gene transfer. Supposing some new genes are found in the E. coli bacteria and some unrelated ones, how can one rule out the possibility that at least some of the genes evolved in the E. coli and spread to the others, without begging the question? I'll be thankful for any clarifications. Frost122585: How does horizontal gene transfer bring us any closer to "real probabilities"? As far as I know, HGT is less well understood than mutations, which makes it harder to estimate the probabilities. Am I missing something obvious?Hu_{December 6, 2007
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I have wordpress problems with internet explorer and copying and pasting does not work.Collin_{December 6, 2007
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Thanks Joseph for bringing a little clarity. I'm still wondering. "What study do you base this prediction on idnet.com.au.?" "I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer." I dug out Dr. Behe's EOE book and found what he had to say about E-coli. pg. 141-142 In the early 1990's Lenski and coworkers began to grow E.coli in flasks; the flasks reached their capacity of bacteria after about 6 or 7 doublings. Everyday he transferred a portion of the bugs to a fresh flask. By now over thirty thousand generations of E. coli, roughly the equivalent of a million years in the (supposed) history of humans, have been born and died in Lenski's lab. In each flask the bacteria would grow to a population size of five hundred million. Over the whole course of the experiment, perhaps ten trillion, 10^13, E coli. have been produced. Although ten trillion sounds like a lot(it's probably more than the number of primates on the (supposed) line from chimp to human), it's viryually nothing compared to the number of malaria cells that have infested the earth. In the past fifty years there have been about a billion times as many of those as E. coli in the Michigan lab, which makes the study less valuable than our data on malaria. Nonetheless, the E coli. work has pointed in the same general direction. The lab bacteria performed much like the wild pathogens: A host of incoherent cahnges have slightly altered pre-existing systems. Nothing fundamentally new has been produced. No new protein-protein interactions, no new molecular machines. As with thalasswemia in humans, some large evolutionary advantages have been conferred by breaking things. Several populations of bacteria lost their ability to repair DNA. One of the most beneficial mutations, seen repeatidly in separate cultures, was the bacterium's loss of the ability to make a sugar called ribose, which is a component of RNA. Another was a change in a regulatory gene called spoT, which affected in masse how fifty-nine other genes work, either increasing or decreasing their activity. One likely explanation for the net good effect of this very blunt mutation is that it turned off the energetically costly genes that make bacterial flagellum, saving the cell some energy. Breaking some genes and turning others off, however, won't make much of anything. After a while, beneficial changes from the experiment petered out. The fact that malaria, with a billion fold more chances gave a pattern very similar to the more modest studies on E. coli strongly suggests that's all Darwinism can do. One of the studies of Lenski: Long-term experimental evolution in Escherichia coli. XI. Rejection of non-transitive interactions as cause of declining rate of adaptation J Arjan GM de Visser and Richard E Lenski http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=134600 "Experimental populations of Escherichia coli have evolved for 20,000 generations in a uniform environment. Their rate of improvement, as measured in competitions with the ancestor in that environment, has declined substantially over this period.....Therefore, this and the other evolving populations must have fairly quickly incorporated mutations that provided the greatest gains, and their slower subsequent adaptation reflects beneficial mutations that are fewer in number, smaller in effect, or both." me again: Reading the preceding study on E.coli by J Arjan GM de Visser and Richard E Lenski, and seeing them trying, desperately, to fit the clear evidence for ID/Genetic Entropy into some type of evolutionary framework made me remember this quote. " The final result of all my researches and discussions is that the theory of evolution should be discarded in its entirety, because it always leads to extreme contradictions and confusing consequences when tested against the empirical results of research on the formation of different kinds of living forms and related fields. This assertion would agitate many people. Moreover: my next conclusion is that, far from a benign natural philosophical school of thought, the theory of evolution is a severe obstacle for biological research. As many examples show (this study of Lenski's, being a prime example), it actually prevents the drawing of logical conclusions from even one set of experimental material. Because everything must be bent to fit this speculative theory (evolution), an exact biology cannot develop." Prof. Dr. Heribert Nilsson Lund University Sweden Kudos Dr. Nilsson, Kudos.bornagain77_{December 6, 2007
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I am also having a hard time understanding the point of this post. Bacteria are everywhere and I assume that the bacteria that a baby is born with comes somehow from the mother during the gestation process. But the chance that a bacteria could have been introduced from outside seems immense since bacteria are everywhere in cluding humans eating baboon innards. So what is the big deal here? It seems reasonable that the bacteria could have changed somehow along the way for a variety of reasons.jerry_{December 6, 2007
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I have found that the problem with word press is browser dependent. We have several different Mac computers in our business and there seems to be a problem with Safari but not Firefox. I got three straight "posting too fast" comments using Safari then took the comment and pasted it into Firefox and it posted immediately. I also found that just repeating the post gets it accepted sometimes almost immediately. By the way if your post is long, select it and copy it so if it dissapears you have a copy of what you wrote.jerry_{December 6, 2007
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same problem with wordpress.russ_{December 6, 2007
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When Humans and Baboons had their presumed common ancestor ~ 6 mill years ago, that should be the last time when E Coli in our bowel had a common ancestor with E coli in the bowel of Baboons in the wild.
1- Humans and baboons did not share a common ancestor ~ 6mya. I don't know of anyone who claims that. Humans and chimps (not baboons) allegedly share a common ancestor ~ 7mya. (anti-IDists will shred someone for that mistake) 2- Symbiotes do NOT get passed on from generation to generation. Meaning the e. coli in your parents' guts are not passed on to your gut, they are not inherited (hat tip to Janice comment 10) Bugs in the News:
The fetus of any animal is completely sterile. Immediately after birth however, the newborn acquires all kinds of different bacteria which live symbiotically (we help them to live, and they help us to live) with the newborn and throughout the individual's life.
To Bob OH- The standard theory of evolution doesn't make any predictions based on the proposed mechanisms. As for testing ID- CSI & IC suffice. 1- We only have experience with CSI & IC arising from agency involvement. 2- There isn't any data, evidence nor observation that demonstrates that either (CSI or IC) can arise And yes I am having the same issue with WordPress. It is very frustrating but it has taught me to first save my comment before posting.Joseph_{December 6, 2007
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This should be a interesting sidelight to this topic: http://www.biologynews.net/archives/2007/11/15/princeton_scientists_break_choleras_lines_of_communication.html November 15, 2007 Princeton scientists break cholera's lines of communication. of special note: A team of Princeton scientists has discovered a key (chemical)mechanism in how bacteria communicate with each other, a pivotal breakthrough that could lead to treatments for cholera and other bacterial diseases. "Lots of other bugs like staph, strep and E. coli use the same general type of signaling mechanism as cholera," said Blackwell, an assistant professor of chemistry. "Many people are looking for ways to inhibit the signaling process, and you could imagine using this process to turn off cholera. It suggests a direct pathway into the clinic." This research also suggests a strong symbiotic relationship for bacteria, with their environment, that further constrains a RV/NS scenario.bornagain77_{December 6, 2007
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Lateral Gene Transfer brings it closer to ID then "Boom its a cow" does because you are dealing with real probabilities - "Boom its a 747" just claims that it was all mmajic ungided randomness out of nothing -per se'.Frost122585_{December 6, 2007
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Bob O'H, The Issue that ID.net is subliminally attacking and I will bring it in to he light, is that DE says that all things originate and then are selected. A transformational process of matter that has an unknown guiding force behind it according to Darwin or it just is. ID says that it is far too improbable that these thing just muted “abracadabra style” and boom you have a human out of nothing. The lateral gene transfer type processes are an even greater way of breaking down the explanatory power of “POOF IT’S A COW” into “there is an improbable chain of events that can only be explained by some form of intelligently directed process arranging the relationships between differing units into a super-highly improbable living organism that displays SC.”Frost122585_{December 6, 2007
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idnet - it's still unclear how this is an ID prediction. We know horizontal gene transfer occurs, so it would be a natural prediction that there would be extra genes in human E. coli, say, and that these would be associated with a fitter phenotype. One example might be antibiotic resistance. So, you appear to have a prediction that is in line with predictions from standard evolutionary biology. It doesn't get you nearer to having a test of ID. Bob P.S. over the last week or so I've been having an intermittent problem with Wordpress saying that I'm posting too quickly. Is anyone else having the same problem? It's not that I am posting too quickly (it will happen on my first post of the day).Bob O'H_{December 6, 2007
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G'day Janice, Your comment: "They’re passed environmentally but not only from parents to children." In this particular instance, how else are they passed? Just querying ...AussieID_{December 6, 2007
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jdd "Do you mean you made these predictions based on ID?" Yes. ID predicts that RM and NS will achieve only very minor feats. This may enable processing a substrate with a slightly different side chain at most. ID theory suggests that totally new metabolic pathways and molecular machines do not arise by RM and NS. For example, most antibiotic resistance arises by Gene Transfer via plasmids. "also a small note, the divergence time between humans and baboons is suggested to be ~25 million year." Thanks a lot. This makes the predictions even more risky as the E Coli have about 3 billion generations to evolve. I don't speak with authority in the ID community but I stand by the predictions and think this research should be done.idnet.com.au_{December 6, 2007
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getawitness, i think they are talking about direct darwinian pathways or random mutation and natural selection. If it's too complex then the random "abracadabra" of "poof" "there it is" darwinisn cant be the solution. Therefore, you need somthing guiding a new gene into the mix. My question is are all the darwinists tlaking about lateral gene transfer today? maybe someone who has read Behe's latest could speak on LGT. I plan to read it soon though.Frost122585_{December 6, 2007
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idnet, I think there's a problem with this:
They are passed environmentally from parents to children.
They're passed environmentally but not only from parents to children.Janice_{December 6, 2007
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BA77,
If the e-coli is divergent, between baboons and man, by more than this limit, which you seem to be implying with gene transfer, I think we can safely assert that it did not occur by a totally RV/NS process.
Wha???getawitness_{December 5, 2007
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I am also a little confused by this: "As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E Coli genes as there have been about 730X10^6 generations of separate development." Do you mean you made these predictions based on ID? If so, Could you elaborate on what aspects of ID lead to these predictions? I am very interested. also a small note, the divergence time between humans and baboons is suggested to be ~25 million year.jdd_{December 5, 2007
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idnet.com.au As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E Coli genes as there have been about 730X10^6 generations of separate development. Of special interest would be the flagellar genes. Of special note: "but that the origin of these functioning genes will be gene transfer." From what research do you base this prediction? Genetic Similarities? From my reading of Dr. Behe's work in the "Edge of Evolution" the limit (prediction) to totally random evolution is now severely constricted and estimated to be 2 novel protein/protein binding sites in an organism. If the e-coli is divergent, between baboons and man, by more than this limit, which you seem to be implying with gene transfer, I think we can safely assert that it did not occur by a totally RV/NS process. as well this other research seems to indicate a different "designed" function for gene transfer: http://www.pnas.org/cgi/content/abstract/103/40/14941 of special note: Several pathogenic strains of Escherichia coli exploit type III secretion to inject "effector proteins" into human cells, which then subvert eukaryotic cell biology to the bacterium's advantage. We have exploited bioinformatics and experimental approaches to establish that the effector repertoire in the Sakai strain of enterohemorrhagic E. coli (EHEC) O157:H7 is much larger than previously thought. Genes encoding proven or predicted effectors occur in >20 exchangeable effector loci scattered throughout the chromosome. Crucially, the majority of functional effector genes are encoded by nine exchangeable effector loci that lie within lambdoid prophages. Thus, type III secretion in E. coli is linked to a vast phage "metagenome," acting as a crucible for the evolution of pathogenicity. Thus the main part of the genome of E-coli seems to be conserved (poly-constrained) and "all the action" seems to be occurring in a part of the genome (vast phage "metagenome) that seems to be gathering and sharing information on the environment with other e-coli. Kind of like a communication network among the e-coli from what I can gather. and then this: crucible for the evolution of pathogenicity. It seems to me that the e-coli are polluted of their primary purpose by a random variation in this "communication network", lose their primary function, and then become pathogenic (turn on their host). I may be wrong, as I'm by no means an expert in this, but I feel gene transfer may not be all what you think it is , especially since Behe provided such a strict limit to what evolution can do by natural processes.bornagain77_{December 5, 2007
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As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E Coli genes as there have been about 730X10^6 generations of separate development. Of special interest would be the flagellar genes. Can someone please explain to me what this means?Nochange_{December 5, 2007
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Can you help me understand this in relation to how (some) evolutionary biologists would hypothesize E.coli evolution?getawitness_{December 5, 2007
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lars, did you click on the link to the paper abstract?russ_{December 5, 2007
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This is not a prediction! You lie! ID is not science, so it cannot make predictions! So there! [/sarcasm]StephenA_{December 5, 2007
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I think it's great that you're making true predictions (i.e. not postdictions). Follow the evidence where it leads!
As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli
I'm not sure I understand the prediction... When you say "extra genes in Baboon E Coli", do you mean genes in baboon E Coli that are not in human E Coli?
but that the origin of these functioning genes will be gene transfer.
Sorry, I'm not a biologist... how will we know whether the origin of these (extra?) functioning genes is gene transfer?lars_{December 5, 2007
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