Cheers!
Posted on 04/06/2009 1:04:25 PM PDT by GodGunsGuts
There are numerous species that are living today even though they appear in the fossil record.
“There are two types of animals that rule the world. Ants are one.
Birds the other.
Found on every continent.”
Uh, so are humans. We rule! I can kill a bird or an ant any time I want. Can they say the same thing?
“They’re not taxed and regulated!”
But they do have a Queen.
They don't retrace their steps;
They exercise their senses;
They communicate;
Doesn't sound entirely random to me.
And if randomness DID produce organization, the GOP would have a bigger voice in Congress.
Cheers!
Cheers!
Good point. So much for the average rate of mutation!
Amen to that!
Even if you lower the average rate of mutation, given the time periods involved, every genome should be unrecognizable when compared to the “deep time” organisms we find in the fossil record. But we find the exact opposite. That is, we see sudden appearance, and then stasis. And I find the words you are using quite curious. Nature “offers” the “lesson” that risks are not to be incurred “unnecessarily.” Very teleological, don’t you think?
We are in agreement here. The changes in the fossil record and the divergence of living species from that record is compelling indirect proof that genomes have mutated greatly and produced extraordinary changes in form.
Rates of mutation though vary from species to species and within genomes. In some instances, well adapted species survive with few changes in form and, implicitly, few if any significant changes in their genomes.
Of course, we cannot directly compare DNA from extant species with those in the fossil record. Except for a few instances involving fossils less than a hundred thousand years old, DNA does not survive fossilization.
I was speaking to morphology. We find two things in the fossil record: extinction and stasis. In other words, of the extant species that have relatives in the fossil record, nothing has changed much since the Cambrian Explosion. This is powerful evidence for design IMHO.
Actually, not just powerful evidence for design, but even more so, powerful evidence for the biblical “kinds.”
Why do you suppose a bacteria under stress produces an error prone DNA polymerase instead of its usual high fidelity DNA polymerase?
This thread was about ants.
Please post a link to whatever you are referring to, on pain of confusing me further.
There are relatively few living species that are unchanged from their counterparts in the fossil record. Instead, there is dramatic, extraordinary change.
The Cambrian-Ordovician extinction events some 485 million years ago were followed by five major extinction events, the most recent being the Cretaceous–Tertiary extinction some 65 million years ago that ended the age of dinosaurs.
There is little stasis in that record, and no humans until very recently. And surely no human fossils are to be found with dinosaur fossils, let alone in the Cambrian era.
DNA is replicated using an enzyme called DNA polymerase (because it produces a DNA polymer or chain).
Most DNA polymerase is very high fidelity, with only one mistake ever few thousand DNA bases that it copies; and there are repair enzymes to catch most of those mistakes by recognizing DNA mismatches.
When a bacteria is under stress it turns down its DNA repair enzyme genes and its high fidelity DNA polymerase and instead replicates its DNA using an error prone DNA polymerase that will introduce “errors” when copying DNA.
Why do you suppose bacteria that did this would be at a survival advantage over those that did not have or utilize error prone DNA polymerase?
In other words, what advantage could there be in a bacteria having a gene to make “errors” in DNA? Why would there be an advantage to producing these “errors” and not correcting them when the bacteria is under stress?
The follow up questions are even more interesting.
1) What is the mechanism by which the bacteria "turns down" the DNA repair enzyme genes?
2) How is this gene activated by external conditions?
2a) When/where did this gene originate, and how is its activation correlated with the natural reproductive rate of the species under study (is it functional in higher animals, too; and if so does it lead to cancer?)
3) Do all the population under stress do this at the same time? Do the bacteria in a colony signal each other? Or is it "every microbe for itself" as to when to switch to faulty polymerase?
4) What happens to the mitosis rate? If it too depends on stress, how is this cross-correlated with the change of the DNA repairs?
5) What are the energetic costs of keeping the DNA repair gene turned off? Does the faulty DNA only come on under periods of abundant food, but not under some other stressor?
6) What studies have been done which have simultaneously verified the change in the polymerase genes and the appearance of changes beneficial in the now-altered environment? Were the studies in vitro or in vivo? Is there a "punctuated equilibrium" in the population, so that the relative population of the (by assumption) mutated bacteria and the "original" type shifts back, once the stress is over?
7) Has anyone tried studies where the faulty DNA polymerase is disabled in one colony of bacteria, but left functional in another, and the two colonies subjected to identical stressors? Has anyone then compared the number of mutations helpful in surviving the stress in each colony; the gross number of bacteria in each colony; and then performed a sensitivity analysis on the above using variations in the severity and/or type of applied stressor as a control?
8) What on EARTH did any of that have to do with ants?
Cheers!
As to your questions.
1) by one of any number of known mechanisms whereby transcription factors (that recruit RNA polymerase to the promoter region of a particular gene or set of genes) are inactivated, or repressors are activated that bury the gene in chromatin.
2) In this case probably by protein misfolding in the endoplasmic reticulum.
2a) No. Multicellular animals wouldn't want to use error prone DNA polymerase, it would cause cancer.
3) The stress responses I have studied are individual and inside the cell, although bacteria do form plaques, and can exchange DNA information, and do signal other bacteria.
4)stress usually slows the replication rate.
5)The energetic costs of utilizing repair enzymes is insignificant compared to the costs of low fidelity DNA repair when everything is working. Why would it be turned down during stress is the relevant question?
6 and 7) Check Pubmed. You might find interesting an experiment on heat tolerance that used selective pressure and checked all the permutations of a particular gene that the bacteria went through EVERY SINGLE POSSIBLE CHANGE of a single nucleotide, before arriving at the mutation that eventually predominated within the population. The mutation coded for a protein that had increased function at high temperature.
8) The article was from a “Creation Science” source and discussed evolution. Ants use a random walk process to search for food and I found it relevant to the discussion.
So why do you suppose a bacteria would have an error prone DNA polymerase, and why would it use it while decreasing its ability to correct “errors” during times of stress?
Now, returning to your answers.
1) What I meant was, what in particular *are* the mechanisms by which an event external to the cell affects the substitution of one polymerase for another? If there are specific known mechanisms, great. Point me to them -- it'd be interesting to see how the two forms of polymerase are thought to have come about, why they were both preserved, and how that mutation propagated across species of asexual beings in widely separated physical environments. This would be useful information, and not just for hand-waving.
2) "Endo" plasmic reticulum is internal to the cell. Your point 1 hints at how the change takes place, but not a biochemical rationale for how the information of "help! help! I'm being repressed" makes it from the outside of the cell (environmental conditions) to influence the reticulum. Unless you are saying (as a WAG example) that changes in ionic concentration affect the ionic composition within the cell, which then affect the tertiary structure of the proteins in the ER, which then affect...
If that is the case, you still need to show that the changes sufficient to modify the gene expression don't throw all other kinds of things within the cell out of whack...or that you have "cancellation of errors"; or, that it is an inexact adaptation, many cells get sick and die under stress, and a relative few manage to make anything out of this adaptation anyway.
2a) I just said that it would likely cause cancer. Which leaves unanswered the question about which organisms show the change in the "preferred" polymerase; the question of by what mechanism the polymerase fell out of use in the populations of the higher creatures; and what difference the cancer would make, IF the higher creatures had had time to breed anyway before the cancers took them out. (cf. no evolutionary adaption to smoking or trans-fats yet, since the deaths come after the age of fertility, so no differential effect on populations of offspring).
3) That's exactly what I had in mind. Are the plaques and the signals (I can't remember the term but the concept is something of a biofilm within which the bacteria establish a "quorum" to undertake concerted action) involved in the changeover to the faulty polymerase?
4) If it does, wouldn't that work against the effect of the faulty DNA repair?
5) I was looking at the costs in the *other* direction -- if a cell is under stress, how much energy is really saved by not repairing the DNA; what *other* problems are caused by not repairing the DNA; what is the Return on Investment, so to speak, of turning off the DNA. Please, no hand-waving. I understand the implied ansatz just fine...has it been independently, empirically *observed*?
6) and 7) I was on that thread before RightWingProfessor got kicked off of FR. Did anyone do any follow-up to show that the rate of mutations was in fact due to the change in temperature? ...and the question about in vivo vs. in vitro is relevant here, since if it is a highly artificial situation (no predation, uniformly changing stress, at a relatively slow rate allowing time for adaptation, protection from the elements or anything else which would break up the colony, large population, excess food), it would overstate the rate at which such adaptive modifciations occur in the wild.(*)
8) That I didn't know. I thought they were using ants to model optimum transportation problems, from the thread ("human drivers slow down when they get too close to another car.")
...and from the thread, the ants *still* are a poor example of true randomness.
(*) What would be fun if one had a *much* faster computer, would be to do an exhaustive search of all the proteins possible given mutations of some order (spot mutations, double mutations, up to say six mutations) within the bacteria's genetic code, while still remaining 'viable', to see what in principle the bacteria could come up with. Keith Laumer in a couple of his books Retief's War, Retief's Ransom IIRC) played with ideas like this. In Ransom he has a world populated by spare body parts which join together for mutual protection forming a wide variety of creatures; and those creatures merge to form a higher being, and so on. The highest level beings are sentient, and approximate humans in ability. The plot revolves around two of the sentient beings who merge to form a superbeing/demigod bent on domination. In War, the planet is showered by relatively high radiation, and the crust is rich in metallic instruments. A variety of mechanistic creatures evolve, including wheeled animals and animals similar to helicopters. Given that the owl can swivel its head 360 degrees (or close to it), and the presence of ball-and-socket joints, why *hasn't* any animal developed wheels yet? It'd sure come in handy sometimes, right?
Cheers!
Thanks for the ping!
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