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The seed, which grew from a plant that itself originally grew from a spore, some time during the Devonian era.As seeds are a more effective way to disperse offspring than spores, it's not surprising that the descendants of this first organism came to dominate the kingdom of plants. But plants which reproduce by spores instead of seeds are still with us, and they represent the descendants of some of the first terrestrial, vascular plants.

If you like. Sure, the plant came first. Right, the spore which came from a spore-bearing plant, like today's ferns. What did ferns evolve from? The first terrestrial, vascular plants. What did those evolve from? Vascular plants that grew in the sea, like seaweeds. What did those evolve from? Sea algaes that lived in multicellular colonies.What did those evolve from? Sea algaes that lived unicellularly. Those? Cyanobacteria. (I'm skipping over a lot of steps and about half a billion years.) Cyanobacteria evolved from chemosynthetic bacteria living at sea floor vents, probably. Those evolved from some of the first living things, ever. That takes us all the way back to LUCA, the cenacestor, the organism who was the common ancestor of all species of life on Earth, approximately 3.8 billion years before the present day. If the sense you're getting is that I'm playing a game of this evolved from that, and that from this other, and that from something yet older.... and so on, and you're wondering "ok but where does that all end?", well, it ends at the beginning - with the Last Universal Common Ancestor (LUCA), because all living things on Earth are descended, ultimately, from a single living organism that lived almost 4 billion years ago.It's pretty fuckin' sweet, if you ask me.

That would certainly be a prediction, but it doesn't function as a test of your theory because the prediction will be true regardless of whether your theory is.Whereas the experiments that verified natural selection would have had different results depending on whether or not natural selection actually occurs (of course, if you think about it it's trivially and obviously true that natural selection occurs, because not all members of a species live as long, or have the same number of offspring.)The experiments that verified mutation would have had different results depending on whether or not mutation happens (of course, it's also trivially and obviously true that mutations must occur, because genetic sequences have to be copied for organisms to grow and reproduce, and it would be impossible for those sequences to be copied without errors every single time.) Why not try learning some, sometime? It's pretty useful, you know.

That mutations occur? Ok, sure. I performed this experiment myself so I can recount the results.I had liquid culture of an "Ames strain", a strain of bacteria that cannot biosynthesize the amino acid histidine, which is necessary for life. They're grown in special broth that supplies histidine, which they cannot synthesize for themselves because they have a frameshift mutation that knocks out the operon for histidine synthesis.Also I had phenylamine, a compound suspected of being a mutagen. I took a portion of the Ames strain culture and exposed it to phenylamine, then attempted to culture on so-called minimal media - a solid media in petri dishes that does not contain histidine (or any other amino acid, or basically anything at all but glucose.)The prediction is that, if phenylamine is mutagenic, then some of the Ames strains will be mutated by it; among some of those individuals, the mutation will take the form of an insertion or two deletions that will restore the proper reading frame and reactivate the His operon. Therefore some of these individuals will be able to grow and thrive on minimal media because they can synthesize their own histidine.My plate was inoculated and incubated for 48 hours at the optimum growth temperature for E. coli. The result was approximately 80 discreet colonies, substantiating the existence of mutations and the capacity of phenylamine to cause mutations (in bacteria at least.) When they're not random we usually don't call them "mutations." If you insert a specific sequence at a specific site that's recombinant genetic engineering, not mutation. Frequently specific mutants, like the Ames strains, are produced not by any means of genetic engineering but by causing lots of random mutations and then selecting the ones you want by some means (replica plating, in the case of the Ames strains.)"Mutation" is largely synonymous with "random mutation." And mutations are random because chemistry is stochastic. Causing random changes in DNA is much, much easier than causing specific ones. If you're trying to hang your hat on the notion that mutations aren't random at all, there's just no evidence at all that's true.

I don't see why that would be any less random.In a Vegas casino, for instance, you're more likely to find dice being rolled on the craps tables than at the blackjack or the slots, right? Does that make a roll of the dice any less random?Or, for that matter, on the roll of a pair of dice you're more likely to roll a 7 than a 12. Is that an element of "nonrandomness"? Or is that simply a recognition that "randomness" doesn't mean "equal probability"?I'm not challenging you, I'm just asking what you mean. It's up to you to decide what "random" means, I guess; but while it's true that in some species and under some circumstances some areas of DNA mutate more or less frequently than others, mutation is ultimately a random process because, ultimately, chemistry is a stochastic process.

I gave you one that I myself performed. Could you explain what you found insufficient about it?Be honest. You didn't even understand it, did you?

Genetic loss of what? Natural selection may weed out some individuals and allow other individuals to breed, but the individuals who bred had the same amount of genetics as the individuals who didn't.It's the content of the genes, not the amount of anything, that determines differential success throughout the populations. How do you propose to measure genetic "information"? How much information, for instance, is in the human genome?Be specific.

For a person of average intelligence, capable and willing to think it through with an open mind? No, not at all.For you? Clearly it was. How is that not what happened? How did HisG- bacteria grow on His- media if mutation didn't occur? Remember, prokaryotes are haploid. I don't have a bruise.Edited by crashfrog, : No reason given.

It was produced randomly. The culture on minimal media selected for a certain mutation, but the mutagen produced random mutants.That's how evolution works - mutation produces variability in populations, and selection hones that variability to the individuals best adapted to the environment. Phenylamine doesn't give bacteria the power to synthesize histidine, it mutates genetics. Some of those mutants had a reversion to HisG+, the vast majority did not, but culture on minimal His- media meant that only the ones with the reversion mutation were able to form colonies.Nothing I did actually made any of the bacteria revert; phenylamine doesn't do that. It doesn't have that kind of specificity and the bacteria had no idea they were going to an environment with no histidine. (Trust me, I didn't tell them.)The mutations were random; the selection was specific. I could have performed the exact same experiment with HisG+, ArgG- bacteria and it would have worked. How could that be, if the mutations weren't random? How would the Ames bacteria know to revert to HisG+ in the presence of phenylamine, if the same chemical tells ArgG- bacteria to revert to ArgG+?And if that's what phenylamine does, why didn't it happen to all the Ames bacteria in my sample? Why were there so few colonies? I must have inoculated the plate with billions of individuals, trillions maybe. Why did I only get 80 colonies and not an entire lawn?Of course the mutations were random. The proof of that is how rare they were. (Phenylamine is not a strong mutagen.)

No, I still don't follow you. I'm a biochemistry major, so I'm used to thinking of DNA in terms of chemistry, not "information", whatever that is. So help me understand what is being lost in a chemical sense. Does microevolution shorten DNA sequences, and macroevolution lengthen them? I'm pretty sure that's not true at all. I don't know what "information" is supposed to mean, but mutations that add sequence to DNA are well-documented. Over the short term, a few of those mutations may be microevolution. Add up many of those mutations over a longer period of time and macroevolution would seem to be the result. Large-scale change is just the accumulation of small-scale change over longer amounts of time. You can invent one, or look one up, I don't care; I'm just asking you - what is genetic "information" supposed to be, and how is it measured?I mean, DNA is a physical molecule. As a biochemist I know how to measure many of its physical properties; molecular weight, number of base pairs, ratio of base pairs to the whole, sequence of base pairs, concentration in aqueous solution (usually in nanograms per microliter), and so on.I've never measured anything like "information" in DNA, though. Can you tell me how to measure it, or not? If you don't know how to measure it then how can you say whether there's less or more of it? Not yet you're not. How do you measure genetic "information"? Be specific. If you can't measure it how do you know what processes result in more or less of it?

Why would there be a selection pressure against useful "information"? If it's useful, then natural selection will preserve those sequences, not obliterate them. Under natural selection what is lost is useless or harmful phenotypic traits and the genes that encode them. No, natural selection will preserve and increase the arrangement of chemicals that produce useful "information" and select against useless or harmful "information." Both macro and micro are true, but that's not what is observed at all. Some microevolutionary processes (like mutation) lengthen DNA sequences. Some species macroevolve by shortening their DNA (like parasites.) There's no need to have an "argument" for it, it's fundamental to mutation that additional sequence can be added. Here are the fundamental types of mutation:Point mutation (exchanges)
Insertion
Deletion
Gene duplication
Gene translocationTwo of those are actually the introduction of something new to the genome; insertion adds one or more bases into a genetic sequence, and duplication introduces an entire copy of an existing sequence (usually adjacent to the original.)Mutation is how genetic "information" is added to the genome, as well as how it is taken out. That is why microevolution can increase the information in a genome, and why macroevolution is trivially demonstrated as the sum total of many microevolutionary events. You want proof that mutations occur? That was identified by Darwin 200 years ago and is a trivial observation. You want proof that mutations can add information? Get yourself a strain of Ames bacteria, expose them to a mutagen, and culture on minimal media. You'll see that insertion must have occurred because you'll see colonies of Ames bacteria growing on a media they shouldn't be able to thrive on.Proof positive - mutations add genetic sequence. If they didn't, the only evolutionary trend we could observe would be a shortening of the DNA of every single organism across the board. If mutations could never add sequence, only remove it, eventually life would go extinct because no organism would have enough DNA to live. But we don't observe that - therefore, we know that mutations both add and subtract genetic sequence. Ok, then you agree - mutations which add base pairs to DNA are adding information. Ergo, microevolution adds information; therefore macroevolution must exist as nothing more than the sum of many instances of microevolution.So, you've just agreed with me that evolution is true. Maybe you want to quit while you're behind? Ok. How much information is one teaspoon's-worth? Doubtless, because humans have to synthesize more proteins that bacteria do.But humans have less chemical information, by this measure, than the marbled lungfish, which comes in at an enormous 130 gbp. And the largest genome of all is the single-celled amoeba Ploychaos dubium, at a whopping 670 gbp.As far as chromosomes go, humans have less chromosomes than guinea pigs (64), garden snails (54), chickens (68), and silkworms (56.) So clearly chromosome count isn't an accurate measure of information content, which every student who has ever double-spaced an essay to make a page requirement is aware of.

Transfer from what? It has to start somewhere. In the case of Hallett and Maxwell 1991, their original population of bacteria were descended clonally from a single individual, so there could not have been any resistance plasmids floating around there for HGT until one bacteria evolved the resistance gene, on its own, by random mutation and natural selection. Sometimes they do, but if having such a transport system is maladaptive then isn't it an increase in "information" to remove it?And what about mutations that add a new transport system, one that transports the antibiotic out of the cell faster than it can diffuse or be transported in? For instance, that's the mechanism that MRSA evolved to efflux flouroquinolone. No, of course not. The origin of those genes was random mutation and natural selection, which is the origin of all genes.Edited by crashfrog, : No reason given.

Yes, I know what a plasmid is. But a plasmid is little more than a platform for gene transfer. The genes being transfered have to come from somewhere; in the case of the experiment referenced, they couldn't have come from resistance already present in the population because the population was comprised entirely of clones of a single individual that had no resistance at all.So, again - transfer from what? HGT isn't the origin of resistance genes in bacteria, it's how they share those genes amongst themselves. Non sequitur. Please answer the question. If having a transport system that exposes you to an antibiotic is maladaptive (which it is, in the presence of the antibiotic) then isn't in an increase in "information" to be rid of it altogether? But I have. Remember? How mutations can add sequence as well as subtract? One bong rip too many, I think. Science is best understood with one's sober mind, with a few exceptions (the story goes that Kary Mullis invented PCR while dropping acid in his hot tub.)

You're not doing very well at answering my questions. I'm starting to think you don't know what you're talking about. No, that's just how they're transferred. That's not where the genes come from.Remember every single individual in this population is a clone of a single founder individual, so if mutation can't result in new genes they can engage in all the horizontal gene transfer they like and they'll never get anything new - they all have the same genes, already. They're clones!But we observe that they do gain new genes. Mutation is how they gain these new genes, and natural selection explains why they come to dominate the population as a result of the advantage having them bestows. No, it doesn't, because they're all clones of an organism that had no resistance genes. The genes can't have already existed in the population because the entire population is a clone of a single individual. The resistance genes arise by mutation and are transferred on plasmids. They're not something that could have previously existed in the population. But the genetic material wasn't present inside, or outside, any of the chromosomes of any of the individuals, because they were clones of an individual that had no resistance genes.Mutation is the origin of resistance; horizontal (and vertical) gene transfer is merely how the mutated gene is spread among individual. By eliminating a vulnerability. So why isn't eliminating a vulnerability a gain in information? It seems to me like it would have to be. Already given. Can you please answer my questions, now?

If mutagens didn't restore the ability of bacteria to synthesize histidine - and remember, we didn't do anything else to the bacteria besides expose them to a mutagen - then what did?Did it happen by magic?