Problems with evolution? Submit your questions.

Since the phenotype of organisms is specified by the information in their genetics, then an increase of diversity of phenotypes within a species (variation) must, by definition, be an increase in genetic information within that species. If organisms could never have any more or any different information than what their parents had, all individuals in a species would be clones of each other. Because we can observe that individuals in a species aren't clones of each other, nor of their parents, we know that individuals have access to a source of genetic information beyond heredity, and that source is random mutation. Every individual of a complex organism - say, any mammal - is born with roughly 100 germline mutations that they did not inherit from either parent or from anybody else. These mutations represent novel genetic information.

Right, and that diversity can only increase by adding additional, new information. Copying errors are how new information is introduced into DNA. We call these errors "mutations" to reflect how they represent changes to DNA, and these changes are the means by which new genetic information arises. It's not at all impossible; Liz Taylor famously had violet eyes which were not inherited from either parent but were the result of a mutation. Human eye color is a polygenic trait and mutations to various genes can alter the composition and concentration of iris pigmentation. Right, and asexual species are highly clonal except for where their genetics diversify as a result of new information gained by random mutations. I've been telling you the source throughout, over and over again. Mutation is the source of genetic information not received via heredity. Yes, that's correct - out of the 3.6 billion base pair genome, about 100 bases per individual - per every individual who has ever been born - are altered as a result of random mutation.It is estimated that as many as 150 billion human beings have lived on planet Earth. That's 15 trillion mutations, then - enough for, over 200,000 years of human evolution, every single base pair in the human genome to have been mutated approximately four thousand times. You only believe this because you cannot do math. You're right that the bulk of mutations are "silent"; they result in no effect on organism phenotype. This is largely due to the lack of obligate specificity in most of the structure of the average protein. (Protein function is determined by the small number of residues that make up the protein's active site.) But, rarely, a mutation in a gene results in a protein product that has a dramatically different structure than wild-type. In these cases, the mutation will have an effect on phenotype, and whether or not that mutation is beneficial or harmful is a function of its interaction with environment. Organisms we observe now, after 3.5 billion years of evolution, are sufficiently adapted to their environments that a non-silent mutation will, in most cases, be maladaptive; but rarely, mutations produce beneficial change. Many examples of such mutations can be found, for instance the mutation that allows humans of European descent to consume cow's milk in adulthood.Natural selection, therefore, is the means by which rare beneficial mutations nonetheless come to spread throughout the population due to their survival benefit. Natural selection is, fundamentally, a process that magnifies the incidence of beneficial mutations and reduces the effect of harmful ones, at the species level.

Well, for instance, I performed an experiment in micobiology lab which I detailed in another thread; to summarize, I transformed His-negative Ames E. coli into His-positive E. coli by introducing a small amount of new information by means of random mutation. (The His-neg bacteria were themselves the descendants of His-positive bacteria which had been transformed by removing a small amount of information to disable histadine biosynthesis.)The evidence for my claim is the obvious notion that since DNA contains information, mutations that introduce DNA will introduce new information. I don't know what a "man-ape" is, but new species arise from old ones when so many genetic changes accrue that the new species can no longer successfully breed with the old one. That's what it means to be a "species", after all; a community of individuals defined by the capacity for interbreeding. It very much appears that way to me, because I observed it myself in the lab. Random mutations to Ames-strain E. coli produced reversion mutants with the highly useful ability to synthesize histidine on media that didn't contain it. I know that happened because I performed the experiment myself. Sure. Other examples would be increased plasminogen activator inhibitor function, increased lipioprotein lipase, enhanced immune system function due to a mutation in G protein beta-3, and so on.Don't get me wrong, it turns out that it's a lot easier to create a dramatic failure in a biological system than a dramatic improvement. But natural selection is a "ratchet" that pushes a species forward towards adaptation to environment, and selects against individuals who represent maladaption. Over time that ratchet results in significant, cumulative species change. Obviously. Yes, which is why I continue to wonder why you keep asking where new genetic information comes from, because I know you know where it comes from - genetic mutation. No, I'd like you to respond to me, since I'm the source. I've done the experiment that proves that mutation add new information. What questions would you like me to answer about it?

What "others that are divisible by three"?I think this may be another case where you need to hit the sack and give yourself some time to sober up.

I'm not asking you for "research" I'm asking you to explain what the hell you meant, because your statement as written is unintelligible. The same thing that causes mutations of nucleotides 1,2,4,5,7,8,10,11, etc. Mutations do not have the kind of specificity to attack the first and second base of a codon but ignore the third. I mean, surely you're aware that frameshift mutations are cyclic, right? That there are two ways to reverse them - reverse the indel or add another two to return to the original reading frame, minus or plus one additional residue? (the utility of Ames-strain bacteria for the detection of mutagenesis is based on this incredibly simple principle.)I mean, surely you wouldn't pop up here and not know what you were talking about, right? Maybe you should be researching some of your own claims, first?

Not so. That's not what "random" means.For instance, rolling two dice and adding the result gives you a random number - this is the foundation of games of chance such as craps.Yet, if you have a dozen people each roll two dice a hundred times and chart the results, every single one of them will produce something akin to this graph:This is because "random" is not a synonym for "completely unreproducible." Frequently random results are very reproducible because the outcomes are probabilistic, as they are with mutation (same as with any chemical reaction.)Usually experiments to detect mutations - say, an Ames culture - are selecting for a specific mutation. That doesn't mean that other mutations aren't happening - we know for a fact that they are, because we're using mutagens that simply can't have that kind of specificity - but that we're combining that with selection against all but one specific kind of mutation, so that we can get a general rate of mutation. If there was no selection of any kind there would be no way to distinguish mutants from non-mutants. But, of course, dead organisms don't pass on their genes. Dead organisms don't consume resources or occupy environmental niches (though they frequently are niches.) That means that populations of living organisms come to be dominated by the individuals who had mutations that increased, not decreased their fitness - they are, after all, the only ones left. The source is the same as new nonfunctional genetic code - random mutation. Since mutations are random they produce a mix of functional and nonfunctional new genetic code. Natural selection serves to weed out nonfunctional genetic changes from functional ones.Random mutation and natural selection is the source for functional genetic novelty and explains increases in complexity of organisms. The evidence for this is ample, has been given to you already, and was either not understood by you or simply ignored.

If all organisms were programmed with the complete diversity of their "kind" (whatever that means) programmed into their genome during their creation as two individuals per kind, and that information is being slowly lost as time goes by, then it's very obvious what we should be observing - that species diversity should be declining across the board, as the diverse genomes within those kinds are slowly pruned.But what we see is the complete opposite - that species diversity increases over time, that genomes increase in information content due to random mutation and natural selection, and that two individuals of one diploid species can have at most a diversity of four alleles per gene amongst the two of them.So by simple observation we know that your position is false; the observations we make are of the exact opposite of a gradual decline from one expansive "supergenome." What we observe is most consistent with an evolutionary increase in species diversity due to random mutation and natural selection occurring over geologic time. Wolves are a diploid species so two wolves can, at most, have only four alleles per gene among them. That's not enough alleles to account for all the genotypes present within the Canis lupis familiaris subspecies. While it's known that the effect of breeder selection on the dog genome has been one of contraction of diversity and the fixation on various recessive traits by selection against the dominant phenotype, many of those alleles don't exist in wolves. They're present as a result of mutations specific to dogs. The evidence for universal common ancestry is quite overwhelming. This evidence includes:1) that all organisms use the same 20 basic amino acids, even though there are countless amino acids to choose from;
2) that all organisms use either the same codon-substitution rules or a slightly-modified version of it, even though there's no reason that should be the case;
3) that all organisms use the same four deoxyribonucleotides and the same four ribonucleotides even though there's no reason they should;
4) that we can chart genetic paternity/maternity via 16s ribosomal subunit across every living species, at an incredible level of statistical significance, even though there's no other reason we should be able to do that;
5) genetic engineering is possible; organisms are so fundamentally compatible that we can take toxic genes from bacteria and insert them into plants, or jellyfish luminescence genes into monkeys; we can put any gene into any other organism and, reliably, it will produce precisely the same protein product there as it did before;and so on. There is more evidence for the common ancestry of all living and extinct organisms than for any other scientific proposition known to man; more evidence than there has ever been for any physical law, any medical diagnosis, any mathematical proof, or any finding of fact, guilt, or innocence by any court. Refusing to accept the ample evidence for universal common ancestry means closing your eyes to literally every field of science. But two organisms don't have the genetic diversity to explain even their own species, much less a handful of related genera and families creationists so haphazardly lump as a "kind." It's simply a genetic impossibility. Contrary to physical and chemical law.Therefore what you believe cannot be true. Diversity of population cannot increase to the extent that we observe it based simply on sexual recombination (and not at all in species that do not sexually reproduce), which proves that random mutation and natural selection is the source of the rest of the new information, and is the mechanism by which species diversify to such an extent that some of their members become a new species, altogether.

None - you have to add marbles, just as random mutation and natural selection add functional information to an organism's genome. "Almost"? So, you admit there's been some evidence for microevolutionary change that adds genetic information.

That's correct, but again - 3 dice or 3 million, the dice are going to follow entirely predictable probability distributions.No, we can't predict exactly the outcome of any one roll of the dice. And of course scientific results are never exactly replicated - we use statistical tests to discern what results are simply the result of chance and what results are significant; what results allow us to discard the null hypothesis. "Random" doesn't mean "unreplicatable." It means "probabilistic." The human genome is 3.6 billion base pairs long, so your intuition is largely correct, any particular mutation is fairly rare. When two humans have the same mutation at the same place in their genome the most reasonable explanation is that it's there by heredity. This is the principle that underlies paternity testing. Sure. It's such a trivially observable fact that we let undergrads perform the experiments. It's so trivial, in fact, that these days you can't even publish a paper on one; no journal would publish it because it's just not significant enough. It's like trying to publish an article that says "color of sky found to be blue."Many documented cases have already been given to you. You've simply incorrectly attributed them to horizontal gene transfer or outright ignored them. I think there's plenty on your plate to respond to as it is. Incorrect - we've proved that they're random. Incorrect - we've proved that HGT was not responsible. Incorrect - you've failed to understand what "random" means. There are a countless number, which you have dismissed on entirely spurious grounds.

Yes, those are frame shift mutations. Any single or double indel is going to shift the reading frame regardless of what base it occurs at. No, they do not. Under no circumstances does this occur.Let me be absolutely clear - you have no idea what you're talking about; a frameshift mutation is not a mutation to the third base of a codon, it's an indel at any point in the gene that shifts the reading frame. "Shifts" the reading "frame." "Frameshift." Get it? There is only one form of frameshift mutation - an indel. Point substitutions don't shift the reading frame. It makes perfect sense because the reading frame is three bases long; three indels is going to remove or add an entire codon. 3 modulus 3 equals zero. Frameshift mutation - Wikipedia

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A frameshift mutation (also called a framing error or a reading frame shift) is a genetic mutation caused by indels (insertions or deletions) of a number of nucleotides that is not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by codons, the insertion or deletion can change the reading frame (the grouping of the codons), resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein produced is.

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When you do a number of indels divisible by three there's no frameshift mutation. When you do one indel, that's a frameshift because one is not divisible by three. When you do three indels you've just taken out or added an entire codon so there's no shift to the reading frame. Take out the periods because they're clearly messing you up.Indel 1:TTh eca rwa sre dTh ere dca rha don eke yTA GIndel 2:TTT hec arw asr edT her edc arh ado nek eyT AGIndel 3:TTT The car was red The red car had one key TAGBack to normal.Or let's use your example: Indel 3:The jca rwa sre. dTt hXe red car had one key the TAGFrameshift mutations happen only when the number of indels is not divisible by three. As you can see, the reading frame is restored after the third indel. Divisible-by-three amounts of indels don't shift the reading frame. Organisms don't really rely on the stop codon as much as you think; protein synthesis ends when the ribosome reaches the stop codon but it also ends when the ribosome runs off the end of the RNA. Losing a stop codon doesn't really matter. A frameshift might introduce a spurious stop codon, however, and that will have a drastic effect on the protein product.But again, the difference between your example and the genetic code is that while not every three letters is an intelligable word - our frameshift of a sentence produced garbage until it was reverted - every three bases is a codon. There aren't any unusued codons. A frameshift is more likely to alter the protein product but in only one possible case is it going to actually destroy the product - when a spurious stop codon is produced. But again, I've just shown you how easy it is to reverse a frameshift, you just add more indels until you've restored the reading frame.A frameshift doesn't cause a loss of information in the genome because the codons continue to encode amino acids. They're not lost, they're just interpreted differently. Most of your genome is information with no functional purpose. Well over 98% of the human genome is sequence with no regulatory or protein-encoding function at all.Does that suggest to you, perhaps, that the human genome is the result of mutation? Any frameshift mutation is going to produce new information randomly, because it will shift the reading frame and result in an entirely new translation of the sequence into proteins. It's not possible to produce "nonsense" codons because all possible codons code for something; the codon substitution table is fully "filled in."

Sure, but how many different chromosome homologues are there among two individuals? Four, is all. And then you go and make it worse: Kind of cuts the information available by half, doesn't it, if Eve is Adam's parthenogenetic clone? That's only two different homologues per chromosome; two alleles per gene. That's it, that's all the genetic diversity in human beings inagaddadavida, honey. And regardless how perfect their genome may have been it still has to be a human genome.

Well, to be fair, they're unfit for the wolves' environment. They're quite well fit for the dog's environment - inside human domiciles.That's the thing about fitness - it's context dependent. You'd make a terribly unfit shark, but that's not the environment you inhabit. Presumably you're a little better suited for where you actually do live.

Canonically, perhaps, but the real world of organisms is more complex than that. Organisms have evolved safeguards to mediate ribosome dissociation and residue release when the stop codon is absent. And, of course, we're talking about chemical reactions, so sometimes a stalled ribosome will just drop off on its own. Oh, they're quite important, but organisms have evolved ways to deal with their absence under some conditions. But again, that's not accurate. Every possible codon that isn't a stop codon is used, and has an amino acid equivalent. Any combination of nucleotide bases that gets transcribed to mRNA and fed through a ribosome is going to be translated into a protein. Every single one.There are no "nonsense" combinations of bases, the way that you can combine letters to make nonsense "words." Any combination of nucleotides is going to be able to be translated into a protein. Organisms can even ignore stop codons that are the result of frameshifts, by mutating one of the tRNA's to recognize that codon.Now, not every protein is going to have function. But a lot of them do. A calculation in my Lehninger textbook (an undergraduate biochemistry text) estimates that 1% of randomly-generated polypeptides exhibits kinase activity. The individual contribution to protein function and structure by any particular single amino acid residue is quite minimal, unless the residue is part of the reaction mechanism. (That's usually only a handful of residues, three or four, throughout a hundred or two hundred residue protein.)If you want to make an argument that any mutation at all to a protein is going to result in diminished function, you can try, but that argument is certainly wrong; there's an enormous amount of evidence that mutation rarely alters protein function at all, and many proteins have not been under enormous selection pressure to optimize, so there's much room for mutational improvement.

No, we know exactly how much information Adam would have contained, because Adam was a human being. He had to be, since all his progeny were, and organisms only reproduce after their own kind, right?Adam can't be genetically incompatible with any of his descendants, because then we would be from a different kind than he, and that's the one thing you're adamant (if you will) that can't happen, remember?So we know everything about your Adam's genetics, because he has to have human genetics. And we know that the most copies of any allele a human can have at any given locus is 2, because humans are a diploid species.

It is, isn't it? Maybe you're getting a sense of the deep wonder and amazement those of us feel who have the privilege to study the biological sciences.You could read all the works of Shakespeare in a semester. The Bible in a year. Two years and you could have the entire canon of Great Works under your belt.Take a square meter of your lawn and you could spend a dozen lifetimes studying the biology, chemistry, and ecology of the myriad of species located therein - and God had nothing at all to do with any of it.Yes, it's amazing!