While Percy's definition of information as the number of bits necessary to represent the message in correct, his example of "genes" is misleading. In principle, any mutation that produces a sequence of bases that did not previously exist in a genome is an increase in information since the number of bits necessary to represent the genome has increased. Thus, if the original three sequences of 6 bases (2 codons) mutated as specified, there would be produced an additional sequence of 6 bases (2 codons) that did not exist before. Simple. It becomes obvious when you consider that to represent the bases at these 6 loci has required the writing of an additional line of information to represent the possibilities.
However (and I'm sure that Percy understands this), genes are actually composed of thousands of bases that make up thousands of codons that encode sequences that represent polymers that are thousands of amino acids long. I know that the point may seem obvious, unless you are unfamiliar with the topic. It's not all that important, I just thought it should be pointed out.
"Increase of genetic information" is just another way of saying genetic diversity. Any increase of genetic diversity is therefore, by definition, an increase in information. The specific example that Percy gave is an example of an increase in the molecular diversity of a hypothetical genome. While the example is a case of the addition of a new molecular allele, it is not a new genetic allele. You see, GGx (x being any of cytosine, adenine, guanine or uracil/thymine) always encodes the amino acid glycine, and ACx always encodes the amino acid Threonine. In other words, all 4 molecular alleles produce exactly the same sequence of amino acids in the resultant protein, and thus represent the same genetic allele. A mutation in the second G in the codon GGA would encode a different amino acid (GAA = glutamic acid, GCA = Alanine, GUA = Valine). The same principle is true for the other specified codons (GGC, ACG, ACA)
I may be picking nits here, but to someone who is unfamiliar with genetics or molecular biology then the example may be misleading. You can find the genetic code lots of places on the web, even Wikipedia.
Percy is also correct that the paper is about the origin of new genes, not the origin of new alleles.
Also, Mr. Jack is also quite correct. It is the interaction of the proteins involved that produce variations in dominance. Hypothetically, a single point mutation could cause a change that is dominant and shows up in the phenotype - which is, I think, Percy's point.
In the other thread the demand was made for one example of where natural selection added information. Percy correctly responded that it doesn't. In fact, quite the contrary is true. There are several mechanisms of evolution, some of which add genetic diversity (information in the genome) and some which remove it. Percy pointed out that natural selection (sexual selection and artificial selection as well) remove diversity. The same is true of genetic drift, biased variation, and non-random mating, other mechanisms of evolution. On the other hand, mutation, geneflow, moveable elements, and recombination add diversity.
It also occurs to me that the first quote from NanoGecko is actually wrong.
It is just as well that the DNA contains so many base pairs of coded information, and that there is a safety mechanism in that usually both parents need to have the copying error (mutation) before the mutation will express itself in the offspring.
As pointed out later, it depends on the proteins produced. However, in one of the most famous and documented cases of evolution by natural selection, the mutation was immediately apparent. The first notice of a dark morph in the Peppered moth (Biston betularia) was in 1848. Until then all observed moths had been of the light-speckled variety. From then until 1895 the percentage of dark morphs increased until it had reached 95% in polluted areas. As pollution was reduced during the last half of the 20th century, the number of dark morphs also declined.
My point here is that the dark morph (called carbonaria) was caused by a single point mutation. The mutation and the gene has been identified. The mutated gene is dominant. Thus, heterozygous moths are dark.
Should we regard that as evidence that humans descended from ape like animals over millions of years?
Why on earth would you even ask such a question? Why do you feel that moths should be involved in the evolution of humans? All living organisms are the result of evolution. They are all descended from previous organisms that were different.
I can present some evidence that humans share a common ancestor with the other apes. Would you like to learn about it?
Although I would have thought 'evolution in action' would have been an addition of information in the peppered moth population.
Then you would have thought wrong. Evolution does not require an addition of information. There are, of course, several mechanisms of evolution that do, in fact add information to the genome of a population. It is also true that the addition of information to the genome of a population is, by definition, evolution. However, evolution can also happen when information in the genome of a population is reduced. You see, at the most basic level, evolution is a change in the allele frequencies in a population over generations. That is what happened (twice) in the case of the peppered moths. And it happened because of natural selection (one of the mechanisms of evolution).
When creationists claim that a mutation can only destroy information and never create it, they are citing the standard communication theory definition of information. It, of course, has to do with the transmission of a message. In this case, the message contains all of the information that is to be transmitted. If in the process of transmission the message is corrupted, then there has been a decrease in information. It is true that in this case a change cannot add information. So creationists, without any understanding of information theory or biology, claim that no new information can be added.
However, genetics and the genome of a replicating population is not a matter of sending messages between two parties. You see, some additional information has been added to the theory to use it in discussing genetics.
(As a proponent of ID I want you to know that I am not attempting to start a fight. At least I have not been provoked here yet. I am asking questions and exposing my ignorance on genetics.)
You are also exposing the fact that you didn't actually read any of this thread, where all of this was covered before.
GGAACG (green eyes)
GGAACA (blue eyes)
GGCACG (yellow eyes)
GGCACA (brown eyes)
All of the above appear to be variation of two amino acids correct?
No. All of the above are variations in the bases in two codons. Each of the GGx codons always produces glycine and each of the ACx codons produces threonine. As a result, none of those combinations could not possibly produce differences in eye color, even if those particular codons that produce those two amino acids are in the sequence of a protein for eye color.
GGA or GGC - glycine ACG or ACA - threonine
I wonder what would happen if some of those amino acids had mutations that changed into any of the other 18 new amino acids???
Amino acids don't mutate - DNA mutates. The effect of a point mutation can be that a different amino acid in a particular protein can be substituted. That change may or may not have an effect on the function of the protein.
Am I right in thinking that mutations at the beginning of each condon [sic] would more likely result in larger mutations? Or would the eyes start to lose some particular functions?
Not really. A point mutation of one of the bases in either the first or second position, and only sometimes in the third position will produce a different amino acid in the protein sequence. If UAU or UAC mutate to UAA or UAG (stop) the the protein will be truncated at that point. That will usually result in making that protein non-functional. Of course, there are lots of other known types of mutations besides point mutations: indels, inversions, transpositions, duplications. An indel might produce a frame shift mutation like that one that allowed a bacterium to metabolize nylon waste.
For example: ACG becoming UCG instead of ACG becoming AAG
Don't know what you are asking. ACG encodes threonine, UCG encodes serine, and AAG encodes lysine. The changes may or may not change the function of the protein.
I think you failed to appreciate the rather abstract nature of Percy's example.
Actually, it is you who has failed to understand that the example was not abstract but grossly incorrect, and when you use that example and try to ask a question, your question is basically gibberish. Again you demonstrate that you lack the integrity to at least read where all of this was previously explained (in this thread) and thus at least speak from some sort of basic knowledge rather than complete ignorance. None of the discussion so far has exceeded what I ever learned in the first college course I ever took on genetics.
Hmmm, Pandion, good idea to check to whom you are replying, and to whom they in turn were replying. Saves a good bit of egg on your face. Just saying...
Well, I see you are correct there. I responded to traderdrew and assumed that the ignorant response that I received was from him. I owe drew an apology. But that makes WoundedKing's comments even more unintelligible. He then tries to dig himself out of his hole of ignorance by explaining why a question about incorrect data is somehow meaningful. traderdrew asked, essentially that if a mutation from ACG to ACA can produce a different eye color, wouldn't a mutation to UCG or produce a larger mutation? My answer was to explain it correctly. WoundedKing apparently lacks the knowledge to understand that.
As ever qualifications are supremely irrelevant. If Pandion has an actual specific criticism of what I wrote, other than that he didn't understand it, I have yet to make out what it is. If he just didn't understand it I'm happy to explain in greater detail.
Well, that would be just great. Why don't you explain to me what you're talking about. I not only read this thread, I was instrumental in hashing out the errors in the first place. So WoundedKing has a degree. Whoopee! That makes him an expert. So I also have degrees, in biology. I have degrees from St. Mary's College of California, Montana State U, El Instituto de Estudios Superiores de Monterrey, and the University of Montana. Along the way I studied genetics far beyond the level of this discussion.
So after the errors that lead this discussion off track in the first place were corrected early on in this thread, now the thread has been lead off track again because of an unwillingness to actually read the thread. The genetic coding wasn't ever the main point anyway. So, now along comes our resident geneticist, who actually thinks that this is somehow subtle rather than just wrong. How irrelevant can anyone person be. And the rest of you just tumble to an argument because you think that someone is a doc candidate or a post doc or something? You all are so dazzled that you miss the point.
Why on earth would anyone ever imagine that I was responding to Percy since that was ironed out at the beginning of the thread? Jeeze! WoundedKing, can you even find a hat to fit?
If you get dud parts (bad parameters) the machine wont work. It's exactly what Shannon considered noise. Noise degrades information exactly as 2ndLaw degrades the universe.
But, Shannon was concerned with communication, not genetics. Shannon began with the message, encoded it, transmitted it through a medium, received it and decoded it. For Shannon, any change in the message caused by noise was a decrease in information. Thus the oft repeated claim that it is impossible to increase information. For Shannon and communications, that may be true. Correct me if I'm wrong there, but it's been a lot of years since I studied this stuff.
Genetic information doesn't work that way. Genetic information is not Shannon information, but an extension of communication theory. In genetics, information is defined as the number of bits required to represent the message. The message is the genome of a population. Thus, a mutation that creates a sequence in a genome that did not previously exist requires additional bits to represent. Thus, there has been an increase in information. If, as you want to claim, the new information causes a malfunction, then that may be eliminated from the genome. However, since none of this fits Shannon's definition of noise, then neutral or beneficial mutations can certainly add information.
Noise degrades information exactly as 2ndLaw degrades the universe.
Shannon noise degrades Shannon information. Please try to distinguish between communications and genetics.
What a strange view of things you have. Have you ever actually studied thermo?
Re: I don't think 'Point Mutation' means what you think it means.
Wounded King writes:
I am also unaware of any research showing a specific point mutation to be responsible for melanic forms of Biston betularia, as far as I am aware the exact genetic basis is still unclear
Journal of Heredity. 2004 Mar-Apr;95(2):97-102.
Allelic melanism in American and British peppered moths.. Grant BS. Department of Biology, College of William and Mary, Williamsburg, VA 23187-8795, USA.
quote:Parallel evolutionary changes in the incidence of melanism are well documented in widely geographically separated subspecies of the peppered moth (Biston betularia). The British melanic phenotype (f. carbonaria) and the American melanic phenotype (f. swettaria) are indistinguishable in appearance, and previous genetic analysis has established that both are inherited as autosomal dominants. This report demonstrates through hybridizations of the subspecies and Mendelian testcrosses of melanic progeny that carbonaria and swettaria are phenotypes produced by alleles (isoalleles) at a single locus. The possibility of close linkage at two loci remains, but the simpler one-locus model cannot be rejected in the absence of contrary evidence.
While this research does not conclusively show a single point mutation is responsible for melanic Biston betularia, it does indicate that it is the most likely explanation "...in the absence of contrary evidence." But, you are essentially correct that the basis is unclear, i.e., there exists the possibility of a close linkage at two loci.