Mutation and "New Information"

OllieFranz

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One thing that has been confusing me about Creationist arguments about mutation is that even though they agree that retrovirus insertion and replication errors can produce new sequences in the DNA, they do not produce new "information." Some of them, the more easily dismissed, argue that there are only four different "letters" in the DNA "alphabet," (there are actually 64 "letters," but that does not affect this argument or its refutation, so I'll address this point in a later paragraph), and the insertions do not add any new letters. That is like saying that all of our collected human wisdom can be found in the sentence "the quick brown fox jumps over the lazy dog," since it contains all 26 letters used to write in English. Instead, we use those 26 letters to form hundreds of thousands of words, many with unique meanings, and combine those words to convey ideas that even the combined resources of the Library of Congress and the British Museum Library can't contain more than a fraction of.

Others have an objection that is harder to understand, mainly because they do not explain what would constitute "new information." I believe that at last I have considered a way of looking at information -- I have no way of knowing if it is their way of looking at it -- that makes sense, at least as long as you are working with the DNA alphabet of four "letters." With organic molecules, especially proteins and nuclaeic acids, close is good enough. If a diabetic cannot get human insulin, pig insulin will do the job. Anabolic steroids work the way they do because they are similar to human testosterone (which is, itself, an anabolic steroid). There is an enzyme in chocolate (phenylethylamine) that minics endorphins released in our brains when we are in love. So even if a section of a gene, or the protein it generates is different, it is still just a variant which either does the same job (albeit it might do it slightly better, or slightly worse) and is therefore a neutral mutation, or does not do the job and is a detrimental mutation. The chances that it does a completely new job (and that is not even requiring that it does it well) are neglegible (and therefore easily dismissed with a handwave if you are a Creationist).

But as I said, that makes sense if you treat DNA sequences as words written in a four-letter alphabet. But DNA (using RNA as an intermediary) builds protein out of amino acids, and it takes three bases in DNA/RNA to select one amino acid. The DNA "alphabet" can be compared to the ASCII alphabet. Pure machine code is a sequence of "bits." Each bit can be either on or off. Machine code can be thought of as having a two letter "alphabet." But even in the earliest computers, the sequence was broken up into eight-bit segments called "bytes." A one-byte register could be in one of 2^8 = 256 different states. ASCII assigned the first 128of them to correspond with various characters, including the ten digits of the decimal system, the letters of the alphabet in both upper case and lower case, and various punctuation marks. Modern computers can work with longer registers than 8 bits, but the byte is so useful and so entrenched that the registers are always multiples of 8 and are partitioned into bytes.

So it takes a DNA "byte," called a "codon," of three bases to code for each amino acid. An insertion, or deletion which is not divisible by three does not just lengthen or shorten the gene, it changes it completely from that point to the end. In fact, it does worse than that. A gene has to begin with a "start" codon and end with a "stop" codon. But the bits of the "stop" sequence are no longer all in the same codon. The gene has been destroyed. Because there are four or five different codon sequences that can serve as "stops," it is likely that one will turn up in the DNA sequence, but the new resulting gene (and related protein) will look nothing like the original. It is completely new.

Also, in man-made computers every bit is always in the same position in the byte (We never begin a byte on the third bit and end on the second bit of the next register), but this is an artificial rule that does not apply to DNA. So if the old "stop" codon can be connected to a "start" codon (and there are four or five different codons that can act as "starts"), it, too can create a new gene. Altogether, a single mutation which upsets the synchronization of the codons could destroy up to three genes and create up to three brand new, unrelated genes. This kind of mutation is far from common, as most mutagens work on whole codons, but it only takes a few in a thousand generations to produce big changes.
 

rjw

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One thing that has been confusing me about Creationist arguments about mutation is that even though they agree that retrovirus insertion and replication errors can produce new sequences in the DNA, they do not produce new "information." Some of them, the more easily dismissed, argue that there are only four different "letters" in the DNA "alphabet," (there are actually 64 "letters," but that does not affect this argument or its refutation, so I'll address this point in a later paragraph), and the insertions do not add any new letters. That is like saying that all of our collected human wisdom can be found in the sentence "the quick brown fox jumps over the lazy dog," since it contains all 26 letters used to write in English. Instead, we use those 26 letters to form hundreds of thousands of words, many with unique meanings, and combine those words to convey ideas that even the combined resources of the Library of Congress and the British Museum Library can't contain more than a fraction of.

Others have an objection that is harder to understand, mainly because they do not explain what would constitute "new information." I believe that at last I have considered a way of looking at information -- I have no way of knowing if it is their way of looking at it -- that makes sense, at least as long as you are working with the DNA alphabet of four "letters." With organic molecules, especially proteins and nuclaeic acids, close is good enough. If a diabetic cannot get human insulin, pig insulin will do the job. Anabolic steroids work the way they do because they are similar to human testosterone (which is, itself, an anabolic steroid). There is an enzyme in chocolate (phenylethylamine) that minics endorphins released in our brains when we are in love. So even if a section of a gene, or the protein it generates is different, it is still just a variant which either does the same job (albeit it might do it slightly better, or slightly worse) and is therefore a neutral mutation, or does not do the job and is a detrimental mutation. The chances that it does a completely new job (and that is not even requiring that it does it well) are neglegible (and therefore easily dismissed with a handwave if you are a Creationist).

But as I said, that makes sense if you treat DNA sequences as words written in a four-letter alphabet. But DNA (using RNA as an intermediary) builds protein out of amino acids, and it takes three bases in DNA/RNA to select one amino acid. The DNA "alphabet" can be compared to the ASCII alphabet. Pure machine code is a sequence of "bits." Each bit can be either on or off. Machine code can be thought of as having a two letter "alphabet." But even in the earliest computers, the sequence was broken up into eight-bit segments called "bytes." A one-byte register could be in one of 2^8 = 256 different states. ASCII assigned the first 128of them to correspond with various characters, including the ten digits of the decimal system, the letters of the alphabet in both upper case and lower case, and various punctuation marks. Modern computers can work with longer registers than 8 bits, but the byte is so useful and so entrenched that the registers are always multiples of 8 and are partitioned into bytes.

So it takes a DNA "byte," called a "codon," of three bases to code for each amino acid. An insertion, or deletion which is not divisible by three does not just lengthen or shorten the gene, it changes it completely from that point to the end. In fact, it does worse than that. A gene has to begin with a "start" codon and end with a "stop" codon. But the bits of the "stop" sequence are no longer all in the same codon. The gene has been destroyed. Because there are four or five different codon sequences that can serve as "stops," it is likely that one will turn up in the DNA sequence, but the new resulting gene (and related protein) will look nothing like the original. It is completely new.

Also, in man-made computers every bit is always in the same position in the byte (We never begin a byte on the third bit and end on the second bit of the next register), but this is an artificial rule that does not apply to DNA. So if the old "stop" codon can be connected to a "start" codon (and there are four or five different codons that can act as "starts"), it, too can create a new gene. Altogether, a single mutation which upsets the synchronization of the codons could destroy up to three genes and create up to three brand new, unrelated genes. This kind of mutation is far from common, as most mutagens work on whole codons, but it only takes a few in a thousand generations to produce big changes.
A great, and recently observed counter example of "no new information" comes out of Lenski's Long Term Evolution Experiment, where last year they finally published the report on how one of their 12 E. coli lines managed to evolve to metabolise citrate in the presence of oxygen, something E. coli cannot do. It was via gene duplications in which the duplicated gene(s) found themselves near the appropriate genetic operator. The result was a line of E coli with a functionality not found with the other lines of E. coli.


Link to the abstract and figures at a glance:-

Genomic analysis of a key innovation in an experimental Escherichia coli population


From the abstract:-

Link above said:
Evolutionary novelties have been important in the history of life, but their origins are usually difficult to examine in detail. We previously described the evolution of a novel trait, aerobic citrate utilization (Cit+), in an experimental population of Escherichia coli. Here we analyse genome sequences to investigate the history and genetic basis of this trait. At least three distinct clades coexisted for more than 10,000 generations before its emergence. The Cit+ trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter. The clades varied in their propensity to evolve this novel trait, although genotypes able to do so existed in all three clades, implying that multiple potentiating mutations arose during the population’s history. Our findings illustrate the importance of promoter capture and altered gene regulation in mediating the exaptation events that often underlie evolutionary innovations.



Snippets from the paper:-


The paper underlying the link above said:
...

Before the Cit+ trait could evolve, the Ara–3 population had to evolve a genetic background in which that new function was accessible by mutation. Potentiation was demonstrated by ‘replay’ experiments using 270 clones sampled over the population’s history20. The replays produced 17 Cit+ mutants that derived from 13 clones, all from generation 20,000 or later. Fluctuation tests confirmed that potentiated clones had increased mutation rates to Cit+, although such mutations were still extremely rare20.

...

The Cit+ mutants arose by diverse mutational processes (Supplementary Table 12). Eight have citT duplications similar to the original one, though no two share the same boundaries (Fig. 7). In seven of these, the duplications generated alternative versions of the rnk-citT module; in the other, the second citT is downstream of the rna promoter. Six mutants have an IS3 element inserted in the 3′ end of citG (Fig. 7). IS3 carries outward-directed promoter elements that can activate adjacent genes27, 45. Two mutants have large duplications encompassing all or part of the cit operon. One mutant has a large inversion that places most of that operon downstream of the promoter for the fimbria regulatory gene fimB, and another has a deletion in citG that presumably formed a new promoter. Also, most of these mutants have stronger phenotypes (Supplementary Fig. 5) than the earliest Cit+ clones in the main experiment (Fig. 4b and Supplementary Fig. 3). In any case, this new function arose in potentiated backgrounds by a variety of mutational processes that recruited several different promoters to allow CitT expression during aerobic metabolism. Thus, these data do not support the physical-promotion hypothesis, whereas the strain-specific differences in growth on citrate conferred by the rnk-citT module provide clear and compelling evidence for epistasis (Fig. 6). However, these hypotheses are not mutually exclusive, and we cannot reject the possibility that some mutation rendered the genome (or the affected region) more prone to physical rearrangements (including mobile-element insertions) and thereby also contributed to the overall potentiation effect.

...

The evolution of citrate use in an experimental E. coli population provided an unusual opportunity to study the multi-step origin of a key innovation. Comparative studies have shown that gene duplications have an important creative role in evolution by generating redundancies that allow neo-functionalization5, 6, 8, 9, 10. Our findings highlight the less-appreciated capacity of duplications to produce new functions by promoter capture events that change gene regulatory networks38. The evolution of citrate use also highlights that such actualizing mutations are only part of the process by which novelties arise. Before a new function can arise, it may be essential for a lineage to evolve a potentiating genetic background that allows the actualizing mutation to occur or the new function to be expressed. Finally, novel functions often emerge in rudimentary forms that must be refined to exploit the ecological opportunities. This three-step process—in which potentiation makes a trait possible, actualization makes the trait manifest, and refinement makes it effective—is probably typical of many new functions.
 
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