tas8831
Well-Known Member
ANALOGY:
Analogies are (or can be) good teaching tools to convey complex subjects to those who are unfamiliar with the subject matter, by making a comparison with that complex material and something more common and understandable.
It goes something like this - The Nucleotides are like letters, the Exons are like words, a Gene is like a sentence, a Genome is like a book, etc., at least that is how I approached it. This is all very simplistic (by design) , but it usually helps get the basic points across.
I was always sure to make it clear that this is pretty much where the analogy ends. I would explain that genes can be very different from sentences, that genomes, unlike books, contain lots of 'chapters' repeated over and over, or parts of them repeated, etc., but again, that the analogy was good enough to get the basics across.
It seems that many people never got that caution, and were apparently told, or it was implied, that the analogy is almost exactly a 1-to-1 directly applicable comparison. And many of those same folks read a book or more likely an internet essay about "genetic information", where direct analogies - just as inapplicable as the language analogies - are employed in which it is asserted that genes/genomes are exactly like computer code, and subject to the exact same constraints. This is why, for example, we see creationists - even on this forum, even today - claiming, for example that "rearranging the things that are already there is not new information". That claim is usually accompanied by something like "and you need new information to make a new part." I have even seem some intrepid anti-evolutionists provide specific (and wholly indefensible) numbers - one fellow claimed on another forum many years ago that 'we' needed at least 1 "brand new protein" to make a new body part, and that this required at least 333 mutations-worth of new information. I asked why, and how he knew this, but I never got a reply (of course). More recently, I had a rather well-known (at least on the internet) creationist declare that 'we' would need at least 1 million mutations to turn an ape pelvis into a human one. I asked for a list of 10 of these changes that were needed and how many mutations each would require and how he knew this. No answer, and it has been about 11 years... Anyway:
These language/computer code/ "information" constraints that are foisted upon evolution include (but are definitely not limited to):
1. You cannot just rearrange what is there and get anything new
2. You cannot just copy-paste what is already there and get anything new
3. You cannot screw up the code/word and expect something new or good to come of it
I first encountered the language analogy argument against evolution way back in the early 1990s, in the first creationism book I ever read. I don't remember the book, specifically but I later learned that the example in this book had made the rounds and was pretty common amongst creationists. It went something like this, and it basically encompasses the three constraints above:
In reality, we see:
The dog ran fast. The dog ran fast.
Diet and the evolution of human amylase gene copy number variation
Abstract
Starch consumption is a prominent characteristic of agricultural societies and hunter-gatherers in arid environments. In contrast, rainforest and circum-arctic hunter-gatherers and some pastoralists consume much less starch1,2,3. This behavioral variation raises the possibility that different selective pressures have acted on amylase, the enzyme responsible for starch hydrolysis4. We found that copy number of the salivary amylase gene (AMY1) is correlated positively with salivary amylase protein level and that individuals from populations with high-starch diets have, on average, more AMY1 copies than those with traditionally low-starch diets. Comparisons with other loci in a subset of these populations suggest that the extent of AMY1 copy number differentiation is highly unusual. This example of positive selection on a copy number–variable gene is, to our knowledge, one of the first discovered in the human genome. Higher AMY1 copy numbers and protein levels probably improve the digestion of starchy foods and may buffer against the fitness-reducing effects of intestinal disease.
The dog dog ran fast.
Common exon duplication in animals and its role in alternative splicing
Abstract
When searching the genomes of human, fly and worm for cases of exon duplication, we found that about 10% of all genes contain tandemly duplicated exons. In the course of the analyses, 2438 unannotated exons were identified that are not currently included in genome databases and that are likely to be functional. The vast majority of them are likely to be involved in mutually exclusive alternative splicing events. The common nature of recent exon duplication indicates that it might have a significant role in the fast evolution of eukaryotic genes. It also provides a general mechanism for the regulation of protein function.
The ran dog fast.
Evolutionary history of exon shuffling
Abstract
Exon shuffling has been characterized as one of the major evolutionary forces shaping both the genome and the proteome of eukaryotes. This mechanism was particularly important in the creation of multidomain proteins during animal evolution, bringing a number of functional genetic novelties. Here, genome information from a variety of eukaryotic species was used to address several issues related to the evolutionary history of exon shuffling. By comparing all protein sequences within each species, we were able to characterize exon shuffling signatures throughout metazoans. Intron phase (the position of the intron regarding the codon) and exon symmetry (the pattern of flanking introns for a given exon or block of adjacent exons) were features used to evaluate exon shuffling. We confirmed previous observations that exon shuffling mediated by phase 1 introns (1-1 exon shuffling) is the predominant kind in multicellular animals. Evidence is provided that such pattern was achieved since the early steps of animal evolution, supported by a detectable presence of 1-1 shuffling units in Trichoplax adhaerens and a considerable prevalence of them in Nematostella vectensis. In contrast, Monosiga brevicollis, one of the closest relatives of metazoans, and Arabidopsis thaliana, showed no evidence of 1-1 exon or domain shuffling above what it would be expected by chance. Instead, exon shuffling events are less abundant and predominantly mediated by phase 0 introns (0-0 exon shuffling) in those non-metazoan species. Moreover, an intermediate pattern of 1-1 and 0-0 exon shuffling was observed for the placozoan T. adhaerens, a primitive animal. Finally, characterization of flanking intron phases around domain borders allowed us to identify a common set of symmetric 1-1 domains that have been shuffled throughout the metazoan lineage.
The dig ran fast.
Point Mutations with Positive Selection Were a Major Force during the Evolution of a Receptor-Kinase Resistance Gene Family of Rice
ABSTRACT
The rice (Oryza sativa) Xa26 gene, which confers resistance to bacterial blight disease and encodes a leucine-rich repeat (LRR) receptor kinase, resides at a locus clustered with tandem homologous genes. To investigate the evolution of this family, four haplotypes from the two subspecies of rice, indica and japonica, were analyzed. Comparative sequence analysis of 34 genes of 10 types of paralogs of the family revealed haplotype polymorphisms and pronounced paralog diversity. The orthologs in different haplotypes were more similar than the paralogs in the same haplotype. At least five types of paralogs were formed before the separation of indica and japonica subspecies. Only 7% of amino acid sites were detected to be under positive selection, which occurred in the extracytoplasmic domain. Approximately 74% of the positively selected sites were solvent-exposed amino acid residues of the LRR domain that have been proposed to be involved in pathogen recognition, and 73% of the hypervariable sites detected in the LRR domain were subject to positive selection. The family is formed by tandem duplication followed by diversification through recombination, deletion, and point mutation. Most variation among genes in the family is caused by point mutations and positive selection.
I also looked at a couple papers on the Titin gene, as I had remembered from some years ago a discussion on that on a forum, but I could not find the paper I had used before. I did, however, come across this figure - all the red blocks are identical or nearly identical Ig-like domains:
Largest protein we make. LOTS of what we are told is not 'new information' and just 'copies of what is already there' jammed together to make a gene that makes an important protein.
That handles both the language and 'information' "arguments via analogy", I believe, but there is one more 'information' issue that I would like to address - the claim that 'just changing what is already there does not create new information, therefore, no adaptive evolution can occur' or words to that effect.
This paper documents an insertion event (a mutation in which a large chunk of DNA is inserted in one event) within the promoter region of a gene which causes the gene to be over-transcribed, i.e., just more of the same protein is made. No 'new' protein, just "information" that makes more of it. And it confers an adaptive benefit:
A single p450 allele associated with insecticide resistance in Drosophila.
"...Transgenic analysis of Cyp6g1 shows that over-transcription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally. This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene."
I'm sure the fallacy-mongers will be out in force (if they do not just ignore it all) and try to find ways to diminish or deny - I have presented the p450 many times, once had a creationist dismiss it because it did not produce a 'new limb'!!
That analogies are not evidence will be their burden to bear.
Definition of analogy
1a: a comparison of two otherwise unlike things based on resemblance of a particular aspect
b: resemblance in some particulars between things otherwise unlike : SIMILARITY
2: inference that if two or more things agree with one another in some respects they will probably agree in others
3: correspondence between the members of pairs or sets of linguistic forms that serves as a basis for
the creation of another form
When I used to teach Biology 101, I would use the classic English Language analogy when introducing students to DNA and Genetics.1a: a comparison of two otherwise unlike things based on resemblance of a particular aspect
b: resemblance in some particulars between things otherwise unlike : SIMILARITY
2: inference that if two or more things agree with one another in some respects they will probably agree in others
3: correspondence between the members of pairs or sets of linguistic forms that serves as a basis for
the creation of another form
Analogies are (or can be) good teaching tools to convey complex subjects to those who are unfamiliar with the subject matter, by making a comparison with that complex material and something more common and understandable.
It goes something like this - The Nucleotides are like letters, the Exons are like words, a Gene is like a sentence, a Genome is like a book, etc., at least that is how I approached it. This is all very simplistic (by design) , but it usually helps get the basic points across.
I was always sure to make it clear that this is pretty much where the analogy ends. I would explain that genes can be very different from sentences, that genomes, unlike books, contain lots of 'chapters' repeated over and over, or parts of them repeated, etc., but again, that the analogy was good enough to get the basics across.
It seems that many people never got that caution, and were apparently told, or it was implied, that the analogy is almost exactly a 1-to-1 directly applicable comparison. And many of those same folks read a book or more likely an internet essay about "genetic information", where direct analogies - just as inapplicable as the language analogies - are employed in which it is asserted that genes/genomes are exactly like computer code, and subject to the exact same constraints. This is why, for example, we see creationists - even on this forum, even today - claiming, for example that "rearranging the things that are already there is not new information". That claim is usually accompanied by something like "and you need new information to make a new part." I have even seem some intrepid anti-evolutionists provide specific (and wholly indefensible) numbers - one fellow claimed on another forum many years ago that 'we' needed at least 1 "brand new protein" to make a new body part, and that this required at least 333 mutations-worth of new information. I asked why, and how he knew this, but I never got a reply (of course). More recently, I had a rather well-known (at least on the internet) creationist declare that 'we' would need at least 1 million mutations to turn an ape pelvis into a human one. I asked for a list of 10 of these changes that were needed and how many mutations each would require and how he knew this. No answer, and it has been about 11 years... Anyway:
These language/computer code/ "information" constraints that are foisted upon evolution include (but are definitely not limited to):
1. You cannot just rearrange what is there and get anything new
2. You cannot just copy-paste what is already there and get anything new
3. You cannot screw up the code/word and expect something new or good to come of it
I first encountered the language analogy argument against evolution way back in the early 1990s, in the first creationism book I ever read. I don't remember the book, specifically but I later learned that the example in this book had made the rounds and was pretty common amongst creationists. It went something like this, and it basically encompasses the three constraints above:
Here is a simple sentence:
The dog ran fast.
Now let us 'evolve' it:
The dog ran fast. The dog ran fast.
The dog dog ran fast.
The ran dog fast.
The dig ran fast.
Isn't that CRAZY??? Those sentences don't make any sense! Obviously, this is not how evolution works. Because it DOESN'T work!
The dog ran fast.
Now let us 'evolve' it:
The dog ran fast. The dog ran fast.
The dog dog ran fast.
The ran dog fast.
The dig ran fast.
Isn't that CRAZY??? Those sentences don't make any sense! Obviously, this is not how evolution works. Because it DOESN'T work!
In reality, we see:
The dog ran fast. The dog ran fast.
Diet and the evolution of human amylase gene copy number variation
Abstract
Starch consumption is a prominent characteristic of agricultural societies and hunter-gatherers in arid environments. In contrast, rainforest and circum-arctic hunter-gatherers and some pastoralists consume much less starch1,2,3. This behavioral variation raises the possibility that different selective pressures have acted on amylase, the enzyme responsible for starch hydrolysis4. We found that copy number of the salivary amylase gene (AMY1) is correlated positively with salivary amylase protein level and that individuals from populations with high-starch diets have, on average, more AMY1 copies than those with traditionally low-starch diets. Comparisons with other loci in a subset of these populations suggest that the extent of AMY1 copy number differentiation is highly unusual. This example of positive selection on a copy number–variable gene is, to our knowledge, one of the first discovered in the human genome. Higher AMY1 copy numbers and protein levels probably improve the digestion of starchy foods and may buffer against the fitness-reducing effects of intestinal disease.
The dog dog ran fast.
Common exon duplication in animals and its role in alternative splicing
Abstract
When searching the genomes of human, fly and worm for cases of exon duplication, we found that about 10% of all genes contain tandemly duplicated exons. In the course of the analyses, 2438 unannotated exons were identified that are not currently included in genome databases and that are likely to be functional. The vast majority of them are likely to be involved in mutually exclusive alternative splicing events. The common nature of recent exon duplication indicates that it might have a significant role in the fast evolution of eukaryotic genes. It also provides a general mechanism for the regulation of protein function.
The ran dog fast.
Evolutionary history of exon shuffling
Abstract
Exon shuffling has been characterized as one of the major evolutionary forces shaping both the genome and the proteome of eukaryotes. This mechanism was particularly important in the creation of multidomain proteins during animal evolution, bringing a number of functional genetic novelties. Here, genome information from a variety of eukaryotic species was used to address several issues related to the evolutionary history of exon shuffling. By comparing all protein sequences within each species, we were able to characterize exon shuffling signatures throughout metazoans. Intron phase (the position of the intron regarding the codon) and exon symmetry (the pattern of flanking introns for a given exon or block of adjacent exons) were features used to evaluate exon shuffling. We confirmed previous observations that exon shuffling mediated by phase 1 introns (1-1 exon shuffling) is the predominant kind in multicellular animals. Evidence is provided that such pattern was achieved since the early steps of animal evolution, supported by a detectable presence of 1-1 shuffling units in Trichoplax adhaerens and a considerable prevalence of them in Nematostella vectensis. In contrast, Monosiga brevicollis, one of the closest relatives of metazoans, and Arabidopsis thaliana, showed no evidence of 1-1 exon or domain shuffling above what it would be expected by chance. Instead, exon shuffling events are less abundant and predominantly mediated by phase 0 introns (0-0 exon shuffling) in those non-metazoan species. Moreover, an intermediate pattern of 1-1 and 0-0 exon shuffling was observed for the placozoan T. adhaerens, a primitive animal. Finally, characterization of flanking intron phases around domain borders allowed us to identify a common set of symmetric 1-1 domains that have been shuffled throughout the metazoan lineage.
The dig ran fast.
Point Mutations with Positive Selection Were a Major Force during the Evolution of a Receptor-Kinase Resistance Gene Family of Rice
ABSTRACT
The rice (Oryza sativa) Xa26 gene, which confers resistance to bacterial blight disease and encodes a leucine-rich repeat (LRR) receptor kinase, resides at a locus clustered with tandem homologous genes. To investigate the evolution of this family, four haplotypes from the two subspecies of rice, indica and japonica, were analyzed. Comparative sequence analysis of 34 genes of 10 types of paralogs of the family revealed haplotype polymorphisms and pronounced paralog diversity. The orthologs in different haplotypes were more similar than the paralogs in the same haplotype. At least five types of paralogs were formed before the separation of indica and japonica subspecies. Only 7% of amino acid sites were detected to be under positive selection, which occurred in the extracytoplasmic domain. Approximately 74% of the positively selected sites were solvent-exposed amino acid residues of the LRR domain that have been proposed to be involved in pathogen recognition, and 73% of the hypervariable sites detected in the LRR domain were subject to positive selection. The family is formed by tandem duplication followed by diversification through recombination, deletion, and point mutation. Most variation among genes in the family is caused by point mutations and positive selection.
I also looked at a couple papers on the Titin gene, as I had remembered from some years ago a discussion on that on a forum, but I could not find the paper I had used before. I did, however, come across this figure - all the red blocks are identical or nearly identical Ig-like domains:
Largest protein we make. LOTS of what we are told is not 'new information' and just 'copies of what is already there' jammed together to make a gene that makes an important protein.
That handles both the language and 'information' "arguments via analogy", I believe, but there is one more 'information' issue that I would like to address - the claim that 'just changing what is already there does not create new information, therefore, no adaptive evolution can occur' or words to that effect.
This paper documents an insertion event (a mutation in which a large chunk of DNA is inserted in one event) within the promoter region of a gene which causes the gene to be over-transcribed, i.e., just more of the same protein is made. No 'new' protein, just "information" that makes more of it. And it confers an adaptive benefit:
A single p450 allele associated with insecticide resistance in Drosophila.
"...Transgenic analysis of Cyp6g1 shows that over-transcription of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated with a single Cyp6g1 allele that has spread globally. This allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6g1 gene."
I'm sure the fallacy-mongers will be out in force (if they do not just ignore it all) and try to find ways to diminish or deny - I have presented the p450 many times, once had a creationist dismiss it because it did not produce a 'new limb'!!
That analogies are not evidence will be their burden to bear.
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