Comments for ASA Book Discussion http://www.asa3online.org/Book A members' forum for discussion of selected books Mon, 23 Aug 2010 05:09:04 -0500 http://wordpress.org/?v=2.8.6 hourly 1 Comment on Complex Specified Information Without an Intelligent Source by Intelligent Design - Page 13 - Christian Forums http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-389 Intelligent Design - Page 13 - Christian Forums Mon, 23 Aug 2010 05:09:04 +0000 http://www.asa3online.org/Book/?p=75#comment-389 [...] an intelligent source does not withstand scrutiny.The full explanation of antibody production is here, and the full argument against Signature of the Cell here. Both pages are maintained under the ASA [...] [...] an intelligent source does not withstand scrutiny.The full explanation of antibody production is here, and the full argument against Signature of the Cell here. Both pages are maintained under the ASA [...]

]]> Comment on Complex Specified Information Without an Intelligent Source by Charles Austerberry http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-388 Charles Austerberry Tue, 13 Jul 2010 14:26:46 +0000 http://www.asa3online.org/Book/?p=75#comment-388 Dear Ide: Thanks again for your post, and for your gracious comments.  I enjoy learning and facilitating the learning of others, especially about biology, and you have been a patient and persistent correspondent, for which I am grateful. Regarding the SNPs: indeed, many are deleterious, and do cause disease, at least in some contexts.  Most seem neutral, as far as we can tell.  But many  can be advantageous, at least in some contexts (for just one example, in cultures raising livestock for milk, a mutation that causes continued expression of the lactase gene through adulthood would provide an advantage).  Many SNPs  provide benefit. The more I learn about somatic hypermutation and N-segment nucleotide insertion, for example, the more I am struck by the elegance of the immune system's balanced use of random and nonrandom mechanisms to achieve remarkable function. My thanks to Craig Story, Randy Isaac, Jon Tandy, other posters, and you, Ide, for the discussion we've had.  Best wishes, Ide, for a wonderful family reunion! God bless, Chuck Dear Ide:
Thanks again for your post, and for your gracious comments.  I enjoy learning and facilitating the learning of others, especially about biology, and you have been a patient and persistent correspondent, for which I am grateful.
Regarding the SNPs: indeed, many are deleterious, and do cause disease, at least in some contexts.  Most seem neutral, as far as we can tell.  But many  can be advantageous, at least in some contexts (for just one example, in cultures raising livestock for milk, a mutation that causes continued expression of the lactase gene through adulthood would provide an advantage).  Many SNPs  provide benefit.
The more I learn about somatic hypermutation and N-segment nucleotide insertion, for example, the more I am struck by the elegance of the immune system’s balanced use of random and nonrandom mechanisms to achieve remarkable function.
My thanks to Craig Story, Randy Isaac, Jon Tandy, other posters, and you, Ide, for the discussion we’ve had.  Best wishes, Ide, for a wonderful family reunion!
God bless,
Chuck

]]> Comment on Complex Specified Information Without an Intelligent Source by Jon Tandy http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-387 Jon Tandy Tue, 13 Jul 2010 05:00:12 +0000 http://www.asa3online.org/Book/?p=75#comment-387 Ide, I had wanted to reply to your last message to me on June 26 regarding some specifics on the examples I had given, to explain how I see CSI increasing in an information technology example, as one way to work back into the biological examples.  But I got buried in several things, and anyway I think Chuck's comments to you on DNA really get closer to the kinds of details you have been looking for, and I wouldn't want to get in the way of that conversation, given your limited time resources. And on the biology score, I certainly can't claim to be able to contribute a great deal of in-depth knowledge.  However, let me comment at a bit of a high level response.  You seem to be grasping at any possible reason not to accept that genuinely new information might be created in biological systems, but seem to want to attribute new biological developments to the existing "pool of CSI". You also suggest that duplication of existing code is in a different category from "new code" or "new CSI".  I will just say that this is a non sequitur, whether you look at it from the point of view of biology or computer science.  I've written enough computer programs to know that you might be right, but not necessarily.  I can copy and paste existing code, with modifications, and create entirely different code with significantly different function. And in the biological realm, although far from my expertise, I would suggest that you need to look at this from the point of view of the biological evidence, rather than through the narrow lens of CSI.  Remember that ID advocates created the concept of CSI, but biologists are the ones doing the actual work in the field.  The fact is, biologists have some pretty good ideas about where novel features come from in the DNA.  It comes from point mutations, gene duplication, substitutions, and all the other things that Chuck has written about it.  These are random or semi-random rearrangements and modifications of existing DNA, that were in many cases not anticipated in the original sequence.  There is no intelligence directing these modifications, at least that we can observe in laboratory experiments (I certainly leave open the possibility of God guiding quantum and classical events through providential action, but that's a matter of faith, not empirical evidence). So even if there are duplications of existing code, it doesn't matter in the slightest that the DNA is reusing what you might term "existing CSI".  The resulting functional features are in many notable cases NOT just copies of existing functionality, and are therefore truly novel features.  If we didn't have the "Intelligent Design" paradigm in mind when looking at it, we would have to conclude that random modifications occur in DNA, which result in the development of new features that in some cases provide greater survival benefits.  Whether or not we put ID labels on this and frame the discussion around CSI, the facts are still the facts.  In this sense, I fail to see what ID actually contributes to our knowledge of biology. Jon Ide,

I had wanted to reply to your last message to me on June 26 regarding some specifics on the examples I had given, to explain how I see CSI increasing in an information technology example, as one way to work back into the biological examples.  But I got buried in several things, and anyway I think Chuck’s comments to you on DNA really get closer to the kinds of details you have been looking for, and I wouldn’t want to get in the way of that conversation, given your limited time resources.

And on the biology score, I certainly can’t claim to be able to contribute a great deal of in-depth knowledge.  However, let me comment at a bit of a high level response.  You seem to be grasping at any possible reason not to accept that genuinely new information might be created in biological systems, but seem to want to attribute new biological developments to the existing “pool of CSI”.

You also suggest that duplication of existing code is in a different category from “new code” or “new CSI”.  I will just say that this is a non sequitur, whether you look at it from the point of view of biology or computer science.  I’ve written enough computer programs to know that you might be right, but not necessarily.  I can copy and paste existing code, with modifications, and create entirely different code with significantly different function.

And in the biological realm, although far from my expertise, I would suggest that you need to look at this from the point of view of the biological evidence, rather than through the narrow lens of CSI.  Remember that ID advocates created the concept of CSI, but biologists are the ones doing the actual work in the field. 

The fact is, biologists have some pretty good ideas about where novel features come from in the DNA.  It comes from point mutations, gene duplication, substitutions, and all the other things that Chuck has written about it.  These are random or semi-random rearrangements and modifications of existing DNA, that were in many cases not anticipated in the original sequence.  There is no intelligence directing these modifications, at least that we can observe in laboratory experiments (I certainly leave open the possibility of God guiding quantum and classical events through providential action, but that’s a matter of faith, not empirical evidence).

So even if there are duplications of existing code, it doesn’t matter in the slightest that the DNA is reusing what you might term “existing CSI”.  The resulting functional features are in many notable cases NOT just copies of existing functionality, and are therefore truly novel features.  If we didn’t have the “Intelligent Design” paradigm in mind when looking at it, we would have to conclude that random modifications occur in DNA, which result in the development of new features that in some cases provide greater survival benefits. 

Whether or not we put ID labels on this and frame the discussion around CSI, the facts are still the facts.  In this sense, I fail to see what ID actually contributes to our knowledge of biology.

Jon

]]> Comment on Complex Specified Information Without an Intelligent Source by Ide Trotter http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-386 Ide Trotter Tue, 13 Jul 2010 00:33:26 +0000 http://www.asa3online.org/Book/?p=75#comment-386 Chuck,   Wow! And many thanks again.  I can’t pretend to have fully assimilated all that you have provided here.  I’m sure we are completely together that “duplication of existing CSI differs from <em>de novo</em> production of CSI.  I’m only noting that duplication and replication are integral aspects of biological phenomena.”   In your earlier section on, “When is there “new code”? it seems most of the actions you bring to my attention fall into my “making use of old code category.”  However, “point substitutions such as those occurring in germline mutations responsible for most human single nucleotide polymorphisms (SNPs)” seems on first impression to be a different animal and possibly closer to what I would call “new.”  (Keep in mind that I’m learning here under your patient tutelage.) Anyhow, I went to Wikipedia and find that SNPs are generally discussed as defects leading to dysfunction.  I believe we have stipulated that we haven’t settled on a mutually agreed understanding of how best to define CSI. Nevertheless, I have a feeling that I would be unlikely to eventually agree that mutations leading to dysfunction represent the type of functionally constructive CSI on which life is based.  So I’m not inclined to think it is what I’m looking for.   I hope to get your reaction to this thinking on my part before I go into recess.  But after that I’m afraid I’ll have to drop out of the discussion for a while.  We are about to have a family gathering (ten grandchildren, the 11th in China for the summer won’t make it, and assorted parents) buried so far in the Colorado mountains that our cell ‘phones don’t work and we are thankful to have slow dial up email.  I’ll be back playing catch-up around the middle of August.   Thanks again for your patient instruction.  Your paying students are most fortunate to have a teacher like you.   Ide Chuck,
 
Wow! And many thanks again.  I can’t pretend to have fully assimilated all that you have provided here.  I’m sure we are completely together that “duplication of existing CSI differs from de novo production of CSI.  I’m only noting that duplication and replication are integral aspects of biological phenomena.”
 
In your earlier section on, “When is there “new code”? it seems most of the actions you bring to my attention fall into my “making use of old code category.”  However, “point substitutions such as those occurring in germline mutations responsible for most human single nucleotide polymorphisms (SNPs)” seems on first impression to be a different animal and possibly closer to what I would call “new.”  (Keep in mind that I’m learning here under your patient tutelage.) Anyhow, I went to Wikipedia and find that SNPs are generally discussed as defects leading to dysfunction.  I believe we have stipulated that we haven’t settled on a mutually agreed understanding of how best to define CSI. Nevertheless, I have a feeling that I would be unlikely to eventually agree that mutations leading to dysfunction represent the type of functionally constructive CSI on which life is based.  So I’m not inclined to think it is what I’m looking for.
 
I hope to get your reaction to this thinking on my part before I go into recess.  But after that I’m afraid I’ll have to drop out of the discussion for a while.  We are about to have a family gathering (ten grandchildren, the 11th in China for the summer won’t make it, and assorted parents) buried so far in the Colorado mountains that our cell ‘phones don’t work and we are thankful to have slow dial up email.  I’ll be back playing catch-up around the middle of August.
 
Thanks again for your patient instruction.  Your paying students are most fortunate to have a teacher like you.
 
Ide

]]> Comment on Complex Specified Information Without an Intelligent Source by Charles Austerberry http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-385 Charles Austerberry Mon, 12 Jul 2010 20:42:10 +0000 http://www.asa3online.org/Book/?p=75#comment-385 I need to correct something I wrote in this post.  I wrote: "Somatic hypermutation, on the other hand, usually causes substitutions rather than insertions or deletions.  It’s a fascinating process whereby double-stranded breaks in DNA are repaired by somewhat error-prone DNA repair mechanisms." When I mentioned double-stranded breaks in DNA I was thinking of switch recombination, not somatic hypermutation.  Both are initiated by activation-induced cytidine deaminase (AID) in the heavy chain antibody-encoding DNA of B cells, but only switch recombination is known to involve double-stranded breaks.  Let's get into switch recombination only if you want to; somatic hypermutation is more pertinent to the diversification of antigen-binding capability. In the case of somatic hypermutation,  DNA polymerases often causes mutations when replicating DNA upon which AID has acted.  In some cases, the deaminated base (being "wrong") directly leads to a mutation when the DNA polymerase uses it as a template.  In other cases the deaminated base is removed by an enzyme called UNG, and it's the base-lacking position in the DNA template that confuses DNA polymerase.  Finally, sometimes base excision repair (BER) or mismatch repair (MMR) follows the deamination, and both BER and MMR frequently make mistakes (more often in the antibody genes than elsewhere in the genome, for unknown reasons).  Here's how a recent article summarizes it: "Several things can happen following AID-catalyzed C deamination. The resulting U opposite G upon normal DNA replication leads to C → T transitions. On the other hand, U can be removed by UNG, and the resulting abasic site, when copied by an error-prone DNA polymerase that can insert T or C opposite the lesion, causes C → A and C → G transversions. Alternatively, U can undergo MMR or BER, which, in the presence of error-prone polymerases, can yield various transitions and transversions." The reference for this is: http://www.jbc.org/content/284/41/27761.abstract Cheers! Chuck     I need to correct something I wrote in this post.  I wrote: “Somatic hypermutation, on the other hand, usually causes substitutions rather than insertions or deletions.  It’s a fascinating process whereby double-stranded breaks in DNA are repaired by somewhat error-prone DNA repair mechanisms.”
When I mentioned double-stranded breaks in DNA I was thinking of switch recombination, not somatic hypermutation.  Both are initiated by activation-induced cytidine deaminase (AID) in the heavy chain antibody-encoding DNA of B cells, but only switch recombination is known to involve double-stranded breaks.  Let’s get into switch recombination only if you want to; somatic hypermutation is more pertinent to the diversification of antigen-binding capability.
In the case of somatic hypermutation,  DNA polymerases often causes mutations when replicating DNA upon which AID has acted.  In some cases, the deaminated base (being “wrong”) directly leads to a mutation when the DNA polymerase uses it as a template.  In other cases the deaminated base is removed by an enzyme called UNG, and it’s the base-lacking position in the DNA template that confuses DNA polymerase.  Finally, sometimes base excision repair (BER) or mismatch repair (MMR) follows the deamination, and both BER and MMR frequently make mistakes (more often in the antibody genes than elsewhere in the genome, for unknown reasons).  Here’s how a recent article summarizes it:
“Several things can happen following AID-catalyzed C deamination. The resulting U opposite G upon normal DNA replication leads to C → T transitions. On the other hand, U can be removed by UNG, and the resulting abasic site, when copied by an error-prone DNA polymerase that can insert T or C opposite the lesion, causes C → A and C → G transversions. Alternatively, U can undergo MMR or BER, which, in the presence of error-prone polymerases, can yield various transitions and transversions.”
The reference for this is:
http://www.jbc.org/content/284/41/27761.abstract
Cheers!
Chuck
 
 

]]> Comment on Complex Specified Information Without an Intelligent Source by Charles Austerberry http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-13/#comment-384 Charles Austerberry Mon, 12 Jul 2010 18:56:19 +0000 http://www.asa3online.org/Book/?p=75#comment-384 Dear Ide: Here I just want to note that while activation-induced deaminase indeed converts one pyrimidine (cytosine or 5-methylcytosine) into another pyrimidine (uracil or thymine, respectively), the range of possible outcomes is really quite large and to a great degree "independent of any preceding order."  Here's why: 1) The U:G or T:G mismatch is a type of DNA damage that is then repaired by error-prone DNA repair.  It's the DNA repair process that actually causes the sequence change (mutation), and the range of possible errors (DNA mutations) resulting from the repair is quite large. 2) Given the nature of the genetic code, even if the range of possible mutations via DNA repair errors were quite limited (for example,  always replacing a C:G basepair with a T:A basepair), such transitions can have a variety of effects on the encoded amino acid sequence depending upon the affected triplet codon and the position of the base (1st, 2nd, or 3rd) that is changed within the codon. I'd be happy to explain the details more if you wish, but perhaps first it would be best to review the three separate posts I wrote earlier today that probably appear farther down in the post list. Cheers! Chuck Dear Ide:
Here I just want to note that while activation-induced deaminase indeed converts one pyrimidine (cytosine or 5-methylcytosine) into another pyrimidine (uracil or thymine, respectively), the range of possible outcomes is really quite large and to a great degree “independent of any preceding order.”  Here’s why:
1) The U:G or T:G mismatch is a type of DNA damage that is then repaired by error-prone DNA repair.  It’s the DNA repair process that actually causes the sequence change (mutation), and the range of possible errors (DNA mutations) resulting from the repair is quite large.
2) Given the nature of the genetic code, even if the range of possible mutations via DNA repair errors were quite limited (for example,  always replacing a C:G basepair with a T:A basepair), such transitions can have a variety of effects on the encoded amino acid sequence depending upon the affected triplet codon and the position of the base (1st, 2nd, or 3rd) that is changed within the codon.
I’d be happy to explain the details more if you wish, but perhaps first it would be best to review the three separate posts I wrote earlier today that probably appear farther down in the post list.
Cheers!
Chuck

]]> Comment on Complex Specified Information Without an Intelligent Source by Charles Austerberry http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-383 Charles Austerberry Mon, 12 Jul 2010 14:29:26 +0000 http://www.asa3online.org/Book/?p=75#comment-383 Ide, note that I did not even include duplication of DNA in my list, because while duplication of genes followed by diversification is very important in evolution (including the evolution of the immunoglobulin superfamily of genes), to my knowledge duplication of DNA is not involved in the antibody gene assembly process happening within a maturing B cell (except for limited DNA replication as part of DNA repair).  Now by "gene duplication" I do not mean DNA replication prior to cell division.  Rather, I mean new copies of genes or other segments of DNA in a genome apart from replication of the entire genome. DNA replication prior to cell division is also important, of course, because a larger population of cells provides the raw material (multiple copies of DNA) in which diversification can happen. This is true within an individual's immune system in multiple senses.  It's true in the development and differentiation of various blood cell lineages in the bone marrow to give rise to (among others) diverse B and T cells.  It's also true later when a particular B or T lymphocyte encounters antigen and become activated.  Immunologists specifically refer to this latter case as "clonal expansion." We can extend these concepts to phylogenetic evolution too as long as we are speaking of the germline DNA that gets passed on to the next generation rather than somatic DNA (such as in B cells) which does not get passed on to the next generation. So to summarize, both gene duplication within a genome, and cell/organism reproduction, can provide multiple copies of DNA that can then diversify. I appreciate your sense that duplication of existing CSI differs from <em>de novo</em> production of CSI.  I'm only noting that duplication and replication are integral aspects of biological phenomena. Cheers! Chuck Ide, note that I did not even include duplication of DNA in my list, because while duplication of genes followed by diversification is very important in evolution (including the evolution of the immunoglobulin superfamily of genes), to my knowledge duplication of DNA is not involved in the antibody gene assembly process happening within a maturing B cell (except for limited DNA replication as part of DNA repair).  Now by “gene duplication” I do not mean DNA replication prior to cell division.  Rather, I mean new copies of genes or other segments of DNA in a genome apart from replication of the entire genome.
DNA replication prior to cell division is also important, of course, because a larger population of cells provides the raw material (multiple copies of DNA) in which diversification can happen.
This is true within an individual’s immune system in multiple senses.  It’s true in the development and differentiation of various blood cell lineages in the bone marrow to give rise to (among others) diverse B and T cells.  It’s also true later when a particular B or T lymphocyte encounters antigen and become activated.  Immunologists specifically refer to this latter case as “clonal expansion.”
We can extend these concepts to phylogenetic evolution too as long as we are speaking of the germline DNA that gets passed on to the next generation rather than somatic DNA (such as in B cells) which does not get passed on to the next generation.
So to summarize, both gene duplication within a genome, and cell/organism reproduction, can provide multiple copies of DNA that can then diversify.
I appreciate your sense that duplication of existing CSI differs from de novo production of CSI.  I’m only noting that duplication and replication are integral aspects of biological phenomena.
Cheers!
Chuck

]]> Comment on Complex Specified Information Without an Intelligent Source by Charles Austerberry http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-382 Charles Austerberry Mon, 12 Jul 2010 13:07:45 +0000 http://www.asa3online.org/Book/?p=75#comment-382 Just to clarify: different chromosomes do not leave or enter B cells in that last level I mentioned above.  What immunologists refer to as "allelic exclusion" simply means that only one of the light chain-encoding chromosomes,  and only one of the heavy chain-encoding chromosomes, are expressed in a given B cell.  It's analogous to allelic assortment plus fertilization (sexual processes producing new combinations of chromosomes) in a sense, but only in a loose sense because the B cells still have the other, unexpressed chromosomes. Cheers! Chuck Just to clarify: different chromosomes do not leave or enter B cells in that last level I mentioned above.  What immunologists refer to as “allelic exclusion” simply means that only one of the light chain-encoding chromosomes,  and only one of the heavy chain-encoding chromosomes, are expressed in a given B cell.  It’s analogous to allelic assortment plus fertilization (sexual processes producing new combinations of chromosomes) in a sense, but only in a loose sense because the B cells still have the other, unexpressed chromosomes.
Cheers!
Chuck

]]> Comment on Complex Specified Information Without an Intelligent Source by Charles Austerberry http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-14/#comment-381 Charles Austerberry Mon, 12 Jul 2010 12:51:42 +0000 http://www.asa3online.org/Book/?p=75#comment-381 Dear Ide: Thanks for reading the reference, and for continuing the conversation. It is a complicated and confusing subject. Where the text notes that two mechanisms of diversification are “consequences of the recombination," it is referring to the DNA recombination events that assemble variable region encoding DNA from V segments and J segments in the case of antibody light-chain encoding DNA, and from V, D, and J segments in the case of antibody heavy-chain encoding DNA.  One of these two "consequences of the recombination,"  junctional diversification, is probably worth your continued study, because it can result in new base pairs of DNA inserted into so-called "N regions." These N regions created by junctional diversification encode hypervariable regions within the variable regions of the antibody chains. Somatic hypermutation, on the other hand, usually causes substitutions rather than insertions or deletions.  It's a fascinating process whereby double-stranded breaks in DNA are repaired by somewhat error-prone DNA repair mechanisms.  It's well-named.  It also happens much later, after the assembly of the V-(D)-J segments. I appreciate your sense that mutations of existing code differ from insertion of new code.  And as we both noted earlier, changing a DNA sequence (whether by insertion, deletion, or substitution) randomly differs from swapping DNA segments randomly.  All are important in evolution.  Natural selection selects for or against genomic changes of two basic types: 1) those arising from mutations (insertions, deletions, substitutions, and larger-scale rearrangements) and 2) those arising from sexual recombination (meiotic recombination and allelic assortment as gametes are formed followed by random combination of gametes when fertilization occurs). When is there "new code"? Well, one could limit the definition of "new" to only cases where the DNA (or RNA) becomes longer than it was previously.  "Origin of life" experiments that result in longer RNAs, insertional mutations, and many N regions in antibody gene junctional diversification would fit that definition.  These are analogous to new letters being typed in a text. One could also expand the definition to include point substitutions such as those occurring in germline mutations responsible for most human single nucleotide polymorphisms (SNPs) as well as somatic hypermutation in antibody encoding genes.   These are analogous to spelling changes in which a single letter is changed. One could further expand the definition to include rearrangements of existing DNA segments.  That would include DNA recombinations in meiosis, chromosomal translocations and inversions, and the V-(D)-J joining in antibody gene variable region assembly.  These are analogous to moving parts of words, whole words, or word phrases around in a text. And finally, one could further expand the definition to include new combinations of chromosomes, which happens through meiotic allelic assortment plus fertilization in the reproduction of sexual organisms, and which also happens when a particular light chain associates with a particular heavy chain in B cells making antibodies. These are analogous to exchanging paragraphs, chapters, or even books in assembling "new" books or libraries of books. Your choice to limit "new" to the very first definition (a longer sequence, with nucleotides not previously encoded in the genome) is fine with me, as long as we all understand the big picture. Cheers! Chuck       Dear Ide:
Thanks for reading the reference, and for continuing the conversation.
It is a complicated and confusing subject.
Where the text notes that two mechanisms of diversification are “consequences of the recombination,” it is referring to the DNA recombination events that assemble variable region encoding DNA from V segments and J segments in the case of antibody light-chain encoding DNA, and from V, D, and J segments in the case of antibody heavy-chain encoding DNA.  One of these two “consequences of the recombination,”  junctional diversification, is probably worth your continued study, because it can result in new base pairs of DNA inserted into so-called “N regions.” These N regions created by junctional diversification encode hypervariable regions within the variable regions of the antibody chains.
Somatic hypermutation, on the other hand, usually causes substitutions rather than insertions or deletions.  It’s a fascinating process whereby double-stranded breaks in DNA are repaired by somewhat error-prone DNA repair mechanisms.  It’s well-named.  It also happens much later, after the assembly of the V-(D)-J segments.
I appreciate your sense that mutations of existing code differ from insertion of new code.  And as we both noted earlier, changing a DNA sequence (whether by insertion, deletion, or substitution) randomly differs from swapping DNA segments randomly.  All are important in evolution.  Natural selection selects for or against genomic changes of two basic types: 1) those arising from mutations (insertions, deletions, substitutions, and larger-scale rearrangements) and 2) those arising from sexual recombination (meiotic recombination and allelic assortment as gametes are formed followed by random combination of gametes when fertilization occurs).
When is there “new code”?
Well, one could limit the definition of “new” to only cases where the DNA (or RNA) becomes longer than it was previously.  “Origin of life” experiments that result in longer RNAs, insertional mutations, and many N regions in antibody gene junctional diversification would fit that definition.  These are analogous to new letters being typed in a text.
One could also expand the definition to include point substitutions such as those occurring in germline mutations responsible for most human single nucleotide polymorphisms (SNPs) as well as somatic hypermutation in antibody encoding genes.   These are analogous to spelling changes in which a single letter is changed.
One could further expand the definition to include rearrangements of existing DNA segments.  That would include DNA recombinations in meiosis, chromosomal translocations and inversions, and the V-(D)-J joining in antibody gene variable region assembly.  These are analogous to moving parts of words, whole words, or word phrases around in a text.
And finally, one could further expand the definition to include new combinations of chromosomes, which happens through meiotic allelic assortment plus fertilization in the reproduction of sexual organisms, and which also happens when a particular light chain associates with a particular heavy chain in B cells making antibodies. These are analogous to exchanging paragraphs, chapters, or even books in assembling “new” books or libraries of books.
Your choice to limit “new” to the very first definition (a longer sequence, with nucleotides not previously encoded in the genome) is fine with me, as long as we all understand the big picture.
Cheers!
Chuck
 
 
 

]]> Comment on Complex Specified Information Without an Intelligent Source by Ide Trotter http://www.asa3online.org/Book/2010/02/16/complex-specified-information-without-an-intelligent-source/comment-page-13/#comment-380 Ide Trotter Sat, 10 Jul 2010 22:31:09 +0000 http://www.asa3online.org/Book/?p=75#comment-380   Thanks Chuck and with apologies for the delay in responding.    This reference is the closest yet to what I have been looking for.  For the benefit of other readers it is a section titled,”The diversity of the immunoglobulin repertoire is generated by four main processes.”  It classifies two of the processes as “consequences of the recombination” and a third as “due to the different possible combinations.”  To may way of thinking neither combination or recombination produces new code or CSI.   The fourth, “somatic hypermutation,” initially sounded more promising.  However, Wikipedia, my easiest source, describes somatic hypermutation (SHM) as follows: “Experimental evidence supports the view that the mechanism of SHM involves deamination of cytosine to uracil in DNA by an enzyme called Activation-Induced (Cytidine) Deaminase, or AID.[6][7] A cytosine:guanine pair is thus directly mutated a to a uracil:guanine mismatch.”   I read this to say it is exactly as I have suspected.  All these antibody development process really depend on the preexisting code.  In the forth or SMH case some process simply makes a C to U swap.  Different code, yes, but clearly not “new” in the sense of a new order independent of any preceding order. I hope you will agree with this interpretation?   Thanks again for the reference.   Ide  
Thanks Chuck and with apologies for the delay in responding. 
 
This reference is the closest yet to what I have been looking for.  For the benefit of other readers it is a section titled,”The diversity of the immunoglobulin repertoire is generated by four main processes.”  It classifies two of the processes as “consequences of the recombination” and a third as “due to the different possible combinations.”  To may way of thinking neither combination or recombination produces new code or CSI.
 
The fourth, “somatic hypermutation,” initially sounded more promising.  However, Wikipedia, my easiest source, describes somatic hypermutation (SHM) as follows:

“Experimental evidence supports the view that the mechanism of SHM involves deamination of cytosine to uracil in DNA by an enzyme called Activation-Induced (Cytidine) Deaminase, or AID.[6][7] A cytosine:guanine pair is thus directly mutated a to a uracil:guanine mismatch.”
 
I read this to say it is exactly as I have suspected.  All these antibody development process really depend on the preexisting code.  In the forth or SMH case some process simply makes a C to U swap.  Different code, yes, but clearly not “new” in the sense of a new order independent of any preceding order. I hope you will agree with this interpretation?
 
Thanks again for the reference.
 
Ide

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