Thursday, December 22, 2005
Several Notes on Human/Primate Baraminology
When I tell people that creationists believe that, in general, creationists believe that the "created kind" are usually at family level of taxonomy, they are truly surprised. After they get over their initial shock, they usually then ask, "are chimps and other primates considered one created kind?" The simple answer is no. This is one of several cases where traditional taxonomy does not help us out. The Bible clearly records the non-common-ancestry of humans, stating that we were formed from the dust of the ground.
So, is there any evidence of this position? What about other hominid fossils --- are they human?
David DeWitt gives us two pieces of evidence. In The Neandertal's Role in Human History [Virginia Journal of Science 51(2):83, 2000; DeWitt, D. and Skinner, W.], he explains that the differences between Neandertal and human mtDNA occur at genetic "hotspots", while the hotspots differ between human and other primates. Note that this is mtDNA, not a whole-genome comparison, but it is interesting nonetheless. Marvin Lubenow contributes other interesting facts to the discussion of Neanderthal being fully human.
Historically, chimp/human genome comparisons have been done only on some genes, because we have not had the genome of the chimp sequenced. However, now it has. Just this year the Chimpanzee Sequence and Analysis Consortium published their results in Nature: Initial sequence of the chimpanzee genome and comparison with the human genome. David DeWitt analyzes some of their data in his TJ article "Chimp genome sequence very different from man" [TJ 19(3) 4-5, 2005].
I haven't had the chance to view the Nature article myself (our library is a bit slow on these things) but I will share DeWitt's analysis.
Retroviral elements:
73 human-specific
45 chimp-specific
Proteins-coding sequences:
29% of proteins are identical
5% of proteins have in-frame indels (insertion or deletion of three nucleotides, i.e. the code for a single amino acid)
Proteins with the most differences: transcription factors
In order for chimps and humans to share a common ancestor, there would have had to be 40 million mutation events, a chromosome fusion event, a modification to the length of the Y chromosome, all becoming fixed in the population in 300,000 generations.
However, what I would really like to know is how different the transposons are between chimps and humans, as that is how Todd Wood hypothesized the major differences between baramins would be shown.
Another interesting article in TJ is a short one called Was Lucy Bipedal? [TJ 19(3):13, 2005] by Marvin Lubenow. He points out that the major indications that Lucy was bipedal come from (1) the Laetoli footprints (which appear to be human) and (2) the reconstruction of Lucy. Now, the interesting thing about the reconstruction of A. afarensis (Lucy) is that the foot is based on a mixture of fossils, including those of Homo habilis! So, by mixing multiple species, you can find an intermediate fossil! Unfortunately, I do not know what the status is of Homo habilis, and whether he is considered a human by baraminologists or not.
Of course, in studying human ancestry, everyone has an axe to grind -- both creationists and evolutionists. The difference being that it is obvious that creationists have a stake in the outcome, but not so obvious the other way around. Marvin Lubenow developed an interesting study to do with his students to help them realize this.
I have not read this one yet, but I found it while searching for other references in this note: Homo erectus 'to' modern man: evolution or human variability?
Sorry this article was so thrown together. I have had it on the back burner for a while, and just wanted to get it done and out the door. In addition, I was hoping to find information on the transposon differences between humans and chimps, but was unable to do so. If anyone can help me here, please email johnnyb@eskimo.com.
So, is there any evidence of this position? What about other hominid fossils --- are they human?
David DeWitt gives us two pieces of evidence. In The Neandertal's Role in Human History [Virginia Journal of Science 51(2):83, 2000; DeWitt, D. and Skinner, W.], he explains that the differences between Neandertal and human mtDNA occur at genetic "hotspots", while the hotspots differ between human and other primates. Note that this is mtDNA, not a whole-genome comparison, but it is interesting nonetheless. Marvin Lubenow contributes other interesting facts to the discussion of Neanderthal being fully human.
Historically, chimp/human genome comparisons have been done only on some genes, because we have not had the genome of the chimp sequenced. However, now it has. Just this year the Chimpanzee Sequence and Analysis Consortium published their results in Nature: Initial sequence of the chimpanzee genome and comparison with the human genome. David DeWitt analyzes some of their data in his TJ article "Chimp genome sequence very different from man" [TJ 19(3) 4-5, 2005].
I haven't had the chance to view the Nature article myself (our library is a bit slow on these things) but I will share DeWitt's analysis.
Retroviral elements:
73 human-specific
45 chimp-specific
Proteins-coding sequences:
29% of proteins are identical
5% of proteins have in-frame indels (insertion or deletion of three nucleotides, i.e. the code for a single amino acid)
Proteins with the most differences: transcription factors
In order for chimps and humans to share a common ancestor, there would have had to be 40 million mutation events, a chromosome fusion event, a modification to the length of the Y chromosome, all becoming fixed in the population in 300,000 generations.
However, what I would really like to know is how different the transposons are between chimps and humans, as that is how Todd Wood hypothesized the major differences between baramins would be shown.
Another interesting article in TJ is a short one called Was Lucy Bipedal? [TJ 19(3):13, 2005] by Marvin Lubenow. He points out that the major indications that Lucy was bipedal come from (1) the Laetoli footprints (which appear to be human) and (2) the reconstruction of Lucy. Now, the interesting thing about the reconstruction of A. afarensis (Lucy) is that the foot is based on a mixture of fossils, including those of Homo habilis! So, by mixing multiple species, you can find an intermediate fossil! Unfortunately, I do not know what the status is of Homo habilis, and whether he is considered a human by baraminologists or not.
Of course, in studying human ancestry, everyone has an axe to grind -- both creationists and evolutionists. The difference being that it is obvious that creationists have a stake in the outcome, but not so obvious the other way around. Marvin Lubenow developed an interesting study to do with his students to help them realize this.
I have not read this one yet, but I found it while searching for other references in this note: Homo erectus 'to' modern man: evolution or human variability?
Sorry this article was so thrown together. I have had it on the back burner for a while, and just wanted to get it done and out the door. In addition, I was hoping to find information on the transposon differences between humans and chimps, but was unable to do so. If anyone can help me here, please email johnnyb@eskimo.com.
Monday, December 12, 2005
Two Must-Reads from Sternberg on Genome Reconfiguration
I just finished two great articles by Sternberg:
Both are excellent, but I recommend that every person go straight to their library, and do an Interlibrary-loan request for the latter. Take it home, read it with a dictionary, and re-read it until you understand every word. It is fabulous.
Both of these articles have a unifying purpose: clarifying the genotype/phenotype distinction, and how it occurs.
The first article is good. It contains a hypothesis that genomes are just as much a product of cell structure as cell structure is a product of the genome. The cell structure has intelligence (us creationists would say "designs" or "programming") to try out new genomic designs, a form of "research and development" carried out by the cell itself. It's main purpose is to show that phenotype can affect genotype just as much as the genotype affects phenotype. Traditional biology holds that this occurs in one direction alone, but recent advances show that this is actually co-recursive.
The second article is absolutely fabulous. He discusses in-depth the roles of repetitive elements and transposable elements. He notes many reasons that the idea of junk in the DNA is false. His main thesis is that repetitive and mobile elements are integral, functional parts of the genome software system.
Some interesting things he notes on the genome:
There is a TON of stuff in the article, and I can't even begin to do it justice in a short post after a first reading. Also, for those of you who argue against neo-Darwinism, most of the article contains direct arguments against such thinking. However, those arguments are outside the scope of this blog, but they are _fabulous_.
Anyway, I might return to this article later. There's too much here to really absorb. But in reality, I'll probably be too busy to revisit it in any meaningful way. But, again, I suggest that you get it from interlibrary loan and read it through. Sternberg is absolutely great.
- Genomes and Form: The Case for Teleomorphic Recursivity
- On the Roles of Repetitive DNA Elements in the Context of A Unified Genomic-Epigenetic System
Both are excellent, but I recommend that every person go straight to their library, and do an Interlibrary-loan request for the latter. Take it home, read it with a dictionary, and re-read it until you understand every word. It is fabulous.
Both of these articles have a unifying purpose: clarifying the genotype/phenotype distinction, and how it occurs.
The first article is good. It contains a hypothesis that genomes are just as much a product of cell structure as cell structure is a product of the genome. The cell structure has intelligence (us creationists would say "designs" or "programming") to try out new genomic designs, a form of "research and development" carried out by the cell itself. It's main purpose is to show that phenotype can affect genotype just as much as the genotype affects phenotype. Traditional biology holds that this occurs in one direction alone, but recent advances show that this is actually co-recursive.
The second article is absolutely fabulous. He discusses in-depth the roles of repetitive elements and transposable elements. He notes many reasons that the idea of junk in the DNA is false. His main thesis is that repetitive and mobile elements are integral, functional parts of the genome software system.
Some interesting things he notes on the genome:
- The "selfish DNA" hypothesis relies on genes being context-independent. However, we have found more and more that genes are actually highly context-dependent.
- The fluidity of a thing does not imply the non-function of a thing. With respect to the genome, the fluidity of transposable and repetetive elements does not imply that they aren't functional, but in fact their fluidity is what makes them highly functional
- Genomic change through transposable elements occurs in fairly large leaps, all of which maintain internal consistency, context, and cohesion. While being fluid, it maintains an internal consistency. (note that this gives credence to the idea that the change process is informationally directed, and operates according to a stable semantic).
- While transposable elements can change the biochemical nature of the cell in many ways, they are not responsible for macro-evolution, because such elements are taxonomically restricted. Despite the fact that species can undergo massive configuration changes in a single generation, none of the changes would cause a taxonomic reclassification.
- The genetic/epigenetic system is a continuous one
- Transposable elements appear to be rapidly-deployable DNA units for the cell to reconfigure itself with in response to specific inputs, stresses, or events
There is a TON of stuff in the article, and I can't even begin to do it justice in a short post after a first reading. Also, for those of you who argue against neo-Darwinism, most of the article contains direct arguments against such thinking. However, those arguments are outside the scope of this blog, but they are _fabulous_.
Anyway, I might return to this article later. There's too much here to really absorb. But in reality, I'll probably be too busy to revisit it in any meaningful way. But, again, I suggest that you get it from interlibrary loan and read it through. Sternberg is absolutely great.
Saturday, December 10, 2005
Evidence for Todd Wood's Altruistic Genes
We talked earlier about Todd Wood's hypothesis of transposons, calling them "altruistic genetic elements" (AGEs). His hypothesis was that transposons were, instead of being parasitic genetic elements, were actually altruistic -- helping the genome reconfigure itself for adaptation. He thought that the following would come to light:
These are his specific predictions. He also describes unprocessed pseudogenes, which are unexpressed genes. On page 20, Wood proposes that some unprocessed pseudogenes are latent genes that have not been activated yet, or have been deactivated by AGEs. Barry Hall provides evidence for this in a recent paper (this was actually published before Wood's paper, but Wood did not reference this paper, so it is unlikely that Wood had access to Hall's work, though it does not really matter).
Barry Hall's paper is called Transposable elements as activators of cryptic genes in E. coli. From what I can tell, cryptic genes and unprocessed pseudogenes are two terms for basically the same thing. The only difference I could tell is that the term "unprocessed pseudogene" usually refers to genes that are similar to genes with known function, but are currently unexpressed.
Anyway, a quick summary is that, while biological tradition has held that transposons are essentially purposeless, "selfish", and parasitic in the genome, there are clear examples of transposons which are beneficial, targetted, and environmentally activated.
The main example used is a suite of genes that are used to metabolize a certain type of sugars, called Beta-glucoside sugars. Normally E. Coli is unable to process these sugars, but not because it lacks the genes to do so. The genes are presesnt, but inactive. However, they are also well-preserved by the genome. There are three operons involved -- bgl, cel, and asc, each built from multiple genes. All of these can be activated by insertion sequences placing themselves in the proper places. And, in fact, empirical analysis indicates that these insertions DO NOT occur except under starvation conditions, and then ONLY in the presence of beta-glucoside sugars (arbutin was the one used in the experiments).
So, it seems that transposons are explicitly being used by the cell to enable specified, adaptive responses. It also seems that cells can have suites of genes which are inactive, only to be activated in specific conditions. Wood proposed that this was the case for C3 and C4 photosynthesis -- many plants have both pathways encoded in their genes, but one or the other is switched off by default, enabled by transposons under certain environmental conditions.
- The difference between two species in the same baramin would be mostly due to transposons
- Some AGEs would be physically associated with genes responsible for species-specific traits
- Populations living immediately after the flood were more adaptable than populations living now
These are his specific predictions. He also describes unprocessed pseudogenes, which are unexpressed genes. On page 20, Wood proposes that some unprocessed pseudogenes are latent genes that have not been activated yet, or have been deactivated by AGEs. Barry Hall provides evidence for this in a recent paper (this was actually published before Wood's paper, but Wood did not reference this paper, so it is unlikely that Wood had access to Hall's work, though it does not really matter).
Barry Hall's paper is called Transposable elements as activators of cryptic genes in E. coli. From what I can tell, cryptic genes and unprocessed pseudogenes are two terms for basically the same thing. The only difference I could tell is that the term "unprocessed pseudogene" usually refers to genes that are similar to genes with known function, but are currently unexpressed.
Anyway, a quick summary is that, while biological tradition has held that transposons are essentially purposeless, "selfish", and parasitic in the genome, there are clear examples of transposons which are beneficial, targetted, and environmentally activated.
The main example used is a suite of genes that are used to metabolize a certain type of sugars, called Beta-glucoside sugars. Normally E. Coli is unable to process these sugars, but not because it lacks the genes to do so. The genes are presesnt, but inactive. However, they are also well-preserved by the genome. There are three operons involved -- bgl, cel, and asc, each built from multiple genes. All of these can be activated by insertion sequences placing themselves in the proper places. And, in fact, empirical analysis indicates that these insertions DO NOT occur except under starvation conditions, and then ONLY in the presence of beta-glucoside sugars (arbutin was the one used in the experiments).
So, it seems that transposons are explicitly being used by the cell to enable specified, adaptive responses. It also seems that cells can have suites of genes which are inactive, only to be activated in specific conditions. Wood proposed that this was the case for C3 and C4 photosynthesis -- many plants have both pathways encoded in their genes, but one or the other is switched off by default, enabled by transposons under certain environmental conditions.
