Sunday, February 26, 2006
Repetitive Elements and Genome Function
Two of my favorite biologists, Sternberg and Shapiro, have teamed up to co-author a paper! The paper is Why repetitive DNA is essential to genome function. They also have coauthored another paper that focuses on retroelements, but I have not gotten around to reading it yet.
Their main thesis is that DNA is essentially a cell's storage mechanism, and that repetitive elements are used to help organise the genome for proper access and function. The repetitive elements serve many functions, including being "generic signals so that operational hardware can locate and process the stored information". They also point out that formatting signals are more-or-less required to have less informational content than the signal, in order to function as formatting signals. Think about a carrier wave versus the data contained therein. Without the carrier wave, it would not be possible to locate the data, but the carrier wave itself does not contain interesting information.
As for the repetitive nature of repetitive elements, they point out that robust systems have redundant components. A minimum is required for function, but excesses are compatible with normal operation.
They also point out that genome size is related to the life cycle length, and that repetitive element size is related to genome size. I _think_ that the point was that larger genomes need more formatting.
They also point out that the ratio of repetitive elements to protein can have phenotypic effects. They use that to indicate that the ratio is "flexible but not adaptively neutral".
They separate storage into "long-term" (DNA codes), "intermediate-term" (epigenetic effects through protein, RNA, and DNA complexes), and "short-term" (DNA, RNA, and protein complexes that are lifecycle-dependent).
They also list several functions genomes are required to perform besides coding for proteins. This includes:
They then discuss the idea that repetitive elements hierarchically organize the genome into series of folders for indexing and access. They did not elaborate this point much, but mostly pointed to other literature.
They discuss at length the interactions of proteins and DNA and their reliance on repetitive elements to work. It helps regulate transcription in response to specific cell states. They relate the function of such repetitive elements to a "multi-layered fuzzy logic system".
As for transposable elements. They say that they allow the cell to "have the ability to introduce a pre-organized constellation of functional signals into any location in the genome". So, transposons are basically a collection of functionality that can be deployed to modulate specific parts of genome function.
Finally, they point out that repetitive elements are highly taxonomically restricted. They say, "Operationally, it is much easier to identify the species of origin of a DNA, cell culture or tissue sample by examining reptitive DNA than coding or unique sequences". This indicates that different types of animals have different cell architectures. The repetitive elements are the primary ways of knowing the cell architectures. They point out that E. Coli and Bacillus subtilis both monitor external glucoses, they each use different mechanisms with repetitive elements to connect the monitoring systems to the genomic repression systems.
They criticize the classical view of the genome (the selfish DNA hypothesis) by proposing a more "systems" view of biology:
The paper also included a fabulous table documenting the various types of repeat elements and some of the functions they are known to play within the genome. Having these descriptions of repeat element types and their functions is worth the price of the article itself.
This is all very interesting for creationists. It implies that genomes have semantics. Viewing the genome's architecture holistically rather than historically seems to be a prime example of a creationist research endeavor. Likewise, it would be interesting to look at how well repetitive elements are able to differentiate baramins, if at all, and also to look and see if these genome restructurings that Shapiro and Sternberg point to in almost every paper involve changes in repetitive elements, or if the repetitive elements remain somewhat static. This may also be a key (or may not be) to Wood's biological similarity problem.
Their main thesis is that DNA is essentially a cell's storage mechanism, and that repetitive elements are used to help organise the genome for proper access and function. The repetitive elements serve many functions, including being "generic signals so that operational hardware can locate and process the stored information". They also point out that formatting signals are more-or-less required to have less informational content than the signal, in order to function as formatting signals. Think about a carrier wave versus the data contained therein. Without the carrier wave, it would not be possible to locate the data, but the carrier wave itself does not contain interesting information.
As for the repetitive nature of repetitive elements, they point out that robust systems have redundant components. A minimum is required for function, but excesses are compatible with normal operation.
They also point out that genome size is related to the life cycle length, and that repetitive element size is related to genome size. I _think_ that the point was that larger genomes need more formatting.
They also point out that the ratio of repetitive elements to protein can have phenotypic effects. They use that to indicate that the ratio is "flexible but not adaptively neutral".
They separate storage into "long-term" (DNA codes), "intermediate-term" (epigenetic effects through protein, RNA, and DNA complexes), and "short-term" (DNA, RNA, and protein complexes that are lifecycle-dependent).
They also list several functions genomes are required to perform besides coding for proteins. This includes:
- Regulating the timing of coding sequence expression
- Regulating coding sequence expression itself
- Coordinating protein expression for proteins that need to function together or in a sequence
- Packaging DNA for retrieval within the cell
- Restructuring the genome (either as part of the cell life cycle, or in response to stress)
- In mitosis, to structure the genome division and copying process
They then discuss the idea that repetitive elements hierarchically organize the genome into series of folders for indexing and access. They did not elaborate this point much, but mostly pointed to other literature.
They discuss at length the interactions of proteins and DNA and their reliance on repetitive elements to work. It helps regulate transcription in response to specific cell states. They relate the function of such repetitive elements to a "multi-layered fuzzy logic system".
As for transposable elements. They say that they allow the cell to "have the ability to introduce a pre-organized constellation of functional signals into any location in the genome". So, transposons are basically a collection of functionality that can be deployed to modulate specific parts of genome function.
Finally, they point out that repetitive elements are highly taxonomically restricted. They say, "Operationally, it is much easier to identify the species of origin of a DNA, cell culture or tissue sample by examining reptitive DNA than coding or unique sequences". This indicates that different types of animals have different cell architectures. The repetitive elements are the primary ways of knowing the cell architectures. They point out that E. Coli and Bacillus subtilis both monitor external glucoses, they each use different mechanisms with repetitive elements to connect the monitoring systems to the genomic repression systems.
They criticize the classical view of the genome (the selfish DNA hypothesis) by proposing a more "systems" view of biology:
As we enter the era of 'systems biology', it is useful to recall that a system is more than a collection of components. Those components need ot integrate functionality so they can accomplish ssystemic tasks requiring cooperative action. One way to state our argument is to say that repetitive DNA elements provide the physical basis within the genome for functional integration. As Britten and Davidson realized, dispersed regulatory sites connect unlinked coding sequences into coordinately controlled subsystems. Similarly, replication and genome transmission processes are organised by generic signals that determine origins, telomeres, centromeres and other nucleoprotein complexes involved in genome maintenance...distributed sites for attachment to cellular or nuclear structures provide a dynamic overall physical organisation of the genome that we are just beginning to comprehend.
The paper also included a fabulous table documenting the various types of repeat elements and some of the functions they are known to play within the genome. Having these descriptions of repeat element types and their functions is worth the price of the article itself.
This is all very interesting for creationists. It implies that genomes have semantics. Viewing the genome's architecture holistically rather than historically seems to be a prime example of a creationist research endeavor. Likewise, it would be interesting to look at how well repetitive elements are able to differentiate baramins, if at all, and also to look and see if these genome restructurings that Shapiro and Sternberg point to in almost every paper involve changes in repetitive elements, or if the repetitive elements remain somewhat static. This may also be a key (or may not be) to Wood's biological similarity problem.
Thursday, February 23, 2006
Baraminology of Camelidae
It appears that baby is coming today, so I thought I'd post a little something before being distracted by a little something :)
Anyway, this is an old one, but one I missed. The 1999 BSG Conference apparently had a focus on Camelidae. This proceedings has more extended abstracts, especially with regards to Camelidae. The Camelidae papers start about halfway through the proceedings.
The proceedings have other good things in them, such as the role of hybridization in determining baramins.
Anyway, this is an old one, but one I missed. The 1999 BSG Conference apparently had a focus on Camelidae. This proceedings has more extended abstracts, especially with regards to Camelidae. The Camelidae papers start about halfway through the proceedings.
The proceedings have other good things in them, such as the role of hybridization in determining baramins.
Tuesday, February 21, 2006
Wood on Biological Similarity
Wood comes out again with a fantastic paper on biological similarity. It is honestly too information-dense for me to summarize -- you will just have to read it yourself. Don't let yourself get put off by the technical jargon at the beginning of the paper -- towards the end he talks in plainer terms about the implications of everything.
One of the things that I enjoy most about the baraminologists is that they are willing to (a) admit tough questions, and not poo-poo them away, (b) they are uncompromising in their adherence to Biblical revelation, and, most importantly, (c) they are willing to acknowledge when they don't have answers to all the questions.
The basic theme of the paper is that (a) humans and chimpanzees have a much larger phenotypic difference than is expected from their genomic differences, and (b) Creationists need to work on a theory for why biological features are similar. He mentions the "common Creator" argument, and, while he agrees with it, he thinks it is too trivial. It is the role of the baraminologist to at least attempt to discover the reason for the specific similarities, and to try to find out for what purpose God created the similarities. He mentions ReMine's "message theory" as the only current systematic attempt at this, but criticizes it primarily on the basis that message theory is based on life being a strict hierarchy, while in fact modern results are showing that life is more of a network than a hierarchy.
One thing that Wood mentioned, but I don't think he emphasized enough, was the differences in gene expression. I think any good systematic approach to the subject will have to look at why the expressions of genes are so different in each baramin.
Anyway, Wood does a good job of critiquing many creationist claims, including parts of claims made by me (Doppleganger -- you would probably be interested in these yourself). While he does not refute these per se, he minimizes to a great amount their importance.
Finally, he points out that genetic similarity may not be baraminically important. He mentions the idea that, at creation, humans and chimps could possibly have even had the same genome, and that the great differences between the creatures aren't genomically based at all. In referencing this, I was quite surprised that he did not reference Sternberg's excellent paper on this subject of the primacy or non-primacy of genes.
Wood finishes not by answering the questions of biological similarity, but by outlining the form that such an answer must have.
Anyway, this paper, like most at the BSG, is a must read for everyone.
One of the things that I enjoy most about the baraminologists is that they are willing to (a) admit tough questions, and not poo-poo them away, (b) they are uncompromising in their adherence to Biblical revelation, and, most importantly, (c) they are willing to acknowledge when they don't have answers to all the questions.
The basic theme of the paper is that (a) humans and chimpanzees have a much larger phenotypic difference than is expected from their genomic differences, and (b) Creationists need to work on a theory for why biological features are similar. He mentions the "common Creator" argument, and, while he agrees with it, he thinks it is too trivial. It is the role of the baraminologist to at least attempt to discover the reason for the specific similarities, and to try to find out for what purpose God created the similarities. He mentions ReMine's "message theory" as the only current systematic attempt at this, but criticizes it primarily on the basis that message theory is based on life being a strict hierarchy, while in fact modern results are showing that life is more of a network than a hierarchy.
One thing that Wood mentioned, but I don't think he emphasized enough, was the differences in gene expression. I think any good systematic approach to the subject will have to look at why the expressions of genes are so different in each baramin.
Anyway, Wood does a good job of critiquing many creationist claims, including parts of claims made by me (Doppleganger -- you would probably be interested in these yourself). While he does not refute these per se, he minimizes to a great amount their importance.
Finally, he points out that genetic similarity may not be baraminically important. He mentions the idea that, at creation, humans and chimps could possibly have even had the same genome, and that the great differences between the creatures aren't genomically based at all. In referencing this, I was quite surprised that he did not reference Sternberg's excellent paper on this subject of the primacy or non-primacy of genes.
Wood finishes not by answering the questions of biological similarity, but by outlining the form that such an answer must have.
Anyway, this paper, like most at the BSG, is a must read for everyone.
Friday, February 17, 2006
New Baby on the Way
My wife is dialated to 2 centimeters. If posts suddenly stop for a time, that's because I'm busy :)
Friday, February 10, 2006
More on Directed Mutagenesis
Our understanding of mutagenesis is showing that mutagenesis is not the haphazard process it was previously thought to be.
Creationists are sometimes falsely accused of having a static view of organisms (and in fact, many lay creationists who have not studied the issue have this view). However, there is no discrepancy between genomic change and creationism. The creationist view is distinctive, however, in that it views multiple categories of change. Cell-directed mutagenesis is characteristically adaptive and beneficial to the cell. Non-directed mutagenesis is almost always damaging to the cells (it can, on occasion, generate some form of benefit, but this is rare, and it is usually outweighed by problems, as in sickle-cell anemia, which prevents malaria.
Anyway, I thought I'd put together a list of articles and ideas supporting directed mutagenesis for those interested. Most of these are investigated in single-celled organisms. Whether or not they are applicable to multicellular organisms has not been as thoroughly examined.
First of all, contingency loci are hypermutable spots of genomes. These spots have been well-known in biology for some time. The interesting things about contingency loci is that these locations are (1) they usually allow a specific, discrete amount of variation, and (2) they are very useful for adaptive purposes, such as antibiotic resistance.
The definitive paper describing contingency loci seems to be Adaptive evolution of highly mutable loci in pathogenic bacteria. I have not read this paper, but a number of papers I have been reading reference this one. From the abstract:
By directing mutation to specific genes, you lessen the problems of error catastrophe by restricting change to specific locations which are built for it.
The paper Environmental regulation of mutation rates at specific sites gives several lines of evidence showing that the rate of changes to these hypermutable loci are specifically affected by environmental conditions which affect the loci. The cell may not know which specific mutation is necessary (that was not determined in the paper), but it does seem to at least know which contingency loci needs to be tampered with.
The paper A Biochemical Mechanism for Nonrandom Mutations and Evolution describes a very interested idea for the mechanism for directed mutations in bacteria. In this review, Wright noted that there are many destabilizing factors in the genome, including proofreading errors during replication, recombination, transcription, and repair. The question is, which of these mechanisms get activated by the cell when the cell is in trouble? The answer is, transcription.
When the DNA is separated into separate strands, it forms stem-loop structures when there are complementary segments which are separaated by 5 to 10 noncomplementary bases. The complementary segments line up, and the noncomplementary bases are subject to numerous types of mutations, such as deamination, deletion, replacment, or complementation.
This seems to be quite an ingenious mechanism that God used to isolate the changeable portions of genes. It seems kind of like a snap-on-tool-like mechanism. Wherever there is a stem-loop, we can substitute various pieces into the DNA to modify it in predictable, specific ways at specific sites.
An interesting quote from the article is this:
The overall gist of the paper is that we can use the secondary structures formed by DNA to predict where mutations are likely to be directed to. In addition, the cell can choose to transcribe certain regions of the genome under stress, in order to activate mutation in those areas to respond to the stressor.
Wright developed an "algorithm for evolution" which looks like this:
Transposons will have to be saved for another time. It's late and I'm tired.
Hopefully I have demonstrated here that genomic change is an active, not a passive mechanism, with respect to adaptive changes. There are spots which are specifically intended for mutation, and these changes are directed by the cell in response to environmental conditions.
This is especially reasonable in a Creationist framework, as it indicates that the cell is "aware" of its own constraints of change, and knows which changes do and do not conform with the cell's overall semantics. It also suggests a method of comparative genomics which examines the differences in secondary structure (and thus hypermutable spots) in different taxa. My guess would be that different baramins would have different hypermutable spots in genes responsible for consumption and other environmental factors, in order to facilitate integration with that baramin's own semantic restrictions.
Creationists are sometimes falsely accused of having a static view of organisms (and in fact, many lay creationists who have not studied the issue have this view). However, there is no discrepancy between genomic change and creationism. The creationist view is distinctive, however, in that it views multiple categories of change. Cell-directed mutagenesis is characteristically adaptive and beneficial to the cell. Non-directed mutagenesis is almost always damaging to the cells (it can, on occasion, generate some form of benefit, but this is rare, and it is usually outweighed by problems, as in sickle-cell anemia, which prevents malaria.
Anyway, I thought I'd put together a list of articles and ideas supporting directed mutagenesis for those interested. Most of these are investigated in single-celled organisms. Whether or not they are applicable to multicellular organisms has not been as thoroughly examined.
Contingency Loci
First of all, contingency loci are hypermutable spots of genomes. These spots have been well-known in biology for some time. The interesting things about contingency loci is that these locations are (1) they usually allow a specific, discrete amount of variation, and (2) they are very useful for adaptive purposes, such as antibiotic resistance.
The definitive paper describing contingency loci seems to be Adaptive evolution of highly mutable loci in pathogenic bacteria. I have not read this paper, but a number of papers I have been reading reference this one. From the abstract:
Bacteria have specific loci that are highly mutable. We argue that the coexistence within bacterial genomes of such 'contingency' genes with high mutation rates, and 'housekeeping' genes with low mutation rates, is the result of adaptive evolution, and facilitates the efficient exploration of phenotypic solutions to unpredictable aspects of the host environment while minimizing deleterious effects on fitness.
By directing mutation to specific genes, you lessen the problems of error catastrophe by restricting change to specific locations which are built for it.
The paper Environmental regulation of mutation rates at specific sites gives several lines of evidence showing that the rate of changes to these hypermutable loci are specifically affected by environmental conditions which affect the loci. The cell may not know which specific mutation is necessary (that was not determined in the paper), but it does seem to at least know which contingency loci needs to be tampered with.
Transcription-directed Evolution
The paper A Biochemical Mechanism for Nonrandom Mutations and Evolution describes a very interested idea for the mechanism for directed mutations in bacteria. In this review, Wright noted that there are many destabilizing factors in the genome, including proofreading errors during replication, recombination, transcription, and repair. The question is, which of these mechanisms get activated by the cell when the cell is in trouble? The answer is, transcription.
When the DNA is separated into separate strands, it forms stem-loop structures when there are complementary segments which are separaated by 5 to 10 noncomplementary bases. The complementary segments line up, and the noncomplementary bases are subject to numerous types of mutations, such as deamination, deletion, replacment, or complementation.
This seems to be quite an ingenious mechanism that God used to isolate the changeable portions of genes. It seems kind of like a snap-on-tool-like mechanism. Wherever there is a stem-loop, we can substitute various pieces into the DNA to modify it in predictable, specific ways at specific sites.
An interesting quote from the article is this:
It is noteworthy that the experiments described above on the effects of artificially induced transcription on mutation rates in growing cells are all examples of specifically directed mutations. However, none of the researchers come to that conclusion or challenge the assumptions and implications inherent in the experiments of Luria and Delbruck, which reinforce neo-Darwinism. This situation may be due to the dominance of current dogma and to the assumption that mechanisms operative during growth cannot also be critical during evolution under conditions of environmental stress.
The overall gist of the paper is that we can use the secondary structures formed by DNA to predict where mutations are likely to be directed to. In addition, the cell can choose to transcribe certain regions of the genome under stress, in order to activate mutation in those areas to respond to the stressor.
Wright developed an "algorithm for evolution" which looks like this:
- Environmental Stress
- Targets Specific Genes for Derepression
- Exposes the Non-transcribed DNA Strand and Drives Supercoiling
- Forms and Stabilizes Secondary Structures
- Creates Unpaired and Mispaired bases
- Causes Hypermutation at Vulnerable sites
- Increases Availability of Variants Most Likely to Survive the Stress
- Selects the Fittest
Transposons
Transposons will have to be saved for another time. It's late and I'm tired.
Conclusion
Hopefully I have demonstrated here that genomic change is an active, not a passive mechanism, with respect to adaptive changes. There are spots which are specifically intended for mutation, and these changes are directed by the cell in response to environmental conditions.
This is especially reasonable in a Creationist framework, as it indicates that the cell is "aware" of its own constraints of change, and knows which changes do and do not conform with the cell's overall semantics. It also suggests a method of comparative genomics which examines the differences in secondary structure (and thus hypermutable spots) in different taxa. My guess would be that different baramins would have different hypermutable spots in genes responsible for consumption and other environmental factors, in order to facilitate integration with that baramin's own semantic restrictions.
Tuesday, February 07, 2006
The New Science of Eco-Devo
Well, not exactly new, but getting new energy. A while ago I read the paper Ecological Developmental Biology: Developmental Biology Meets the Real World by Scott Gilbert. I have no idea if Gilbert is a creationist, but his research should certainly be of interest to creationists.
This paper discusses several ways in which the environment impacts the development of organisms. He points out that this area of research has been hampered by the fact that the specimens chosen for in-depth study were chosen precisely because they could grow reliably in a lab environment. Therefore, the sample of organisms used to study development are very irregular in the fact that their development doesn't count on environmental factors.
Some basic examples are:
The paper focused on predator-induced polyphenisms. Specifically, kairomones, which are soluble chemicals released by animals (kind of like aqueous pheromones). Basically, a prey, during its development, can detect the fact that it is sharing the water with a predator, and have an adaptive change induced.
Some examples:
What's even more interesting (especially to creationists) is the concept of genetic assimilation. If a phenotype is induced environmentally for enough generations, the inducer can internalize such that future progeny will have the phenotype even in the absence of the inducer. Examining the mechanisms behind this would be an excellent project for a baraminologist (there are some papers referenced, but I have not read them and do not know how well they cover the subject).
On an ecological consideration, Gilbert points out that the lack of research in this area may mean that some of the chemicals we introduce into the environment may cause developmental problems in organisms. This is something that is not normally considered to the extent that it should.
I thought that the most interesting parts were (a) that organisms during development can sense the animals in their ecology and respond appropriately, and (b) these changes can be converted into internally-generated, thus giving another mechanism for baraminic diversification.
Lots of good things to think about. In fact, the paper covers lots of things I just didn't have time to mention. This is a must-read.
This paper discusses several ways in which the environment impacts the development of organisms. He points out that this area of research has been hampered by the fact that the specimens chosen for in-depth study were chosen precisely because they could grow reliably in a lab environment. Therefore, the sample of organisms used to study development are very irregular in the fact that their development doesn't count on environmental factors.
Some basic examples are:
- Some butterflies have different color phenotypes based on what season they were born in (dependent on day-length and temperature
- Snapping turtles are born male and female depending on the temperature
- Ant larva become workers/queens depending on diet
- Some toads can develop alternate phenotypes depending on whether or not the pond is drying up
- Orthodontic problems in humans may be caused by overly-soft diets in children (it is the increased chewing and tension in the jaw that stimulates the bone and muscle growth
The paper focused on predator-induced polyphenisms. Specifically, kairomones, which are soluble chemicals released by animals (kind of like aqueous pheromones). Basically, a prey, during its development, can detect the fact that it is sharing the water with a predator, and have an adaptive change induced.
Some examples:
- If you raise Daphnia in water in which Chaoborus was previously cultured, it will induce a neck spine or helmet.
- If the carp Carassius carassius is developing in the water with a pike that has already eaten a carp, it will have induced a morphology that will not fit into the pike's jaws.
- Gilbert pointed to the human immune system as a giant example of a predator-induced polyphenic system (antibodies produced by our mothers give us passive immunity when we are born).
What's even more interesting (especially to creationists) is the concept of genetic assimilation. If a phenotype is induced environmentally for enough generations, the inducer can internalize such that future progeny will have the phenotype even in the absence of the inducer. Examining the mechanisms behind this would be an excellent project for a baraminologist (there are some papers referenced, but I have not read them and do not know how well they cover the subject).
On an ecological consideration, Gilbert points out that the lack of research in this area may mean that some of the chemicals we introduce into the environment may cause developmental problems in organisms. This is something that is not normally considered to the extent that it should.
I thought that the most interesting parts were (a) that organisms during development can sense the animals in their ecology and respond appropriately, and (b) these changes can be converted into internally-generated, thus giving another mechanism for baraminic diversification.
Lots of good things to think about. In fact, the paper covers lots of things I just didn't have time to mention. This is a must-read.
The Baraminology of Snakes
Tom Hennigan has a new paper out concerning the baraminology of snakes. For those of you who have forgotten, baraminology is the creationist biosystematics/taxonomy methodology. You can read more about it at the beginning of the blog archives.
Anyway, while not identifying holobaramins (original created kinds), Tom was able to identify several monobaramins (organisms part of a single created kind, but that may be joined with other monobaramins to form the complete created kind).
By several lines of evidence, he identified the following monobaramins.
From Boidae: Morelia/Liasis, Python, and Antaresia
From Colubridae: Nerodia, Pantherophis/Lampropeltis/Ptuophis, Diadophis, Thamnophis, Tolucaa/Conopsis, and Chilomeniscus
From Viperidae: Crotalus/Sistrurus, Agkistrodon, and Bitis
Tom identified the question of whether or not snakes represent a holobaramin as an open question.
Anyway, while not identifying holobaramins (original created kinds), Tom was able to identify several monobaramins (organisms part of a single created kind, but that may be joined with other monobaramins to form the complete created kind).
By several lines of evidence, he identified the following monobaramins.
From Boidae: Morelia/Liasis, Python, and Antaresia
From Colubridae: Nerodia, Pantherophis/Lampropeltis/Ptuophis, Diadophis, Thamnophis, Tolucaa/Conopsis, and Chilomeniscus
From Viperidae: Crotalus/Sistrurus, Agkistrodon, and Bitis
Tom identified the question of whether or not snakes represent a holobaramin as an open question.
Research on Rapid Metamorphism
Andrew Snelling just posted an impact article reviewing research (both secular and YEC) on rapid metamorphism.
It's an interesting article, but geology is one of my weakest subjects, so there's not much I can comment on in it.
Biotite was not in the precursor granulites, so it had to form as a result of both their metamorphism to eclogite and the fluid flows. Of course, these radiohalos could only have been produced in the biotite grains after they formed. Furthermore, because there was no source of either parent uranium-238 or its radioactive decay products within either the eclogites or the precursor granulites, the large quantities of polonium-210 required to generate these radiohalos had to have been transported from external sources into the biotite flakes within these rocks by the hot fluids. But the polonium-210 only has a half-life of 138 days, and the radiohalos would only have formed and survived after the temperature in the rocks fell below 150°C. So this drastically restricts the duration of the earthquake-triggered hot fluid flows and associated eclogite metamorphism even more, perhaps to only a few weeks or months! And because the heat flow into the granulites to metamorphose them would have been primarily by convection associated with the fluid flows, rather than just by conduction, such a drastically short timescale of only weeks for this eclogite metamorphism is entirely feasible.
It's an interesting article, but geology is one of my weakest subjects, so there's not much I can comment on in it.
