After rereading the paper in light of Dr. Wolfe's comments, I can tell that we went a bit too far with the yeast nomenclature. The actual point is that at sometime in the past, what were seen as being short and long arms were standardized as left and right arms (Hong, personal communication). As maps improved, they didn't redo the left and right designations to reflect new sizes. Even if this is also wrong, the spirit of the standardization should still be embraced.
read full comment
Article mis-states the yeast convention (Ken Wolfe, 01 March 2011)
The article mis-states the yeast convention. The Watson strand is the strand with its 5' end at the left telomere, but the left arm is not always the shorter arm of a yeast chromosome. In fact, the L arm is longer than the R arm for 7 of the 16 yeast chromosomes (up to 4 times longer, in the cases of chromosomes IX and XIV).
The left/right nomenclature for yeast chromosome arms dates back to the early days of yeast genetic maps, but I do not know who introduced it. Cytogenetics is not really possible for Saccharomyces because the chromosomes are too small and do not have extensive heterochromatin at centromeres, so nobody knew which arm was the shorter one until chromosome-sized genetic (and eventually genomic) maps became available. Oliver et al (Nature 357:38, 1992) then...
read full comment
I am suppose that PyrD polarization in this article is incorrect (Valery Anisimov, 07 December 2010)
For sure this paper propose a new interesting method for the indels polarization based on the structural analysis. But on the same time we should be careful in this point because without clear rules of it implementation sometimes we can come to the wrong conclusions. I think that PyrD polarization made by authors in this paper is exactly the case of applying such muddy logic. First of all the authors claims that polarization of the PyrD indel using HemE protein as an outgroup made by Skophammer and others is questionable. I am totally agree with this statement. But then they are also rejected polarization of the PyrD based on the consideration of HisA and HisF proteins as outgroup, claimed that "indel arguments contradict themselves". I do not see a logic in the last statement. Why if...
read full comment
I am particularly agree with the author in some points. (Valery Anisimov, 02 December 2010)
According to myself investigations based on the analysis of the percentage of the genes shared by different bacterial clades, closest clade to Archaea is Actinobacteria and for Bacillus closest one of course Clostridia but on the second place we can see again Actinobacteria. So it is quite possible that Actinobacteria, Neomura and Bacillus had the common ancestor. But based on the analysis of the genes reading directions distributions inside bacterial genomes I guess that this common ancestor was close to Clostridia clade. LUCA probably had RNA-based chromosome which in the secondary structure was organized as one huge stem. So during transcription process ribosome can move only one way. As consequence all genes had the same reading direction. Afterwards when RNA-based genome was...
read full comment
GC% and AG% not independent (Donald Forsdyke, 25 November 2010)
There is a reciprocal relationship between GC% and AG%.
There are two ways to modulate (G+C)% when the total number of bases is constant; either by changing the number of G’s, or by changing the number of C’s. As (G+C)% increases, trading A for G would not affect the AG%. Likewise, trading T for C would not affect the AG%. However, if T were replaced by G, the AG% would increase as (G+C)% increases. Conversely, if A were replaced with C the AG% would decrease as (G+C)% increases.
The latter inverse relationship is observed in bacteria (Lao & Forsdyke 2000; Mortimer & Forsdyke 2003) and eukaryotes (Cristillo et al 2001), and is extensively discussed in my textbook - Evolutionary Bioinformatics (Springer 2006). ...
read full comment
Correction of Acknowledgement (Mark Ragan, 07 June 2010)
This paper was developed from a talk I gave at ISHPSSB-2009 on the invitation of Maureen O'Malley (Exeter University). An incorrect attribution is given in the Acknowledgements.
read full comment
BIO INSIPER NANOTECH: COST ACTION 2010 (Paolo Manzelli, 06 April 2010)
BIO-INSPIRED NANOTECH. EUROPEAN COST ACTION 2010. Notes and suggestion by Paolo Manzelli <pmanzelli@gmail.com>
To Jean-Jacques Toulmé <jean-jacques.toulme@inserm.fr> and colleagues in address .
I would like to suggest to develop a section on Quantum Entanglement and Biological information Exhange on the basis of the following considerations.
As a matter of facts the basic question of Bio-inspired technology is focused on undestanding a physical model of self-molecular assembly, in order to create complex systems of Bio-inspired Tech.at nano scale. To understand the underlining criteria of self assembly I think that science need to overcome the traditional mechanical approach of physics and need to to develop a complete...
read full comment
ImRNA or RNA antibody model? (Donald Forsdyke, 09 October 2009)
The author's appendix (p. 11) summarizes nine steps in the proposed "imRNA response mechanism." Two of these are weak. Step 3: Recognition of foreign viral mRNA "possibly by host reverse transcriptases RT." But how does reverse transcriptase distinguish between self and not-self RNAs? Step 6: Integration into host genome. But there is no distinction between somatic cells and germline cells. How is the "Weismann barrier" breached in the case of germline cells? As Koonin points out, there is Lamarckian element here. While there is much indirect evidence, ably summarized by Flegel, that support his model (especially bacterial CRISPR systems), the above objections are overcome in the "RNA antibody" model we suggested (see read full comment
good idea, again (William Martin, 24 September 2009)
In 2003, Ford Doolittle called this the "Genome of Eden" constraint, in Phil Trans Roy Soc Lond B. In 2007 (PNAS) and 2008 (PNAS), Tal Dagan used it to estimate LGT frequency and cumulative impact among prokaryotes. Good idea, again.
read full comment
An early warning against rejection-free claim for iPS cells (Shi Liu, 04 September 2009)
I have been wondering why almost all the transplantations of iPSCs (induced pluripotent stem cells) were done on SCID mice rather than on normal mice. As a matter of fact I even publicly questioned the study design of a study and asked: Why a study aimed at showing a "circumvention of the immune rejection barrier" by using iPSC-based therapy would still use sub-lethally irradiated mice as the recipients? (see publication at http://im1.biz/displayimage.php?album=84&pos=1 ).
I think the results presented here should serve as a warning against many naive claims for cell therapy. Immunity may be more tricky than we have thought of and reprogramming cells may even present or expose some antigens subject to rejection reactions. read full comment
Response from the authors (Robson Francisco De Souza, 26 August 2009)
1) The sequences corressponding to the structures in PDB for the Anabaena protein are indeed different from those derived from the genomic sequence. Given that the domain is short any such change, even if at the termini, appear to distort the key structural elements. This justifies our exclusion of the Anabaena structures from further analysis.
2) This is indeed true and this observation reinforces our basic inference that there is no strict link between functions of solo ASRAH proteins and ASR-type sensory rhodopsins.
1) The authors claim that "Examination of the structures reveals that key structural elements of the Anabaena representative have been mutated to obtain its crystal structure." I believe this is incorrect. There are parts of the structure which are missing due to disorder, but there are no mutations in the main sequence, with the exception of His-tags added on either of the termini.
2) Not only there are many rhodopsin-less species in which ASRT homologs are found, but there are also several bacterial species having homologs of ASR, but no ASRT.
read full comment
A great example of science in action (Stephen Curry, 30 March 2009)
I thought this a very interesting paper that shed important light on the difficulties inherent in predicting structure from sequence - and in correcting earlier errors. The insights derived from the exchanges between reviewers and authors were particularly illuminating. I've mentioned the paper on my blog as an example of the great value of openness in the publication procedure.
Among the "Whole genome duplication" scenario proponents there are two versions of Ohno,s hypothesis, some has suggested two round (2R) scenario (leading to octaploids), whereas others only one round (1R) of whole genome duplication (leading to tetraploids, please see Ref 25 of this manuscript, and also see Gu et al 2002 Nat.Genet.31, 205-209 and Durand Dannie TRENDS in Genetics Vol.19 No1 Jan 2003). The title of the manuscript refers to 1R. However in the text I provide a critical overview of 2R also (please see in particular the sections “Paralogy regions in the Human genome” and “HOX cluster duplication and the history of vertebrate genome evolution”. I can hope this comment will let the readers to understand the title of this manuscript. <br><br>I...
read full comment
Two rounds of genome duplication would generate from diploids -> tetraploids and from tetraploids -> octaploids. <br><br>So I do not understand the title of the paper. <br><br>In fact there is a paper on this issue that indeed refers to octaploidy.<br>TJ Gibson and J Spring (2000) Evidence in favour of ancient octaploidy in the vertebrate genome, Biochem Soc Trans 28:259–264.
read full comment
Correction and citation (Dustin Holloway, 07 October 2008)
Although the KEGG database is mentioned at several points within the text, readers should also note that the layout of the WNT pathway as seen in Figure 4 was modeled after that seen in the KEGG WNT Signaling Pathway(http://www.genome.jp/kegg/pathway/hsa/hsa04310.html).Please also note that, in Figure 2, the y-axis is the Positive Predictive Value (PPV).Finally, identifiers for several of the TFs in the bottom portion of Figure 6A are missing. The TFs should be labeled (from left to right) SRF, E2F, Mef2a, T3R, YY1, and CebpB.We apologize for any inconvenience this may have caused the sophisticated reader.
read full comment
Figure Correction (Dustin Holloway, 07 October 2008)
Please note the following minor correction to Figure 1:The small box on the bottom right hand corner of Figure 1 contains the following text: "100X Average Accuracy." This should instead read "50X Average Accuracy." (The Figure legend provides the correct number). Also, the text directly next to the box should read "Average the Accuracy Estimates Over 50 Repeats", rather than "...Over 100 Repeats."
read full comment
additional supporting information for the article (Neil Smalheiser, 03 April 2008)
In my article (section 5d, Cargo proteins within postsynaptic exosomes, subsection b, AMPA receptors), I made the statement that “to my knowledge, no physiologic role for presynaptic AMPA receptors has been described.” Thus, I surmised that AMPA receptor proteins and/or mRNAs carried from postsynaptic to presynaptic terminals would have no physiological significance, but might instead provide a way for the postsynaptic terminal to shed AMPA receptors. However, more recently, I have become aware that there is an extensive literature documenting the presence and physiological relevance of presynaptic AMPA receptors in hippocampal and sensory ganglion neurons, among other neuronal cell types. (See Matsuda et al (2008) [1] for discussion and a partial list of references.) This...
read full comment
Acknowledging an earlier observation of orphan SelD (Daniel Haft, 04 March 2008)
Just after publication of our manuscript, we came across the following reference: Zhang Y, Romero H, Salinas G, Gladyshev VN., Dynamic evolution of selenocysteine utilization in bacteria: a balance between selenoprotein loss and evolution of selenocysteine from redox active cysteine residues. Genome Biol. 2006;7(10):R94. Epub 2006 Oct 20. We launched our study from the observation that SelD proteins explained by neither selenocysteine nor selenouridine pathways might imply a third SelD-dependent trait. The orphan status of SelD in Enterococcus faecalis and Haloarcula marismortui and possibility of SelD-dependence for selenium-dependent molybdenum hydroxylases were raised previously by Zhang, et al., and should have been cited as background to this paper. We regret having been unaware of...
read full comment
Darwin Was Indeed Wrong but Koonin’s Revolution May Not Be Novel (Shi Liu, 22 October 2007)
In 1991 I already pointed out the major mistakes made by Darwin which included his assertion that all extent lives were descended from a common ancestor cell and his simple and exclusive treatment of similarity with genealogically inherited identity (1). My alternative view on the origin and evolution is that life might have independently originated from multiple acellular ancestors and that similarity among different organisms may be a reflection of non-phylogenetic formations by a common mechanism (1). My theory treats biotic evolution as a companion process to the abiotic evolution and thus the events and history of biotic evolution should naturally reflect the abiotic course of evolution. Like the Big Bang events happened in the formation and evolution of the abiotic world, similar...
read full comment
Examine macroevolutionary concepts carefully (Nicholas Matzke, 29 August 2007)
Well, since it is clear that this paper will be on every ID/creationist blog on the planet in under 12 hours, I might as well put in my 2 cents early. I will say at the outset that I have immense respect for Eugene Koonin and his contributions to numerous fields, and criticize his work with some trepidation. However, I think with this paper he has unfortunately tumbled into a series of mistakes that have repeatedly afflicted those trying to understand macroevolution without taking sufficient care in examining the concepts they are relying upon.I will enumerate some of them, in no particular order:1. Treating Linnaean categories as "real", and thinking about them in a typological manner rather than phylogeneticallyThis is most clearly exposed in Koonin's discussion of the Cambrian phyla...
read full comment
Absence of evidence or evidence of absence? (Daniel Silvestre, 23 August 2007)
The presented hypothesis is quite ingenious and is something pleasant to read in these days of pragmatic science. But, I can see that something is missing. This article demonstrate clearly that viruses share "common" features (synapomorphies?) not shared by any kind of cellular life. Hence, is reasonable to assume that all viruses descend from a common ancestor. The missing point is: how one can decide who appeared first (cells or viruses) with this type of evidence? There is no possible outgroups/transition analysis to handle this issue, to my known experience. There is no fossil evidence of viruses predating cellular life nor evidence of absence of cellular with the presence of viruses. Therefore, with the evidence and arguments presented in this paper give sound basis to the existence of...
read full comment
Re: Running before walking (Albert de Roos, 20 June 2007)
In reply to the comment of Niles Lehman, it is true that I do assume single-stranded oligonucleotides to be available and where I write that single stranded RNA (ssRNA) preceded double-stranded RNA, I mean ssRNA as the carrier of catalytic function.I also notice that my perception of OOL research is different from that of the mainstream scientists in the field, as also indicated by the reviewers of the manuscript and would like to expand a little on it. I do assume the presence of ribonucleotides as the building blocks of life, but recognize that this is indeed not trivial and I do not deny that there seem important chemical hurdles to take for an abiotic generation of oligo-ribonucleotides (or its precursors). However, ribonucleotides are the actual building blocks of Life as we know it...
read full comment
Running before walking? (Niles Lehman, 18 June 2007)
I read the article by DeRoos with interest. However, it is not clear to me how dsRNA could preceed ssRNA. If dsRNA is the precursor to ssRNAs with some activities or phenotypes, how would the dsRNA arise in the first place? The hybridization model presented in Figure 2 presupposes the existence of ssRNA oligomers. This seems counterintuitive ... or am I missing some key point?
read full comment
RSS
Latest comments
Yeast Standards (Reed Cartwright, 08 March 2011)
After rereading the paper in light of Dr. Wolfe's comments, I can tell that we went a bit too far with the yeast nomenclature. The actual point is that at sometime in the past, what were seen as being short and long arms were standardized as left and right arms (Hong, personal communication). As maps improved, they didn't redo the left and right designations to reflect new sizes. Even if this is also wrong, the spirit of the standardization should still be embraced. read full comment
Comment on: Cartwright et al. Biology Direct, 6:7
Article mis-states the yeast convention (Ken Wolfe, 01 March 2011)
The article mis-states the yeast convention. The Watson strand is the strand with its 5' end at the left telomere, but the left arm is not always the shorter arm of a yeast chromosome. In fact, the L arm is longer than the R arm for 7 of the 16 yeast chromosomes (up to 4 times longer, in the cases of chromosomes IX and XIV).
The left/right nomenclature for yeast chromosome arms dates back to the early days of yeast genetic maps, but I do not know who introduced it. Cytogenetics is not really possible for Saccharomyces because the chromosomes are too small and do not have extensive heterochromatin at centromeres, so nobody knew which arm was the shorter one until chromosome-sized genetic (and eventually genomic) maps became available. Oliver et al (Nature 357:38, 1992) then... read full comment
Comment on: Cartwright et al. Biology Direct, 6:7
I am suppose that PyrD polarization in this article is incorrect (Valery Anisimov, 07 December 2010)
For sure this paper propose a new interesting method for the indels polarization based on the structural analysis. But on the same time we should be careful in this point because without clear rules of it implementation sometimes we can come to the wrong conclusions. I think that PyrD polarization made by authors in this paper is exactly the case of applying such muddy logic.
First of all the authors claims that polarization of the PyrD indel using HemE protein as an outgroup made by Skophammer and others is questionable. I am totally agree with this statement. But then they are also rejected polarization of the PyrD based on the consideration of HisA and HisF proteins as outgroup, claimed that "indel arguments contradict themselves". I do not see a logic in the last statement. Why if... read full comment
Comment on: Valas et al. Biology Direct, 4:30
I am particularly agree with the author in some points. (Valery Anisimov, 02 December 2010)
According to myself investigations based on the analysis of the percentage of the genes shared by different bacterial clades, closest clade to Archaea is Actinobacteria and for Bacillus closest one of course Clostridia but on the second place we can see again Actinobacteria. So it is quite possible that Actinobacteria, Neomura and Bacillus had the common ancestor. But based on the analysis of the genes reading directions distributions inside bacterial genomes I guess that this common ancestor was close to Clostridia clade. LUCA probably had RNA-based chromosome which in the secondary structure was organized as one huge stem. So during transcription process ribosome can move only one way. As consequence all genes had the same reading direction. Afterwards when RNA-based genome was... read full comment
Comment on: Cavalier-Smith Biology Direct, 5:7
GC% and AG% not independent (Donald Forsdyke, 25 November 2010)
There is a reciprocal relationship between GC% and AG%.
There are two ways to modulate (G+C)% when the total number of bases is constant; either by changing the number of G’s, or by changing the number of C’s. As (G+C)% increases, trading A for G would not affect the AG%. Likewise, trading T for C would not affect the AG%. However, if T were replaced by G, the AG% would increase as (G+C)% increases. Conversely, if A were replaced with C the AG% would decrease as (G+C)% increases.
The latter inverse relationship is observed in bacteria (Lao & Forsdyke 2000; Mortimer & Forsdyke 2003) and eukaryotes (Cristillo et al 2001), and is extensively discussed in my textbook - Evolutionary Bioinformatics (Springer 2006).
... read full comment
Comment on: Zhang et al. Biology Direct, 5:63
Correction of Acknowledgement (Mark Ragan, 07 June 2010)
This paper was developed from a talk I gave at ISHPSSB-2009 on the invitation of Maureen O'Malley (Exeter University). An incorrect attribution is given in the Acknowledgements. read full comment
Comment on: Ragan Biology Direct, 4:43
BIO INSIPER NANOTECH: COST ACTION 2010 (Paolo Manzelli, 06 April 2010)
BIO-INSPIRED NANOTECH. EUROPEAN COST ACTION 2010.
Notes and suggestion by Paolo Manzelli <pmanzelli@gmail.com>
To Jean-Jacques Toulmé <jean-jacques.toulme@inserm.fr> and colleagues in address .
I would like to suggest to develop a section on Quantum Entanglement and Biological information Exhange on the basis of the following considerations.
As a matter of facts the basic question of Bio-inspired technology is focused on undestanding a physical model of self-molecular assembly, in order to create complex systems of Bio-inspired Tech.at nano scale. To understand the underlining criteria of self assembly I think that science need to overcome the traditional mechanical approach of physics and need to to develop a complete... read full comment
Comment on: Ogryzko Biology Direct, 3:15
ImRNA or RNA antibody model? (Donald Forsdyke, 09 October 2009)
The author's appendix (p. 11) summarizes nine steps in the proposed "imRNA response mechanism." Two of these are weak.read full comment
Step 3: Recognition of foreign viral mRNA "possibly by host reverse transcriptases RT." But how does reverse transcriptase distinguish between self and not-self RNAs?
Step 6: Integration into host genome. But there is no distinction between somatic cells and germline cells. How is the "Weismann barrier" breached in the case of germline cells? As Koonin points out, there is Lamarckian element here.
While there is much indirect evidence, ably summarized by Flegel, that support his model (especially bacterial CRISPR systems), the above objections are overcome in the "RNA antibody" model we suggested (see
Comment on: Flegel Biology Direct, 4:32
good idea, again (William Martin, 24 September 2009)
In 2003, Ford Doolittle called this the "Genome of Eden" constraint, in Phil Trans Roy Soc Lond B. In 2007 (PNAS) and 2008 (PNAS), Tal Dagan used it to estimate LGT frequency and cumulative impact among prokaryotes. Good idea, again. read full comment
Comment on: Isambert et al. Biology Direct, 4:28
An early warning against rejection-free claim for iPS cells (Shi Liu, 04 September 2009)
I have been wondering why almost all the transplantations of iPSCs (induced pluripotent stem cells) were done on SCID mice rather than on normal mice. As a matter of fact I even publicly questioned the study design of a study and asked: Why a study aimed at showing a "circumvention of the immune rejection barrier" by using iPSC-based therapy would still use sub-lethally irradiated mice as the recipients? (see publication at http://im1.biz/displayimage.php?album=84&pos=1 ).
I think the results presented here should serve as a warning against many naive claims for cell therapy. Immunity may be more tricky than we have thought of and reprogramming cells may even present or expose some antigens subject to rejection reactions.
read full comment
Comment on: Dressel et al. Biology Direct, 4:31
Response from the authors (Robson Francisco De Souza, 26 August 2009)
1) The sequences corressponding to the structures in PDB for the Anabaena protein are indeed different from those derived from the genomic sequence. Given that the domain is short any such change, even if at the termini, appear to distort the key structural elements. This justifies our exclusion of the Anabaena structures from further analysis.
2) This is indeed true and this observation reinforces our basic inference that there is no strict link between functions of solo ASRAH proteins and ASR-type sensory rhodopsins.
read full comment
Comment on: De Souza et al. Biology Direct, 4:25
A few remarks (Leonid Brown, 20 August 2009)
1) The authors claim that "Examination of the structures reveals that key structural elements of the
Anabaena representative have been mutated to obtain its crystal structure." I believe this is incorrect. There are parts of the structure which are missing due to disorder, but there are no mutations in the main sequence, with the exception of His-tags added on either of the termini.
2) Not only there are many rhodopsin-less species in which ASRT homologs are found, but there are also several bacterial species having homologs of ASR, but no ASRT. read full comment
Comment on: De Souza et al. Biology Direct, 4:25
A great example of science in action (Stephen Curry, 30 March 2009)
I thought this a very interesting paper that shed important light on the difficulties inherent in predicting structure from sequence - and in correcting earlier errors. The insights derived from the exchanges between reviewers and authors were particularly illuminating. I've mentioned the paper on my blog as an example of the great value of openness in the publication procedure.
read full comment
Comment on: Kinch et al. Biology Direct, 4:2
1R or 2R (Amir Abbasi, 22 December 2008)
Among the "Whole genome duplication" scenario proponents there are two versions of Ohno,s hypothesis, some has suggested two round (2R) scenario (leading to octaploids), whereas others only one round (1R) of whole genome duplication (leading to tetraploids, please see Ref 25 of this manuscript, and also see Gu et al 2002 Nat.Genet.31, 205-209 and Durand Dannie TRENDS in Genetics Vol.19 No1 Jan 2003). The title of the manuscript refers to 1R. However in the text I provide a critical overview of 2R also (please see in particular the sections “Paralogy regions in the Human genome” and “HOX cluster duplication and the history of vertebrate genome evolution”. I can hope this comment will let the readers to understand the title of this manuscript. <br><br>I... read full comment
Comment on: Abbasi Biology Direct, 3:50
octaploids (Herman Van Eck, 16 December 2008)
Two rounds of genome duplication would generate from diploids -> tetraploids and from tetraploids -> octaploids. <br><br>So I do not understand the title of the paper. <br><br>In fact there is a paper on this issue that indeed refers to octaploidy.<br>TJ Gibson and J Spring (2000) Evidence in favour of ancient octaploidy in the vertebrate genome, Biochem Soc Trans 28:259–264. read full comment
Comment on: Abbasi Biology Direct, 3:50
Correction and citation (Dustin Holloway, 07 October 2008)
Although the KEGG database is mentioned at several points within the text, readers should also note that the layout of the WNT pathway as seen in Figure 4 was modeled after that seen in the KEGG WNT Signaling Pathway(http://www.genome.jp/kegg/pathway/hsa/hsa04310.html).Please also note that, in Figure 2, the y-axis is the Positive Predictive Value (PPV).Finally, identifiers for several of the TFs in the bottom portion of Figure 6A are missing. The TFs should be labeled (from left to right) SRF, E2F, Mef2a, T3R, YY1, and CebpB.We apologize for any inconvenience this may have caused the sophisticated reader. read full comment
Comment on: Holloway et al. Biology Direct, 3:24
Figure Correction (Dustin Holloway, 07 October 2008)
Please note the following minor correction to Figure 1:The small box on the bottom right hand corner of Figure 1 contains the following text: "100X Average Accuracy." This should instead read "50X Average Accuracy." (The Figure legend provides the correct number). Also, the text directly next to the box should read "Average the Accuracy Estimates Over 50 Repeats", rather than "...Over 100 Repeats." read full comment
Comment on: Holloway et al. Biology Direct, 3:22
additional supporting information for the article (Neil Smalheiser, 03 April 2008)
In my article (section 5d, Cargo proteins within postsynaptic exosomes, subsection b, AMPA receptors), I made the statement that “to my knowledge, no physiologic role for presynaptic AMPA receptors has been described.” Thus, I surmised that AMPA receptor proteins and/or mRNAs carried from postsynaptic to presynaptic terminals would have no physiological significance, but might instead provide a way for the postsynaptic terminal to shed AMPA receptors. However, more recently, I have become aware that there is an extensive literature documenting the presence and physiological relevance of presynaptic AMPA receptors in hippocampal and sensory ganglion neurons, among other neuronal cell types. (See Matsuda et al (2008) [1] for discussion and a partial list of references.) This... read full comment
Comment on: Smalheiser Biology Direct, 2:35
Acknowledged reference (Andrea Melendez, 10 March 2008)
To access the above referenced article please click here. read full comment
Comment on: Haft et al. Biology Direct, 3:4
Acknowledging an earlier observation of orphan SelD (Daniel Haft, 04 March 2008)
Just after publication of our manuscript, we came across the following reference: Zhang Y, Romero H, Salinas G, Gladyshev VN., Dynamic evolution of selenocysteine utilization in bacteria: a balance between selenoprotein loss and evolution of selenocysteine from redox active cysteine residues. Genome Biol. 2006;7(10):R94. Epub 2006 Oct 20. We launched our study from the observation that SelD proteins explained by neither selenocysteine nor selenouridine pathways might imply a third SelD-dependent trait. The orphan status of SelD in Enterococcus faecalis and Haloarcula marismortui and possibility of SelD-dependence for selenium-dependent molybdenum hydroxylases were raised previously by Zhang, et al., and should have been cited as background to this paper. We regret having been unaware of... read full comment
Comment on: Haft et al. Biology Direct, 3:4
Darwin Was Indeed Wrong but Koonin’s Revolution May Not Be Novel (Shi Liu, 22 October 2007)
In 1991 I already pointed out the major mistakes made by Darwin which included his assertion that all extent lives were descended from a common ancestor cell and his simple and exclusive treatment of similarity with genealogically inherited identity (1). My alternative view on the origin and evolution is that life might have independently originated from multiple acellular ancestors and that similarity among different organisms may be a reflection of non-phylogenetic formations by a common mechanism (1). My theory treats biotic evolution as a companion process to the abiotic evolution and thus the events and history of biotic evolution should naturally reflect the abiotic course of evolution. Like the Big Bang events happened in the formation and evolution of the abiotic world, similar... read full comment
Comment on: Koonin Biology Direct, 2:21
Examine macroevolutionary concepts carefully (Nicholas Matzke, 29 August 2007)
Well, since it is clear that this paper will be on every ID/creationist blog on the planet in under 12 hours, I might as well put in my 2 cents early. I will say at the outset that I have immense respect for Eugene Koonin and his contributions to numerous fields, and criticize his work with some trepidation. However, I think with this paper he has unfortunately tumbled into a series of mistakes that have repeatedly afflicted those trying to understand macroevolution without taking sufficient care in examining the concepts they are relying upon.I will enumerate some of them, in no particular order:1. Treating Linnaean categories as "real", and thinking about them in a typological manner rather than phylogeneticallyThis is most clearly exposed in Koonin's discussion of the Cambrian phyla... read full comment
Comment on: Koonin Biology Direct, 2:21
Absence of evidence or evidence of absence? (Daniel Silvestre, 23 August 2007)
The presented hypothesis is quite ingenious and is something pleasant to read in these days of pragmatic science. But, I can see that something is missing. This article demonstrate clearly that viruses share "common" features (synapomorphies?) not shared by any kind of cellular life. Hence, is reasonable to assume that all viruses descend from a common ancestor. The missing point is: how one can decide who appeared first (cells or viruses) with this type of evidence? There is no possible outgroups/transition analysis to handle this issue, to my known experience. There is no fossil evidence of viruses predating cellular life nor evidence of absence of cellular with the presence of viruses. Therefore, with the evidence and arguments presented in this paper give sound basis to the existence of... read full comment
Comment on: Koonin et al. Biology Direct, 1:29
Re: Running before walking (Albert de Roos, 20 June 2007)
In reply to the comment of Niles Lehman, it is true that I do assume single-stranded oligonucleotides to be available and where I write that single stranded RNA (ssRNA) preceded double-stranded RNA, I mean ssRNA as the carrier of catalytic function.I also notice that my perception of OOL research is different from that of the mainstream scientists in the field, as also indicated by the reviewers of the manuscript and would like to expand a little on it. I do assume the presence of ribonucleotides as the building blocks of life, but recognize that this is indeed not trivial and I do not deny that there seem important chemical hurdles to take for an abiotic generation of oligo-ribonucleotides (or its precursors). However, ribonucleotides are the actual building blocks of Life as we know it... read full comment
Comment on: de Roos Biology Direct, 2:12
Running before walking? (Niles Lehman, 18 June 2007)
I read the article by DeRoos with interest. However, it is not clear to me how dsRNA could preceed ssRNA. If dsRNA is the precursor to ssRNAs with some activities or phenotypes, how would the dsRNA arise in the first place? The hybridization model presented in Figure 2 presupposes the existence of ssRNA oligomers. This seems counterintuitive ... or am I missing some key point? read full comment
Comment on: de Roos Biology Direct, 2:12