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Nguyễn Xuân Hưng

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Lời bình cho các bài báo mới và có chất lượng

trang F1000 hiện giờ cung cấp một dịch vụ nhằm bình chọn và đưa ra các lời bình luận cho các bài báo mới và có chất lượng khoa học cao nhất (từ PubMed).

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Đầu tiên là top10

1. F1000 Factor 10.4
http://www.ncbi.nlm.nih.gov/entrez/...ds=15790847&dopt=Abstract&holding=f1000,hulib

Widespread parallel evolution in sticklebacks by repeated fixation of Ectodysplasin alleles.
Colosimo PF, Hosemann KE, Balabhadra S, Villarreal G, Dickson M, Grimwood J, Schmutz J, Myers RM, Schluter D, Kingsley DM
Science 2005 Mar 25 307(5717):1928-33

Trudy Mackay
North Carolina State University, United States of America
DEVELOPMENTAL BIOLOGY

Comments
Trudy Mackay
North Carolina State University, United States of America
DEVELOPMENTAL BIOLOGY

New Finding
This paper provides one answer to two longstanding and open questions regarding the basis of adaptive evolution: is the basis of adaptive evolution due to single genes with large effects or multiple quantitative trait loci (QTL) with individually small effects; and if the former, is the repeated evolution of the same adaptation attributable to multiple independent mutations in the same gene, a single mutation event harbored at low frequency in multiple populations, or mutations in different genes? While marine threespine sticklebacks have extensive bony armour, freshwater populations have repeatedly evolved a reduction in this armour. Colosimo et al. show that the reduction in armour is largely attributable to a single QTL with large effect, with minor modifier loci. High resolution mapping and positional cloning of the major QTL revealed the candidate gene to be Ectodysplasin (Eda). Thus, adaptive evolution can at least sometimes have a simple genetic basis. Further, the same Eda haplotype was found in several North American and European freshwater populations, while a different Eda haplotype was observed in a Japanese population. Thus, at least two independent mutations in the same gene led to the same adaptive phenotype, and there is a single genetic basis for the evolution of reduced armour in the North American and European populations.

Evaluated 3 May 2005


Richard Harrison
Cornell University, United States of America
GENOMICS & GENETICS

This paper uses positional cloning and linkage disequilibrium mapping to identify the gene responsible for major differences in armor plate patterning between marine and freshwater sticklebacks. The authors provide gene genealogical data to support the hypothesis that parallel selection of alleles at the Ectodysplasin locus (Eda) has led to repeated evolution of low-plated phenotypes in freshwater environments. By constructing transgenic fish containing the mouse version of the Eda gene, the authors provide additional support for a role for this gene in the parallel evolution of the novel phenotype. This paper is an elegant exemplar of what can be done using modern genomic approaches to document the genetic and molecular basis of an important evolutionary transition driven by natural selection.

Evaluated 26 Apr 2005


Tony Long
University of California, Irvine, United States of America
GENOMICS & GENETICS

Another brilliant piece of work by the Kingsley group on the evolution of armor plating in stickleback fish. The authors positionally clone a gene that leads to an adaptive reduction in body armor in numerous stickleback populations. Cloning this gene was an incredibly difficult piece of work, and represents one of only a handful of examples where we now have insight into the molecular basis of morphological evolution. It was always thought that the stickleback in different watersheds have independently evolved a reduction in armor plating (in fact this character is a textbook example of repeated convergent evolution). Very surprisingly, this paper shows that many different populations harbor the same recessive allele leading to armor reduction that apparently can migrate between populations in marine morphs if covered by the dominant allele. Time to rewrite the textbooks!

Evaluated 25 Apr 2005


Patricia Simpson
University of Cambridge, United Kingdom
DEVELOPMENTAL BIOLOGY

This study presents new hope to all those working in nonmodel systems that, with heroic effort, one can actually identify with some confidence the gene(s) involved in natural adaptations. The authors used QTL mapping, sequencing, and transgenics to indicate that the same Ectodysplasin alleles were fixed in disparate populations causing parallel evolution of armor plating. There is some indication an independent mutation may also have caused the same phenotype in an isolated population, but the evidence for this secondary result was significantly weaker. Hence, it appears repeated selection on the standing genetic variation already present in marine ancestors caused parallel evolution of armor plating in these sticklebacks.

Evaluated 18 Apr 2005


Detlef Weigel
Max Planck Institute for Developmental Biology, Germany
PLANT BIOLOGY

This paper sets a new standard in the identification of adaptive variants found in nature. The authors not only use QTL (quantitative trait locus) cloning to identify a locus controlling plate morphology in natural populations of sticklebacks, but also show that the same rare haplotype present in marine forms was selected during the formation of plateless freshwater forms, where it became fixed. This happened apparently independently all over the world. This paper has almost everything; the only important experiment missing was transformation of a functional natural allele into a background with a reduced-function allele.

Evaluated 6 Apr 2005
 
2. F1000 Factor 10.1
http://www.ncbi.nlm.nih.gov/entrez/...ds=15831759&dopt=Abstract&holding=f1000,hulib

Reconstitution of circadian oscillation of cyanobacterial KaiC phosphorylation in vitro.
Nakajima M, Imai K, Ito H, Nishiwaki T, Murayama Y, Iwasaki H, Oyama T, Kondo T
Science 2005 Apr 15 308(5720):414-5

Katherine Osteryoung
Michigan State University, United States of America
PLANT BIOLOGY

Amazingly, this paper demonstrates that the rhythmic, in vivo cycle of autophosphorylation-dephosphorylation of the cyanobacterial circadian clock protein KaiC can be reconstituted in vitro with recombinant KaiC. All it took was combining KaiC with ATP and two additional clock proteins, KaiA and KaiB.

Evaluated 9 May 2005

Martin Egli
Vanderbilt University, United States of America
STRUCTURAL BIOLOGY

Reports the fascinating and unexpected finding that incubation of the recombinant clock protein KaiC from the cyanobacterium Synechococcus elongatus with KaiA, KaiB and ATP in vitro produces a self-sustainable oscillation of KaiC phosphorylation. The period of this in vitro oscillation is temperature compensated (stable despite temperature change!), demonstrating that the basic features of a biological clock can be reconstituted in vitro and persist without transcription and translation. The work shows that interactions of various kinds between the KaiA, KaiB and KaiC proteins and ATP produce a minimal molecular timer and points the way to a more detailed examination of the clockwork with biochemical, biophyscial and structural tools.

Evaluated 4 May 2005

Ueli Schibler
University of Geneva, Switzerland
CELL BIOLOGY

This spectacular paper shows that robust circadian rhythms of protein phosphorylation can be generated in the test tube with three recombinant proteins and ATP. In cyanobacteria, a circadian clock regulates the expression of virtually all genes. This molecular oscillator depends on a small operon encompassing the three genes KaiA, KaiB, and KaiC. KaiC protein can act as both an autokinase and an autophosphatase, and depending on its phosphorylation status and the transient interactions it establishes with KaiA and KaiB proteins, the kinase or phosphatase activity will prevail temporarily. This leads to a daily cycle of KaiC phosphorylation in vitro similar to that observed in living cyanobacteria kept in constant darkness.

Evaluated 28 Apr 2005

C. Robertson McClung
Dartmouth College, United States of America
PLANT BIOLOGY

This study announces the stunning achievement of in vitro reconstitution of a biological circadian clock; the circadian oscillation in the phosphorylation state of the cyanobacterial clock protein KaiC can be generated simply by incubation of the three clock proteins, KaiA, KaiB and KaiC, together with ATP. In most model organisms, the core oscillator of the circadian clock appears to be a pair of interlocked negative feedback loops in which transcription and translation of clock genes and their mRNAs play critical roles. At least in this simple organism, gene expression is not an essential component of the oscillator; how the activities of and interactions among the three cyanobacterial proteins are sufficient to generate a robust self-sustaining and temperature-compensated circadian rhythm will be a fascinating study.

Evaluated 19 Apr 2005
 
3. F1000 Factor 9.7

http://www.ncbi.nlm.nih.gov/entrez/...ds=15750596&dopt=Abstract&holding=f1000,hulib

Santa Jeremy Ono
University College London, United Kingdom
IMMUNOLOGY

This is the first study to identify a key pathway involved in the resolution of an inflammatory response. The data clearly show that the D6 chemokine receptor is essential for the resolution of beta-chemokine induced inflammation. As beta-chemokines are key drivers of early and late phase allergic inflammation, this finding is very important. The work also has clear implications for the design of new anti-inflammatory compounds based upon modeling of the D6/chemokine interaction, rationale drug design and compound library mining.

Evaluated 29 Apr 2005


Barry Rouse
University of Tennessee, United States of America
MICROBIOLOGY

We know far more about the causes of inflammation than how it is resolved. The provocative paper of Jamieson et al. implies that resolution depends, at least in part, on soaking up and ignoring the signals of chemokines involved in causing inflammation. It seems that a single so-called decoy chemokine receptor D6 serves such a role against numerous b-chemokines. Thus, without D6, inflammatory reactions were far more severe and persistent. Accordingly, D6 helps prevent initiation but it is not clear if it plays a similar role in resolution. Should this be so, there could be a place for overexpressing such decoys to control pathological inflammatory disease.

Evaluated 26 Apr 2005

Steve Ward
University of Bath, United Kingdom
IMMUNOLOGY

This article provides a fascinating and timely insight into how the "silent" chemokine receptor D6 is involved in the clearance of CC chemokines and hence may play a key role in the control and resolution of inflammatory responses. D6 is expressed on lymphatic endothelium of many organs, but it is not coupled to G proteins and so is, therefore, thought unable to generate classic biochemical responses elicited by other G protein-coupled chemokine receptors. The authors used targeted disruption of the gene encoding D6 to identify the biological role of D6, which has so far remained elusive. In models of cutaneous inflammation, they observed significantly higher concentrations of CCL2 and CCL3 in the knock-out mice, consistent with a role for D6 in post-inflammatory clearance of CC chemokines from the skin. The phenotype of the D6 deficient mice is reminiscent of human psoriasis including epidermal hyperproliferation and inflammatory cell (notably T cell and mast cell) infiltration. The inflammatory pathology that develops in D6-null mice is T cell dependent. However, infiltration of T cells into the epidermis is also partially responsible for mast cell recruitment, raising the possibility that these cells and their granule products also contribute to the pathology. Finally, we have some concrete evidence to substantiate the long-held notion that D6 functions to mop up chemokines and thus helps maintain immune homeostasis or resolve inflammation. Great stuff!
 
4. F1000 Factor 9.6
http://www.ncbi.nlm.nih.gov/entrez/...ds=15781854&dopt=Abstract&holding=f1000,hulib

Mammalian motor neurons corelease glutamate and acetylcholine at central synapses.
Nishimaru H, Restrepo CE, Ryge J, Yanagawa Y, Kiehn O
Proc Natl Acad Sci U S A 2005 Apr 5 102(14):5245-9

Judith S. Eisen
University of Oregon, United States of America
NEUROSCIENCE

Vertebrate motor neurons are among the best-studied cholinergic neurons; therefore, it is startling to learn that mammalian motor neurons release both acetylcholine and glutamate at their central synapses. The authors found no evidence for glutamate release from motor neuron peripheral synapses at neuromuscular junctions, providing evidence that these cells have the ability to segregate different neurotransmitters to different synapses. Many conserved genes regulate development of vertebrate and arthropod motor neurons; however, with a few notable exceptions, most arthropod motor neurons apparently use glutamate as their excitatory neurotransmitter at neuromuscular junctions. Thus, in addition to opening up new areas of investigation of motor neuron function, this new finding may shed light on evolutionary relationships between vertebrate and arthropod motor neurons.

Evaluated 9 May 2005

Jan-Marino Ramirez
University of Chicago, United States of America
NEUROSCIENCE

This study reports the unexpected finding that mammalian motoneurons release not only acetylcholine but also glutamate at central synapses. This finding breaks with the long-held notion that these motoneurons exert their excitatory effect only via cholinergic synapses. Equally unexpected and novel is the demonstration that glutamate is only co-released to excite Renshaw cells but not to excite muscles. This finding is incompatible with the principle first coined by Dale in 1935 that the same transmitter is released from all terminals in a single neuron. Mammalian motoneurons may therefore serve as exciting models to unravel the intracellular mechanisms that regulate internal transmitter sorting.

Evaluated 27 Apr 2005
 
5. F1000 Factor 8.2
http://www.ncbi.nlm.nih.gov/entrez/...ds=15802565&dopt=Abstract&holding=f1000,hulib

Structure of the Rotor of the V-Type Na+-ATPase from Enterococcus hirae.
Murata T, Yamato I, Kakinuma Y, Leslie AG, Walker JE

Celerino Abad-Zapatero
Abbott Laboratories / University of Illinois at Chicago, United States of America
STRUCTURAL BIOLOGY

This paper and the following paper {1} provide another window into the structure and function of ATPases. The authors provide the structure of the rotor components of the vacuolar type (V-Type) of two different prokariotes. Structures of this complexity require years of dedicated work to understand their atomic mechanisms. However, these two papers make further inroads into the details. In particular, the symmetry mismatch between the rotor and the catalytic domains of ATPases and other biological nanomachines (i.e. DNA packaging and flagellar motors)seems to be a distinctive feature. {1} Meier et al. Science 2005, 308:659-62 [PMID:15860619].

Evaluated 6 May 2005

Robert Fillingame
University of Wisconsin, United States of America
STRUCTURAL BIOLOGY

The authors report the fascinating but surprising finding that crystals of the membrane traversing rotor of Enterococcus V-type ATPase contains 10 subunits, each folding with 4 transmembrane helices. Each subunit contains a single Na+ binding site and the resolution is sufficient to define liganding groups. Previous Na+ binding studies had suggested 6 saturable sites in the complete V-ATPase {1}. Single particle averaging of electron microscopic images had indicated a ring with 7-fold symmetry {2}. The 68 angstrom high membrane-traversing cylinder has a 39 angstrom wide peripheral belt of hydrophobic amino acid side chains. Its placement in lipid bilayer is of interest. {1} Murata et al. J Biol Chem 2000, 275:13415-9 [PMID:10788452], {2} Murata et al. J Biol Chem 2003, 278:21162-7 [PMID:12651848].

Evaluated 5 May 2005

Wolfgang Junge
Universitaet Osnabrueck, Germany
PLANT BIOLOGY

The authors present the first high-resolution structure (0.21 nm) of the central ring of the rotary 'electromotor' of a Na+-pumping V-ATPase. The C10-symmetrical ring, with twice the diameter of that of the F-ATPase, carries ten Na+-binding sites, each intercalated between two neighbouring double hairpin-shaped protomers and located in the middle of the membrane. The model qualifies previous EM-based speculation on a C7-symmetry of this ring.

Evaluated 28 Apr 2005
 
6. F1000 Factor 8.2
http://www.ncbi.nlm.nih.gov/entrez/...ds=15845854&dopt=Abstract&holding=f1000,hulib

A cellular microRNA mediates antiviral defense in human cells.
Lecellier CH, Dunoyer P, Arar K, Lehmann-Che J, Eyquem S, Himber C, Saïb A, Voinnet O
Science 2005 Apr 22 308(5721):557-60

Andy Maule
John Innes Centre, United Kingdom
PLANT BIOLOGY

It has previously remained a puzzle as to why RNA interference (RNAi)-mediated defence against viruses, which is so prevalent in plants, has not been apparent in humans despite the presence of much of the same core RNAi machinery. This paper reports the exciting discovery that the retrovirus primate foamy virus type 1 (PFV-1) is constrained in human cells by an RNAi-related mechanism. In this case, PFV-1 is targeted fortuitously by an endogenous miRNA (miR-32) that potentially inhibits translation of the PFV-1 target gene, Bet, although the authors do not rule out an additional more direct antiviral effect mediated by siRNAs. PFV-1 is nevertheless able to replicate in the presence of miR-32, a process facilitated by Tas, a PFV-1 protein also shown to have RNAi suppressor activity. Thus, as for plant viruses, it appears that PFV-1 has co-evolved to overcome RNAi by developing suppressor functions.

Evaluated 5 May 2005

Fritz Eckstein
Max Planck Institute for Experimental Medicine, Germany
CHEMICAL BIOLOGY

This is a most interesting finding showing that a cellular microRNA restricts the accumulation of a retrovirus in human cells. This expands the role of microRNAs from a regulatory role to that of a defense mechanism, targeting foreign genetic material. Interestingly, the virus has developed a counter measure by encoding a protein that suppresses the microRNA function.

Evaluated 3 May 2005

Jim Smiley
University of Alberta, Canada
MICROBIOLOGY

Provides perhaps the most compelling evidence to date for RNA silencing as an innate antiviral defense mechanism in mammals, just as is so in plants and insects. The authors show that human miR-32 microRNA targets mRNAs of the primate retrovirus PFV-1 for translational silencing; a viral protein (Tas) in turn serves as a broad-spectrum RNA silencing suppressor that reverses this inhibition. Remarkably, Tas is active in both mammals and plants. Taken with previous data documenting that adeno- and pox-viruses also encode RNA silencing suppressors, the results strengthen the case that RNA silencing represents an ancient and highly conserved anti-viral defense mechanism.

Evaluated 29 Apr 2005
 
7. F1000 Factor 8.1
http://www.ncbi.nlm.nih.gov/entrez/...ds=15758953&dopt=Abstract&holding=f1000,hulib

Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage.
Falck J, Coates J, Jackson SP
Nature 2005 Mar 31 434(7033):605-11

Stephen Elledge
Harvard Medical School, United States of America
CELL BIOLOGY

This is a nice study because it points out that the PIKK family DNA-dependent protein kinases, DNA-PK, ATM, and ATR, which are structurally related, bind their distinct specificity subunits in a similar manner. An interesting future area of investigation is whether these specificity subunits, MRN, ATRIP and KU, actually bind to a related sequence on the PIKK family member. Overall, this study contributes to understanding part of the structural relationships between these subunits, which will be fully resolved when the structures are eventually solved.

Evaluated 27 Apr 2005

William Earnshaw
University of Edinburgh, United Kingdom
CELL BIOLOGY

Just when I had thought that the mechanism of ATM recruitment to DNA breaks was totally obscure, this elegant study reports a simple mechanism for recruitment of all the phosphoinositide-3-kinase-related protein kinases (PIKKs) to breaks. Starting with a peptide-binding assay using the conserved C-terminus of Nbs1 (mutated in Nijmegen breakage syndrome), the authors show that ATM, ATR and DNA-PKcs are all recruited directly to DNA breaks by interactions with the C-termini of partner proteins. This is an elegant and convincing study that provides a major step forward in our understanding of the DNA damage checkpoint responses of mammalian cells.

Evaluated 22 Apr 2005

Michael B. Yaffe
Massachusetts Institute of Technology, United States of America
CELL BIOLOGY

In an elegant example of sequence gazing, Jackson and colleagues have identified a novel evolutionarily conserved sequence motif at the C termini of several DNA damage signaling molecules that is essential for recruiting DNA damage kinases to DNA lesions. The short motif, which appears to involve two pairs of acidic residues within a span of ~10 amino acids, allows Nbs1 to bind and target ATM to double strand breaks, allows Ku80 to bind and target DNA-PK to free DNA ends, and allows ATRIP to bind and target ATR to single strand DNA. In each case, the motif is required for activation of checkpoint signaling events to occur downstream from these DNA damage kinases. While the structural basis for interaction of the motif with these PI 3-kinase-related protein kinases has yet to be fully explored, the intriguing observation that the HEAT repeats of ATM are required for the interaction with the motif in Nbs1 suggests a novel function for this part of ATM whose function has remained largely mysterious. In addition, the conserved nature of the motif in 3 distinct types of DNA damage signaling attests to its evolutionary utility in regulating kinase activity through a common as-yet-unknown mechanism.

Evaluated 11 Apr 2005
 
7. F1000 Factor 8.1

http://www.ncbi.nlm.nih.gov/entrez/...ds=15758953&dopt=Abstract&holding=f1000,hulib

Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage.
Falck J, Coates J, Jackson SP
Nature 2005 Mar 31 434(7033):605-11

Stephen Elledge
Harvard Medical School, United States of America
CELL BIOLOGY

This is a nice study because it points out that the PIKK family DNA-dependent protein kinases, DNA-PK, ATM, and ATR, which are structurally related, bind their distinct specificity subunits in a similar manner. An interesting future area of investigation is whether these specificity subunits, MRN, ATRIP and KU, actually bind to a related sequence on the PIKK family member. Overall, this study contributes to understanding part of the structural relationships between these subunits, which will be fully resolved when the structures are eventually solved.

Evaluated 27 Apr 2005


William Earnshaw
University of Edinburgh, United Kingdom
CELL BIOLOGY

Just when I had thought that the mechanism of ATM recruitment to DNA breaks was totally obscure, this elegant study reports a simple mechanism for recruitment of all the phosphoinositide-3-kinase-related protein kinases (PIKKs) to breaks. Starting with a peptide-binding assay using the conserved C-terminus of Nbs1 (mutated in Nijmegen breakage syndrome), the authors show that ATM, ATR and DNA-PKcs are all recruited directly to DNA breaks by interactions with the C-termini of partner proteins. This is an elegant and convincing study that provides a major step forward in our understanding of the DNA damage checkpoint responses of mammalian cells.

Evaluated 22 Apr 2005


Michael B. Yaffe
Massachusetts Institute of Technology, United States of America
CELL BIOLOGY

In an elegant example of sequence gazing, Jackson and colleagues have identified a novel evolutionarily conserved sequence motif at the C termini of several DNA damage signaling molecules that is essential for recruiting DNA damage kinases to DNA lesions. The short motif, which appears to involve two pairs of acidic residues within a span of ~10 amino acids, allows Nbs1 to bind and target ATM to double strand breaks, allows Ku80 to bind and target DNA-PK to free DNA ends, and allows ATRIP to bind and target ATR to single strand DNA. In each case, the motif is required for activation of checkpoint signaling events to occur downstream from these DNA damage kinases. While the structural basis for interaction of the motif with these PI 3-kinase-related protein kinases has yet to be fully explored, the intriguing observation that the HEAT repeats of ATM are required for the interaction with the motif in Nbs1 suggests a novel function for this part of ATM whose function has remained largely mysterious. In addition, the conserved nature of the motif in 3 distinct types of DNA damage signaling attests to its evolutionary utility in regulating kinase activity through a common as-yet-unknown mechanism.

Evaluated 11 Apr 2005
 
8. F1000 Factor 8.0

http://www.ncbi.nlm.nih.gov/entrez/...ds=15829956&dopt=Abstract&holding=f1000,hulib

DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis.
Bartkova J, Horejsí Z, Koed K, Krämer A, Tort F, Zieger K, Guldberg P, Sehested M, Nesland JM, Lukas C, Ørntoft T, Lukas J, Bartek J
Nature 2005 Apr 14 434(7035):864-70

Michael B. Yaffe
Massachusetts Institute of Technology, United States of America
CELL BIOLOGY

A new beam of light into the confusion regarding DNA damage signaling and human tumorigenesis! In this fascinating paper, Lukas, Bartek and colleagues report that early stage precancerous lesions and low-grade malignant tumors in humans contain evidence of activated DNA damage signaling pathways, prior to the emergence of mutations in p53, the acquisition of genomic instability, or the display of invasive behaviour. Activation of the ATM/Chk2 pathway in bladder, breast, colon, and lung tumors was seen in human tissue samples, and the activation of this pathway could be recapitulated in cultured U2OS cells by forced unscheduled DNA replication induced by S-phase promoting oncogenes. Interestingly, many of the lesions appeared to contain RPA, a marker of single stranded DNA that one naively associated with ATR/Chk1 activation as well. The authors propose that activation of the DNA damage response early in tumorigenesis may help to suppress cell proliferation, and that tumors arise when cells somehow escape from these early lesion checkpoints. It now seems clear that defining the role of additional checkpoint pathways and the mechanisms underlying checkpoint bypass will prove instrumental in developing a better understanding of tumor progression in vivo.

Evaluated 6 May 2005


Tom Misteli
National Cancer Institute, NIH, USA, United States of America
CELL BIOLOGY


This study shows that DNA damage pathways are activated in early tumors. The concept is put forth that these pathways contribute to preventing tumorigenesis upon oncogenic insult and that mutations compromising DNA damage checkpoints facilitate tumor progression. See also comments on Gorgoulis et al., Nature 2005, 434:907-13 [PMID:15829965].

Evaluated 20 Apr 2005
 
9. F1000 Factor 6.6

http://www.ncbi.nlm.nih.gov/entrez/...ds=15824132&dopt=Abstract&holding=f1000,hulib

Inhibition of the anaphase-promoting complex by the Xnf7 ubiquitin ligase.
Casaletto JB, Nutt LK, Wu Q, Moore JD, Etkin LD, Jackson PK, Hunt T, Kornbluth S
J Cell Biol 2005 Apr 11 169(1):61-71

Arp Schnittger
University of Cologne, Germany
PLANT BIOLOGY

"One RING to bind them" - A new regulator of the anaphase-promoting complex/cyclosome (APC/C) that also links this ubiquitin ligase with the spindle check point opens the door to a whole lot of new and exciting questions about one of the best studied protein complexes in cell biology. APC/C is an important E3 ligase, which facilitates the timely degradation of many cell cycle regulators, allowing cell cycle progression. APC/C has recently been found to be regulated by binding of a class of inhibitors (comprising EMI1, RCA1, XErp1). Casaletto and coworkers present now yet another inhibitor of APC/C, designated Xnf7. Interesingly, Xnf7 itself is a RING finger and displays ubiquitin ligase activity, which was found be required for its inhibitory function.

Evaluated 4 May 2005

Timothy Yen
Fox Chase Cancer Center, United States of America
CELL BIOLOGY

This paper reports a new spindle checkpoint assembly mechanism in Xenopus egg extracts that regulates the timing of mitosis by directly inhibiting the anaphase promoting complex (APC). The authors identify Xnf7 as a ubiquitin ligase that binds to and can directly inhibit the APC, and is required for spindle assembly checkpoint function. This mechanism differs from the accepted model where the checkpoint indirectly inhibits the APC by sequestering its specificity factor, Cdc20.

Evaluated 25 Apr 2005


Rebecca Heald
University of California, Berkeley, United States of America
CELL BIOLOGY

This study identifies the protein Xnf7 as a negative regulator of the anaphase promoting complex (APC) in Xenopus egg extracts that may link spindle status to APC activity. Xnf7 binds to APC core subunits and possesses E3 ubiquitin ligase activity that is required for its regulation of the APC, though its substrates are unknown.

Evaluated 21 Apr 2005


Mary Dasso
National Institutes of Health, United States of America
CELL BIOLOGY

This paper shows that the RING finger ubiquitin ligase Xnf7 inhibits the anaphase-promoting complex/cyclosome (APC/C) in a manner that is important for activation or maintenance of the spindle assembly checkpoint in Xenopus egg extracts. Xnf7 binds directly to the APC/C and inhibits it in a manner that is dependent on Xnf7 ubiquitin ligase activity; this mechanism is distinct from other known APC/C inhibitors, which have been reported to modulate APC/C activity through its accessory factors, Cdc20 and Cdh1.

Evaluated 15 Apr 2005
 
10. F1000 Factor 6.6

http://www.ncbi.nlm.nih.gov/entrez/...ds=15845853&dopt=Abstract&holding=f1000,hulib

Comparative metagenomics of microbial communities.
Tringe SG, von Mering C, Kobayashi A, Salamov AA, Chen K, Chang HW, Podar M, Short JM, Mathur EJ, Detter JC, Bork P, Hugenholtz P, Rubin EM
Science 2005 Apr 22 308(5721):554-7

Robert Jackson
Duke University, United States of America
ECOLOGY

This novel paper examines DNA fingerprints of genes rather than of organisms. The authors also tie the genes observed in several environments to the physical characteristics of those environments. Ultimately, we need such approaches to link the molecular ecology of microbes to their biogeochemistry - what they are doing in nature.

Evaluated 4 May 2005

John Jaenike
University of Rochester, United States of America
GENOMICS & GENETICS

This important paper provides the first comparative analysis of both phylogenetic and functional diversity of entire microbial communities. The communities considered include those associated with farm soils, deep-sea whale carcasses, the Sargasso Sea, and an acid mine biofilm. A key finding is that microbial communities have distinctive profiles of encoded functions that are more similar within than between habitat types. Moreover, there are numerous genes whose functions are unknown, suggesting the existence of undiscovered functional systems. The extraordinarily high species diversity of these communities makes genome assembly nearly impossible, thus making it difficult to determine how the various functional systems are compartmentalized within and among species. This community-level analysis of functional genomics is reminiscent of the old idea of an ecological community as a superorganism, which, while no longer considered relevant for communities of macroscopic organisms, may be the only way to proceed in the analysis of microbial communities.

Evaluated 28 Apr 2005

Jeffrey Lawrence
University of Pittsburgh, United States of America
MICROBIOLOGY

This metagenomic survey of both terrestrial and marine environments offers few large contigs, but nonetheless a surprisingly good picture both of taxonomic diversity and functional diversity. For example, bacterial communities from marine "whale falls" were less diverse than those in soil environments, but their metabolic profiles inferred from KEGG classification of 150,000 sequence reads were similar, reflecting a shared, heterotroph-based community. The genes from whale-fall communities were functionally more similar to those from soil than to those from the Sargasso Sea sample or the Iron Mountain acid mine, demonstrating that metagenome profiles lacking large numbers of contiguous sequences can provide insight into community structure and metabolic potential.

Evaluated 27 Apr 2005

Daniel Vaulot
Centre National de la Recherche Scientifique, France
ECOLOGY

This paper proposes a new approach to exploit shot-gun metagenomics data. It does not try to reconstruct whole genomes, a nearly impossible task, but instead it links gene categories and environmental conditions. Metagenomics (Ecogenomics) looks like a very promising approach to assess the diversity of microbe functions in the environment. However, the recent paper by Venter et al. (Science 2004, 304:66-74 [PMID:15001713]) had sent shivers throughout the community because, after a daunting sequencing effort, only two genomes could be reconstructed. The present paper provides a very elegant way to make use of these data by focusing on genes, instead of on whole genomes.

Evaluated 25 Apr 2005
 
cám ơn Casper nhé. Cứ tiếp tục triển khai đê.
Tôi thấy có rất nhiều ng sưu tầm tài liệu về miRNA, mọi ng tham gia bình luận bài này đê.

A cellular microRNA mediates antiviral defense in human cells.
Lecellier CH, Dunoyer P, Arar K, Lehmann-Che J, Eyquem S, Himber C, Saïb A, Voinnet O
Science 2005 Apr 22 308(5721):557-60
 

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