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For a comprehensive review of the most interesting recent articles published in the biological sciences, visit Faculty of 1000 Biology, an online literature awareness tool published by BioMed Central. Faculty of 1000 Biology systematically highlights exciting recent publications on the basis of recommendations of a faculty of well over 1,000 of the world's leading researchers. |
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Deborah Charlesworth
University of Edinburgh, United Kingdom
PLANT BIOLOGY
 Confirmation
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In this study, the authors test and confirm the hypothesis that GC content of genes can be increased due to biased gene conversion between duplicated gene pairs that are not close together in the genome. The clever idea was to use duplicated gene pairs in yeast and Arabidopsis. Some are recent duplicates with highly similar sequences, and these should undergo exchanges that could increase GC content, but other duplicates' sequences would be too different for this. Thus a correlation is expected between GC content of pairs, and their sequence similarity, but this correlation should be due to the first group of duplicates, and not observed for those whose divergence is large. This is exactly what was observed, using GC in 3rd positions of codons, supporting indirect inferences of Innan and colleagues (Science 2004, 306:1367-70 [PMID:15550669]).
Evaluated 23 Aug 2005 |
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R. Scott Hawley
Stowers Institute for Medical Research, United States of America
CELL BIOLOGY
 New Finding
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This paper describes a beautiful study of the effects of heterozygous insertions in C. elegans. The authors first demonstrate that interference can cross the gap in homology created by insertion heterozygosity. Most interestingly, they also show that crossing over is higher on the side of the insertion-bearing chromosome that contains the Pairing Site. The authors propose that the insertion heterozygotes induce heterosynapsis at the site of the insertion which is then propagated distally along the chromosome.
Evaluated 14 Sep 2005 |
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Andy Maule
John Innes Centre, United Kingdom
PLANT BIOLOGY
New Finding
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Here's a virus that does it differently. Most plant viruses encode a suppressor protein that allows them to combat constitutive defences based upon RNA silencing. Unusually, an analysis of the plant virus Red clover necrotic mosaic virus failed to identify a virus protein leading to the suppression phenotype. Rather, suppression was attributed to virus RNA amplification per se, a process that was also sensitive to the Dicer-like 1 (dcl1) mutation in Arabidopsis. Since Dcl1 is necessary for siRNA and miRNA biogenesis and for virus replication, the authors propose that suppression results from competition for this key silencing component.
Evaluated 14 Sep 2005 |
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Fred Dyda
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), United States of America
STRUCTURAL BIOLOGY
 Hypothesis
New Finding
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This paper shows the surprising result that the single-stranded genome of the Vibrio cholerae phage CTXvarphi integrates into the host's genome by folding on itself and thereby creating binding sites for host-encoded site-specific recombinases in the double-stranded regions of the folded structure. The phage uses the host tyrosine recombinases XerC and XerD, and while the presence of both of these are needed, the catalytic activity of only XerC is used, as the recombinases form but do not resolve the Holliday junction between the recombinants.
Evaluated 13 Sep 2005 |
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Benjamin Cravatt
The Scripps Research Institute, United States of America
CHEMICAL BIOLOGY
New Finding
 Tech Advance
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This manuscript describes an innovative strategy for screening libraries of viral protein variants to identify common modes for their inhibition by small molecules. The authors first use phage display to identify alleles in the HIV Nef protein that promote binding to p53, actin, and p56lck and correlate these results with AIDS progression. These findings are fascinating in their own right, as they suggest that Nef alleles that promote interactions with p53 are important for disease progression. The authors then screen the p53-selected allotype library with a small molecule library to identify agents that disrupt Nef-p53 interactions. An intriguing structure-activity relationship emerges where only a subset of the compounds that block the wild type Nef-p53 interaction are effective against the entire allotype library. These studies are highly significant, as they provide an experimental framework for tackling the complex problem of drug resistance through mutation that complicates the treatment of many infectious diseases (as well as cancer).
Evaluated 14 Sep 2005 |
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