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Top 7 in Genomics & Genetics

A snapshot of the most highly ranked articles in genomics, genetics and related areas, from Faculty of 1000

By | November 22, 2011

WIKIMEDIA COMMONS, TOM ELLENBERGER

1. Remote assembly

Polyubiquitin chains bind to proteins in order to direct them towards specific cellular locations or orchestrate the assembly or break down of large molecules. The current study reveals that the chains can still trigger signaling pathways without being attached to any protein.

Z.P. Xia et al., “Direct activation of protein kinases by unanchored polyubiquitin chains,” Nature, Sep. 3; 461(7260):114-9, 2009. Free F1000 Evaluation.

2. Biology manifesto

This classic paper describes the flaws in the current biological paradigm by pointing out how difficult it would be to use biological methods to fix a broken radio. The trouble?  Most of the discipline is descriptive but not predictive, and lacks a formal language. Taking a page from engineering may help biologists make sense of complex living systems, the author argues.

Y. Lazebnik, “Can a biologist fix a radio?—Or, what I learned while studying apoptosis,” Cancer Cell, 2(3):179-82, 2002. Free F1000 Evaluation.

3. Stripping DNA

The expression of DNA can be altered by adding or removing epigenetic tags such as methyl groups, but until recently scientists only recognized one way to strip DNA of its methyl groups. The current study reveals a previously unknown pathway by which methyl tags can be removed from DNA.

Y.F. He et al., “Tet-mediated formation of 5-carboxylcytosine and its excision by TDG in mammalian DNA,” Science, 333(6047):1303-7, 2011. Free F1000 Evaluation.

4. Cellular cannibals

In the face of low energy stores, defective components, or invading bacteria, cells need a way to devour their own parts. Yet just what organelle turned the cell cannibalistic remained a mystery. This research suggests mitochondria are responsible for producing the key components that break down other parts of the cell.

D.W. Hailey et al., “Mitochondria supply membranes for autophagosome biogenesis during starvation,” Cell, 141(4):656-67, 2010. Free F1000 Evaluation.

5. Breast cancer’s secrets

The BRCA1 mutation dramatically increases the risk for breast and ovarian cancer, but scientists couldn’t agree on which defect in the BRCA1 protein was responsible. The study rejects one- proposed mechanism for how BRCA1 mutations cause cancer and  instead, demonstrates BRCA1’s ability to recognize another protein seems to be the important function for keeping cancer in check.

R. Shakya et al., “BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity,” Science, 334(6055):525-8, 2011. Free F1000 Evaluation.

6. Chains in flux

Polyubiquitin chains play an important role in cellular signaling. In this study, the researchers developed new antibody tags that can track the chains as they add or subtract links and interact with other proteins. The new tools will allow scientists to watch proteins bound to the chains in action.

K. Newton et al., “Ubiquitin chain editing revealed by polyubiquitin linkage-specific antibodies,” Cell, 134(4):668-78, 2008. Free F1000 Evaluation.

7. Running interference

At first glance, long, noncoding RNAs may not seem to be good for much. But this study reveals they can actually act as decoys that draw microRNAs away from their targets. In this case, the noncoding RNAs act as a sponge to soak up the microRNAs, thus preventing the microRNAs from repressing signaling that is important for muscle cell differentiation.

M. Cesana et al., “A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA,” Cell. 147(2):358-69, 2011. Free F1000 Evaluation.

The F1000 Top 7 is a snapshot of the highest ranked articles from a 30-day period on Faculty of 1000 Genomics & Genetics, as calculated on November 21, 2011. Faculty Members evaluate and rate the most important papers in their field. To see the latest rankings, search the database, and read daily evaluations, visit http://f1000.com.

 

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