HIV budding from cell membrane.WIKIMEDIA COMMONS, NIH1. Lighting up RNA
A novel technique for tagging and following RNA processes in live cells promises to illuminate RNA biology the way green fluorescent protein (GFP) did for the study of proteins. The tagging method consists of short RNA sequences that bind to GFP-like fluorophores and produce a wide range of colors. These RNA-fluorophore complexes can then be fused to RNAs in the cell.

J.S. Paige et al., “RNA mimics of green fluorescent protein,” Science, 333:642-46, 2011. Free F1000 Evaluation

2. I Spy
Researchers testing the ability of engineered E. coli cells to stabilize unstable proteins in vivo, stumbled upon a new protein chaperone, called Spy, that suppresses protein aggregation and aids protein refolding. Spy is shaped unlike any other previously studied chaperone and can increase the steady-state levels of a set of unstable protein mutants up to 700-fold.


3. Gene expression goes global
Protein levels are regulated by the interplay not merely of protein translation and degradation, but mRNA transcription and destruction. In this first investigation into genome-scale prediction of mRNA and protein synthesis rates, researchers measured both RNA abundance and protein turnover of over 5000 genes, and found that the abundance of proteins in a cell is primarily controlled at the translational level.

B. Schwanhäusser et al., “Global quantification of mammalian gene expression control,” Nature, 473:337-42, 2011. Free F1000 Evaluation

4. Why DNA breaks

Chromosome instability—the propensity of certain places in the genome to break under replicative stress—can contribute to tumorigenesis. Previous work suggested that such common fragile sites were prone to breakage because of secondary structures that arose during replication and blocked the formation of replication forks. In contrast, this study shows that at least one site, FRA3B, is unstable even when few replication events are initiated, suggesting another mechanism must be responsible for the site’s fragility.

A. Letessier et al., “Cell-type specific replication initiation programs set fragility of the FRA3B fragile site,” Nature, 470:120-23, 2011. Free F1000 Evaluation

5. Odd cod immunity
The full genome sequence of the Atlantic cod reveals that the fish have lost the genes for MHCII and CD4, two key players in immunity. Apparently in compensation, the cod’s genome shows that MHC I locus is greatly expanded, and contains a unique complement of Toll-like receptors, another important component of the immune system.

B. Star et al., “The genome sequence of Atlantic cod reveals a unique immune system,” Nature, 477:207-10, 2011. Free F1000 Evaluation

6. HIV evades NK death
Just as T cells are able to pressure HIV to adapt to escape recognition, it now appears NK cells also can drive HIV evolution. Researchers identified polymorphisms in strains of HIV-1 that prevented activation of NK cells with specific killer immunoglobulin-like receptors (KIRs).

G. Alter et al., “HIV-1 adaptation to NK-cell-mediated immune pressure,” Nature, 476:96-100, 2011. Free F1000 Evaluation

7. Molecular fountain of youth?
Replicating cells of complex organisms can reset the cellular clock of progeny, essentially resetting their age. Researchers identify a transcription factor called NDT80, which is essential for gametogenesis in budding yeast, that makes this possible, allowing yeast cells to extend the number of times they replicate. Transient expression of NDT80 in yeast cells that weren’t undergoing gametogenesis could also reset their life span.

E. Unal et al., “Gametogenesis eliminates age-induced cellular damage and resets life span in yeast,” Science, 332:1554-47, 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 September 15, 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

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