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closeComments from Faculty of 1000 Biology
Posted by NiyazAhmed on 29 Jun 2008 at 05:09 GMT
Evaluated by: Joe Heitman with Cecelia Shertz and Maria E. Cardenas, Duke University Medical Center, United States of America [MICROBIOLOGY]
Evaluated 23 Jun 2008
Tags: Hypothesis, New Finding, Novel Drug Target
F1000 Factor: 3.0
Comments:
The ubiquitous Tor nutrient sensor cascade was discovered to evoke G2/M cell cycle transition via the polo-like kinase Cdc5 in Saccharomyces cerevisiae. It was known that inhibition of Tor with rapamycin causes a G1 cell cycle arrest, whereas these new findings by Nakashima et al. demonstrate that disruption of the Tor complex 1 (TORC1) provokes a G2/M delay. This effect is attributable to TORC1-protein phosphatase 2A mediated Cdc5 nuclear import, which has multiple mitotic roles including Swe1 phosphorylation which controls G2/M transition, cytokinesis, and CLB2 expression. This study reveals Tor is active throughout the cell cycle via key cell cycle regulators. This scenario differs from that found in Schizosaccharomyces pombe, where rapamycin stimulates mitotic entry {1}. Future studies should address if TORC1 governs the G2/M transition in multi-cellular eukaryotes such as humans. Reference: {1} Petersen et al. Nat Cell Biol 2007, 9:1263-1272.
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Best,
Niyaz Ahmed
Section Editor, PLoS ONE