Focus
December 12, 2008

Philipp Oberdoerffer (left), David SinclairPATHOLOGY: Potentially Universal Mechanism of Aging Discovered
Researchers have uncovered what may be a universal cause of aging, which applies to both single-cell organisms like yeast and multicellular organisms including mammals. Their findings, reported in the Nov. 28 Cell, show that DNA damage eventually leads to a breakdown in the cell’s ability to regulate which genes are appropriately switched on and off. The study, by Philipp Oberdoerffer (left), David Sinclair, and colleagues, marks the first time that such an evolutionarily conserved aging mechanism has been identified in such diverse organisms. It also introduces hypotheses on how this process might be reversed.

Danny Chou, Stephen Elledge, Sherry Yen, and Qikai XuPROTEOMICS: Protein Stability Profiling Goes Global
By measuring protein stability on a grand scale, Danny Chou, Stephen Elledge, Sherry Yen, and Qikai Xu gauged protein levels in the cell that accounted for both protein synthesis and degradation. Their method is based on a genetic construct that uses fluorescent red and green proteins to take measurements on a cellwide scale. The new technique allows researchers to check the stability of thousands of proteins at the same time to get a picture of the molecular forces at work in the cell during any given cell state. The work appears in two papers in the Nov. 7 Science.

Haoqiang Ying, Ronald DePinho, Hongwu ZhengONCOLOGY: Unlikely Pair of Mutations Drives Brain Cancer
Some glioblastomas develop slowly while others burst through the brain so quickly that a person could be healthy one month and gripped by disease the next. Genetic screens have shown that the faster, or primary, glioblastomas harbor mutant versions of Pten and other genes. Defects in the well-known tumor suppressor p53 have been linked almost solely to the slower-growing, or secondary, glioblastomas. It now appears that corrupted versions of p53 do play a role in the faster-growing variety, especially when joined by mutant versions of Pten. From left, Haoqiang Ying, Ronald DePinho, Hongwu Zheng and colleagues report the findings in the Oct. 23 Nature.

Copyright 2008 by the President and Fellows of Harvard College