Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. Signal., 8 June 2010
Vol. 3, Issue 125, p. ec169
[DOI: 10.1126/scisignal.3125ec169]

EDITORS' CHOICE

Cell Biology Germline Quality Control

L. Bryan Ray

Science, Science Signaling, AAAS, Washington, DC 20005, USA

The p53 tumor suppressor protein plays a key role in protecting organisms from aberrant cancer cells. But during evolution, animals would rarely, if ever, have lived long enough to develop cancer and so need such a function of p53. What, then, were the original functions for which p53 was selected? Lu et al. observed a pulse of p53 activation during Drosophila development in the female germ line. In cancer, p53 is activated in response to DNA damage. Similarly, in this study, breaks in DNA that occur normally during meiosis also caused p53 activation. In animals in which resolution of DNA breaks during crossing over was inhibited, activation of p53 was prolonged; furthermore, when p53 was also lacking, oogenesis was abnormal. Exactly how activation of p53 contributes to the process of chromosome recombination during meiosis remains unclear, but it may provide quality control, only allowing survival of gametes that possess intact DNA.

W.-J. Lu, J. Chapo, I. Roig, J. M. Abrams, Meiotic recombination provokes functional activation of the p53 regulatory network. Science 328, 1278–1281 (2010). [Abstract] [Full Text]

Citation: L. B. Ray, Germline Quality Control. Sci. Signal. 3, ec169 (2010).


To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882