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Cell Growth & Differentiation Vol. 10, 665-675, October 1999
© 1999 American Association for Cancer Research


Articles

p53 Controls Low DNA Damage-dependent Premeiotic Checkpoint and Facilitates DNA Repair during Spermatogenesis1

Dov Schwartz, Naomi Goldfinger, Zvi Kam and Varda Rotter2

Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel 76100

Abstract

Previously, it was implicated that p53 plays a role in spermatogenesis. Here we report that p53 knockout mice exhibit significantly less mature motile spermatozoa than their p53(+/+) counterparts. To better understand the role of p53 in spermatogenesis, we analyzed the response of spermatogenic cells to DNA insult during prophase. It was found that although low-level {gamma}-irradiation activated a p53-dependent premeiotic delay, higher levels of {gamma}-irradiation induced a p53-independent apoptosis during meiosis. Furthermore, p53 knockout mice exhibited reduced in vivo levels of unscheduled DNA synthesis, indicative of compromised DNA repair. Thus, p53 provides another level of stringency in addition to other spermatogenic "quality control" mechanisms.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1999 by the American Association of Cancer Research.