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Molecular and Cellular Biology, August 2005, p. 7203-7215, Vol. 25, No. 16
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.16.7203-7215.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Surveillance of Different Recombination Defects in Mouse Spermatocytes Yields Distinct Responses despite Elimination at an Identical Developmental Stage

Marco Barchi,1 Shantha Mahadevaiah,2 Monica Di Giacomo,1 Frédéric Baudat,1,{dagger} Dirk G. de Rooij,3 Paul S. Burgoyne,2 Maria Jasin,1* and Scott Keeney1*

Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021,1 Division of Stem Cell Research and Developmental Genetics, MRC National Institute for Medical Research, London NW7 1AA, United Kingdom,2 Department of Endocrinology, Faculty of Biology, Utrecht University, and Department of Cell Biology, UMCU, Utrecht, The Netherlands3

Received 28 April 2005/ Returned for modification 24 May 2005/ Accepted 27 May 2005

Fundamentally different recombination defects cause apoptosis of mouse spermatocytes at the same stage in development, stage IV of the seminiferous epithelium cycle, equivalent to mid-pachynema in normal males. To understand the cellular response(s) that triggers apoptosis, we examined markers of spermatocyte development in mice with different recombination defects. In Spo11–/– mutants, which lack the double-strand breaks (DSBs) that initiate recombination, spermatocytes express markers of early to mid-pachynema, forming chromatin domains that contain sex body-associated proteins but that rarely encompass the sex chromosomes. Dmc1–/– spermatocytes, impaired in DSB repair, appear to arrest at or about late zygonema. Epistasis analysis reveals that this earlier arrest is a response to unrepaired DSBs, and cytological analysis implicates the BRCT-containing checkpoint protein TOPBP1. Atm–/– spermatocytes show similarities to Dmc1–/– spermatocytes, suggesting that ATM promotes meiotic DSB repair. Msh5–/– mutants display a set of characteristics distinct from these other mutants. Thus, despite equivalent stages of spermatocyte elimination, different recombination-defective mutants manifest distinct responses, providing insight into surveillance mechanisms in male meiosis.

* Corresponding author. Mailing address for Scott Keeney: Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Ave., Box 97, New York, NY 10021. Phone: (212) 639-5182. Fax: (212) 717-3627. E-mail: s-keeney{at}ski.mskcc.org. Mailing address for Maria Jasin: Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Ave., Box 109, New York, NY 10021. Phone: (212) 639-7438. Fax: (212) 717-3317. E-mail: m-jasin{at}ski.mskcc.org.

{dagger} Present address: Institut de Génétique Humaine, Montpellier, France.

Molecular and Cellular Biology, August 2005, p. 7203-7215, Vol. 25, No. 16
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.16.7203-7215.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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