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First published online June 3, 2009
doi: 10.1242/10.1242/jcs.046706
Research Article |
1 Unidad de Biología Celular, Departamento de Biología, Edificio de Ciencias Biológicas, Facultad de Ciencias, Universidad Autónoma de Madrid, Calle Darwin 2, 28049 Madrid, Spain
2 Biotechnology Program, Centro Nacional de Investigaciones Oncológicas, Calle Melchor Fernández Almagro 3, 28029 Madrid, Spain
3 Departamento de Biología Celular y del Desarrollo, Centro de Investigaciones Biológicas, Calle Ramiro de Maeztu 9, 28040 Madrid, Spain
* Author for correspondence (e-mail: jose.suja{at}uam.es)
Accepted 23 March 2009
Cyclin-dependent kinase 2 (CDK2) was assumed to be essential in the mammalian cell cycle both at the G1-S transition and throughout the S phase. Interestingly, ablation of Cdk2 in mice does not have substantial consequences for embryonic or postnatal development, but both males and females are infertile. In the present study, we have analysed the meiotic alterations leading to infertility in Cdk2–/– male mice. We have studied the distribution and dynamics of several proteins related to meiosis progression, such as synaptonemal complex proteins, cohesin complexes, and centromere-, telomere- and recombination-related proteins. Cdk2–/– spermatocytes show an incomplete chromosome pairing, an extensive non-homologous synapsis and arrest at a pachytene-like stage with unrepaired programmed double-strand breaks. In these spermatocytes, some telomeres do not attach to the nuclear envelope, and sex chromosomes do not form a sex body. Our data demonstrate an unpredicted participation of CDK2 in the accurate pairing and recombination between homologues during mammalian meiosis.
Key words: CDK2, Chromosome synapsis, Meiosis, Meiotic recombination, Mouse, Sex body
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