Mutations that affect meiosis in male mice influence the dynamics of the 
mid-preleptotene and bouquet stages

Liebe, Bodo; Petukhova, G.; Barchi, M.; Bellani, M.; Braselmann, H.; Nakano, T.; Pandita, T. K.; Jasin, M.; Fornace, A.; Meistrich, M. L.; Baarends, W. M.; Schimenti, J.; de Lange, T.; Keeney, S.; Camerini-Otero, R. D.; Scherthan, Harry

doi:10.1016/j.yexcr.2006.07.019

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Mutations that affect meiosis in male mice influence the dynamics of the mid-preleptotene and bouquet stages

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Liebe, Bodo
Max Planck Society;

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Scherthan, Harry
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Liebe, B., Petukhova, G., Barchi, M., Bellani, M., Braselmann, H., Nakano, T., et al. (2006). Mutations that affect meiosis in male mice influence the dynamics of the mid-preleptotene and bouquet stages. Experimental Cell Research, 312(19), 3768-3781. doi:10.1016/j.yexcr.2006.07.019.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-833C-D

Abstract

previous termMeiosisnext term pairs and segregates homologous chromosomes and thereby forms haploid germ cells to compensate the genome doubling at fertilization. Homologue pairing in many eukaryotic species depends on formation of DNA double strand breaks (DSBs) during early prophase I when telomeres begin to cluster at the nuclear periphery (previous termbouquet stage)next term. By fluorescence in situ hybridization criteria, we observe that previous termmid-preleptotene and bouquet stagenext term frequencies are altered in previous termmale micenext term deficient for proteins required for recombination, ubiquitin conjugation and telomere length control. The generally low frequencies of previous termmid-preleptotenenext term spermatocytes were significantly increased in previous termmale micenext term lacking recombination proteins SPO11, MEI1, MLH1, KU80, ubiquitin conjugating enzyme HR6B, and in previous termmicenext term with only one copy of the telomere length regulator Terf1. The previous termbouquet stagenext term was significantly enriched in Atm−/−, Spo11−/−, Mei1m1Jcs/m1Jcs, Mlh1−/−, Terf1+/− and Hr6b−/− spermatogenesis, but not in previous termmicenext term lacking recombination proteins DMC1 and HOP2, the non-homologous end-joining DNA repair factor KU80 and the ATM downstream effector GADD45a. previous termMicenext term defective in spermiogenesis (Tnp1−/−, Gmcl1−/−, Asm−/−) showed wild-type previous termmid-preleptotene and bouquetnext term frequencies. A low frequency of previous termbouquetnext term spermatocytes in Spo11−/−Atm−/− spermatogenesis suggests that DSBs contribute to the Atm−/−-correlated previous termbouquet stagenext term exit defect. Insignificant changes of previous termbouquetnext term frequencies in previous termmicenext term with defects in early previous termstagesnext term of DSB repair (Dmc1−/−, Hop2−/−) suggest that there is an ATM-specific previous terminfluence on bouquet stagenext term duration. Altogether, it appears that several pathways previous terminfluencenext term telomere previous termdynamicsnext term in mammalian previous termmeiosis.next term