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Cohesin SMC1β protects telomeres in meiocytes

¹ Institute of Physiological Chemistry, Medical Faculty Carl Gustav Carus, Dresden University of Technology, 01307 Dresden, Germany
² Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, NY 10029
³ Max Planck Institute of Molecular Genetics, D-14195 Berlin, Germany
⁴ Department of Cell and Developmental Biology, University of Würzburg, 97074 Würzburg, Germany
⁵ Memorial Sloan-Kettering Cancer Center, New York, NY 10044
⁶ Department of Cell and Molecular Biology, Karolinska Institutet, S-171 77 Stockholm, Sweden

Correspondence to Rolf Jessberger: Rolf.Jessberger{at}tu-dresden.de

Meiosis-specific mammalian cohesin SMC1β is required for complete sister chromatid cohesion and proper axes/loop structure of axial elements (AEs) and synaptonemal complexes (SCs). During prophase I, telomeres attach to the nuclear envelope (NE), but in Smc1β^–/– meiocytes, one fifth of their telomeres fail to attach. This study reveals that SMC1β serves a specific role at telomeres, which is independent of its role in determining AE/SC length and loop extension. SMC1β is necessary to prevent telomere shortening, and SMC3, present in all known cohesin complexes, properly localizes to telomeres only if SMC1β is present. Very prominently, telomeres in Smc1β^–/– spermatocytes and oocytes loose their structural integrity and suffer a range of abnormalities. These include disconnection from SCs and formation of large telomeric protein–DNA extensions, extended telomere bridges between SCs, ring-like chromosomes, intrachromosomal telomeric repeats, and a reduction of SUN1 foci in the NE. We suggest that a telomere structure protected from DNA rearrangements depends on SMC1β.

Abbreviations used in this paper: AE, axial element; ALT, alternative lengthening of telomeres; chIP, chromatin IP; DIG, digoxigenin; IF, immunofluorescence; IP, immunoprecipitation; MPTA, meiotic prophase I telomere aberration; NE, nuclear envelope; SC, synaptonemal complex; telo-FISH, telomere FISH; WT, wild type.

© 2009 Adelfalk et al.
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