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Meiotic telomere clustering requires actin for its formation and cohesin for its resolution

MPG-Autoren

Trelles-Sticken,  Edgar
Max Planck Society;

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Adelfalk,  Caroline
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, 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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Zitation

Trelles-Sticken, E., Adelfalk, C., Loidl, J., & Scherthan, H. (2005). Meiotic telomere clustering requires actin for its formation and cohesin for its resolution. The Journal of Cell Biology: JCB, 170(2), 213-223. doi:10.1083/jcb.200501042.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0010-85E8-E
Zusammenfassung
In diploid organisms, meiosis reduces the chromosome number by half during the formation of haploid gametes. During meiotic prophase, telomeres transiently cluster at a limited sector of the nuclear envelope (bouquet stage) near the spindle pole body (SPB). Cohesin is a multisubunit complex that contributes to chromosome segregation in meiosis I and II divisions. In yeast meiosis, deficiency for Rec8 cohesin subunit induces telomere clustering to persist, whereas telomere cluster–SPB colocalization is defective. These defects are rescued by expressing the mitotic cohesin Scc1 in rec8{Delta} meiosis, whereas bouquet-stage exit is independent of Cdc5 pololike kinase. An analysis of living Saccharomyces cerevisiae meiocytes revealed highly mobile telomeres from leptotene up to pachytene, with telomeres experiencing an actin- but not microtubule-dependent constraint of mobility during the bouquet stage. Our results suggest that cohesin is required for exit from actin polymerization–dependent telomere clustering and for linking the SPB to the telomere cluster in synaptic meiosis.