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

被引:113
作者
Trelles-Sticken, E
Adelfalk, C
Loidl, J
Scherthan, H
机构
[1] Max Planck Inst Mol Genet, D-14195 Berlin, Germany
[2] Univ Vienna, Fac Life Sci, Dept Chromosome Biol, A-1030 Vienna, Austria
[3] Inst Radiat Biol Bundeswehr, D-80937 Munich, Germany
关键词
D O I
10.1083/jcb.200501042
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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-SPBcolocalization 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.
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页码:213 / 223
页数:11
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