Published 18 July 2005. doi:10.1083/jcb.200501042
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 170, Number 2, 213-223
Meiotic telomere clustering requires actin for its formation and cohesin for its resolution
Edgar Trelles-Sticken1,
Caroline Adelfalk1,
Josef Loidl2, and
Harry Scherthan1,3
1 Max-Planck-Institute for Molecular Genetics, D-14195 Berlin, Germany
2 Department of Chromosome Biology, Faculty of Life Sciences, University of Vienna, A-1030 Vienna, Austria
3 Institute for Radiation Biology Bundeswehr, D-80937 Munich, Germany
Correspondence to Harry Scherthan: scherth{at}web.de
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 clusterSPB colocalization is defective. These defects are rescued by expressing the mitotic cohesin Scc1 in rec8
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 polymerizationdependent telomere clustering and for linking the SPB to the telomere cluster in synaptic meiosis.
E. Trelles-Sticken and C. Adelfalk contributed equally to this paper.
Edgar Trelles-Sticken's present address is Schuetzenstrasse 31, D-12105 Berlin, Germany.
Abbreviations used in this paper: AE, axial element; DSB, DNA double strand break; Lat B, latrunculin B; MT, microtubule; SC, synaptonemal complex; SPB, spindle pole body.

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