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Set1- and CIb5-deficiencies disclose the differential regulation of centromere and telomere dynamics in Saccharomyces cerevisiae meiosis

MPG-Autoren

Trelles-Sticken,  Edgar
Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50515

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., Bonfils, S., Sollier, J., Géli, V., Scherthan, H., & de La Roche Saint-André, C. (2005). Set1- and CIb5-deficiencies disclose the differential regulation of centromere and telomere dynamics in Saccharomyces cerevisiae meiosis. Journal of Cell Science, 118, 4985-4994. doi:10.1242/10.1242/jcs.02612.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-8577-E
Zusammenfassung
The entry into meiosis is characterized by a lengthy premeiotic S phase and a reorganization of the nuclear architecture. Analysis of centromere and telomere dynamics in wild-type Saccharomyces cerevisiae meiosis suggests that resolution of vegetative centromere and telomere clusters are independent events differently connected to premeiotic S phase. Absence of the B-type cyclin Clb5 or the Set1 histone methyltransferase leads to a delay of premeiotic S phase by separate mechanisms. In clb5{Delta} cells, centromere cluster resolution appears normal, whereas dissolution of the vegetative telomere clusters is impaired and meiosis-specific clustering of telomeres, i.e. bouquet formation, is grossly delayed. In set1{Delta} cells, centromere and telomere redistribution are both impaired and bouquet nuclei are absent, despite proper location of the meiosis-specific telomere protein Ndj1. Thus, centromere and telomere redistribution at the onset of prophase I is differentially regulated, with centromere dispersion occurring independently of premeiotic S phase. The normal kinetics of dissolution of the vegetative telomere clusters in a set1{Delta} mec1-1 mutant suggests the presence of a checkpoint that limits the dispersion of telomeres in absence of Set1.