Two mitotic kinesins cooperate to drive sister chromatid separation during anaphase

Nature ◽  
2003 ◽  
Vol 427 (6972) ◽  
pp. 364-370 ◽  
Author(s):  
Gregory C. Rogers ◽  
Stephen L. Rogers ◽  
Tamara A. Schwimmer ◽  
Stephanie C. Ems-McClung ◽  
Claire E. Walczak ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Separation

scholarly journals Genes Involved in Sister Chromatid Separation and Segregation in the Budding Yeast Saccharomyces cerevisiae

Genetics ◽  
2001 ◽  
Vol 159 (2) ◽  
pp. 453-470
Author(s):  
Sue Biggins ◽  
Needhi Bhalla ◽  
Amy Chang ◽  
Dana L Smith ◽  
Andrew W Murray
Keyword(s):  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Mitotic Spindle ◽  
Budding Yeast ◽  
Temperature Sensitive ◽  
Chromosome Behavior ◽  
Yeast Saccharomyces Cerevisiae ◽  
Sister Chromatids ◽  
Marked Chromosome ◽  
Sister Chromatid Separation

Abstract Accurate chromosome segregation requires the precise coordination of events during the cell cycle. Replicated sister chromatids are held together while they are properly attached to and aligned by the mitotic spindle at metaphase. At anaphase, the links between sisters must be promptly dissolved to allow the mitotic spindle to rapidly separate them to opposite poles. To isolate genes involved in chromosome behavior during mitosis, we microscopically screened a temperature-sensitive collection of budding yeast mutants that contain a GFP-marked chromosome. Nine LOC (loss of cohesion) complementation groups that do not segregate sister chromatids at anaphase were identified. We cloned the corresponding genes and performed secondary tests to determine their function in chromosome behavior. We determined that three LOC genes, PDS1, ESP1, and YCS4, are required for sister chromatid separation and three other LOC genes, CSE4, IPL1, and SMT3, are required for chromosome segregation. We isolated alleles of two genes involved in splicing, PRP16 and PRP19, which impair α-tubulin synthesis thus preventing spindle assembly, as well as an allele of CDC7 that is defective in DNA replication. We also report an initial characterization of phenotypes associated with the SMT3/SUMO gene and the isolation of WSS1, a high-copy smt3 suppressor.

scholarly journals Dual Inhibition of Sister Chromatid Separation at Metaphase

Cell ◽  
2001 ◽  
Vol 107 (6) ◽  
pp. 715-726 ◽  
Author(s):  
Olaf Stemmann ◽  
Hui Zou ◽  
Scott A. Gerber ◽  
Steven P. Gygi ◽  
Marc W. Kirschner
Keyword(s):  
Sister Chromatid ◽  
Dual Inhibition ◽  
Sister Chromatid Separation

scholarly journals CENP-O Class Proteins Form a Stable Complex and Are Required for Proper Kinetochore Function

2008 ◽  
Vol 19 (3) ◽  
pp. 843-854 ◽  
Author(s):  
Tetsuya Hori ◽  
Masahiro Okada ◽  
Katsumi Maenaka ◽  
Tatsuo Fukagawa
Keyword(s):  
Sister Chromatid ◽  
Proteasome Inhibitor ◽  
Stable Complex ◽  
Proteasome Inhibitor Mg132 ◽  
Dt40 Cell ◽  
Phenotype Analysis ◽  
Functional Classes ◽  
Sister Chromatid Separation ◽  
Chicken Dt40 Cell ◽  
Kinetochore Function

We previously identified a multisubunit complex (CENP-H/I complex) in kinetochores from human and chicken cells. We showed that the CENP-H/I complex is divided into three functional classes. In the present study, we investigated CENP-O class proteins, which include CENP-O, -P, -Q, -R, and -50 (U). We created chicken DT40 cell knockouts of each of these proteins, and we found that all knockout lines were viable, but that they showed slow proliferation and mitotic defects. Kinetochore localization of CENP-O, -P, -Q, and -50 was interdependent, but kinetochore localization of these proteins was observed in CENP-R–deficient cells. A coexpression assay in bacteria showed that CENP-O, -P, -Q, and -50 proteins form a stable complex that can associate with CENP-R. Phenotype analysis of knockout cells showed that all proteins except for CENP-R were required for recovery from spindle damage, and phosphorylation of CENP-50 was essential for recovery from spindle damage. We also found that treatment with the proteasome inhibitor MG132 partially rescued the severe mitotic phenotype observed in response to release from nocodazole block in CENP-50–deficient cells. This suggests that CENP-O class proteins are involved in the prevention of premature sister chromatid separation during recovery from spindle damage.

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