Linked Life Data

16443750

Source:http://linkedlifedata.com/resource/pubmed/id/16443750

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 3
pubmed:dateCreated
2006-1-30
pubmed:abstractText
The cohesin complex prevents premature segregation of duplicated chromosomes by providing resistance to the pole-ward pull by spindle microtubules. The centromeric region (or sister kinetochores) bears the majority of this force and undergoes transient separation prior to anaphase, indicative of its elastic nature. A cysteine protease, separase, cleaves the cohesin subunit Scc1 and dissolves cohesion between sister chromatids, initiating their separation. Separase also cleaves the kinetochore protein Slk19 during anaphase. Slk19 has been implicated in stabilization of the mitotic spindle and regulation of mitotic exit, but it is not known what role it plays at the kinetochores. We show that during pre-anaphase arrest, the spindle in slk19Delta cells is excessively dynamic and the nuclei move into mother-daughter junction prematurely. As a result, the chromatin mass undergoes partial division that requires neither anaphase promoting complex (APC) activity nor Scc1 cleavage. Partial division of the chromatin mass is accompanied by the loss of the centromeric region's ability to resist pole-ward pull by the spindle. Slk19 physically associates with Scc1 and this association appears necessary for efficient cleavage of Slk19 by separase. Our results suggest that Slk19 participates in regulating nuclear migration and, in conjunction with cohesin complex, may be involved in the maintenance of centromeric tensile strength to resist the pole-ward pull.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9533
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
519-31
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Deficiency of centromere-associated protein Slk19 causes premature nuclear migration and loss of centromeric elasticity.
pubmed:affiliation
Institute of Molecular and Cell Biology, Proteos, 61 Biopolis Drive, Singapore 138673.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't