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Sld5 Ensures Centrosomal Resistance to Congression Forces by Preserving Centriolar Satellites
Author(s) -
Manpreet Kaur,
Raksha Devi,
Tanushree Ghosh,
Md. Muntaz Khan,
Praveen Kumar,
P. Priyanka,
Ananya Kar,
Aparna Sharma,
Akhil Varshney,
Vipin Kumar,
Sandeep Saxena
Publication year - 2017
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.00371-17
Subject(s) - centrosome , kinesin , biology , microbiology and biotechnology , microtubule , motor protein , mitosis , spindle pole body , chromosome segregation , cytoplasm , spindle apparatus , genetics , chromosome , cell division , cell , cell cycle , gene
The migration of chromosomes during mitosis is mediated primarily by kinesins that bind to the chromosomes and move along the microtubules, exerting pulling and pushing forces on the centrosomes. We report that a DNA replication protein, Sld5, localizes to the centrosomes, resisting the microtubular pulling forces experienced during chromosome congression. In the absence of Sld5, centriolar satellites, which normally cluster around the centrosomes, are dissipated throughout the cytoplasm, resulting in the loss of their known function of recruiting the centrosomal protein, pericentrin. We observed that Sld5-deficient centrosomes lacking pericentrin were unable to endure the CENP-E- and Kid-mediated microtubular forces that converge on the centrosomes during chromosome congression, resulting in monocentriolar and acentriolar spindle poles. The minus-end-directed kinesin-14 motor protein, HSET, sustains the traction forces that mediate centrosomal fragmentation in Sld5-depleted cells. Thus, we report that a DNA replication protein has an as yet unknown function of ensuring spindle pole resistance to traction forces exerted during chromosome congression.

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