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Loss of RanGEF/Pim1 activity abolishes the orchestration of Ran‐mediated mitotic cellular events in S. pombe
Author(s) -
Hirose Eiji,
Mukai Mari,
Shimada Atsushi,
Nishitani Hideo,
Shibata Yosaburo,
Nishimoto Takeharu
Publication year - 2006
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2005.00919.x
Subject(s) - biology , pim1 , cytokinesis , ran , mitosis , microbiology and biotechnology , mutant , mutation , cell division , genetics , gtpase , gene , cell , phosphorylation , serine
RCC1, a conserved chromosomal protein with a seven‐bladed propeller is a GDP/GTP nucleotide exchange factor for RanGTPase that mediates various cellular events. We isolated 16 temperature‐sensitive (ts) mutants of S. pombe RCC1 ‐homolog, pim1 + , by error‐prone PCR. Five pim1 ts mutants had a single mutation. The obtained pim1 ts mutations and previously reported mutations were localized on similar sites in seven RCC1 repeats. Those mutations resulted in a reduced binding of Pim1 with Spi1. All pim1 ts mutants showed a defect in nucleocytoplasmic protein transports, whereas the majority of them showed a normal mRNA export. In all pim1 ts examined, chromosomal DNA replication was completed. However, mitotic spindle formation was abrogated, the septum was formed being uncoupled with nuclear division and abnormally widened, thus resulting in chromosomal DNA mis‐segregation and the accumulation of enucleated cells. As a result, a defect of RanGEF/Pim1 abolished the orchestration of sequential mitotic events, spindle formation, septation and cytokinesis that are essential to produce two identical daughter cells.