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Science 18 March 2005: Vol. 307. no. 5716, pp. 1781 - 1785 DOI: 10.1126/science.1106823
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Reports
A Mitotic Septin Scaffold Required for Mammalian Chromosome Congression and Segregation
Elias T. Spiliotis,1
Makoto Kinoshita,2
W. James Nelson1*
Coordination of cytokinesis with chromosome congression and segregation is critical for proper cell division, but the mechanism is unknown. Here, septins, a conserved family of polymerizing guanosine triphosphatebinding proteins, localized to the metaphase plate during mitosis. Septin depletion resulted in chromosome loss from the metaphase plate, lack of chromosome segregation and spindle elongation, and incomplete cytokinesis upon delayed mitotic exit. These defects correlated with loss of the mitotic motor and the checkpoint regulator centromere-associated protein E (CENP-E) from the kinetochores of congressing chromosomes. Mammalian septins may thus form a mitotic scaffold for CENP-E and other effectors to coordinate cytokinesis with chromosome congression and segregation.
1 Department of Molecular and Cellular Physiology, Beckman Center for Molecular and Genetic Medicine, Stanford University School of Medicine, Stanford, CA 943055435, USA.
2 Biochemistry and Cell Biology Unit, Horizontal Medical Research Organization, Kyoto University Graduate School of Medicine, Yoshida Konoe, Sakyo, Kyoto 6068501, Japan.
* To whom correspondence should be addressed. E-mail: wjnelson{at}stanford.edu
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- Protein Networks Supporting AP-3 Function in Targeting Lysosomal Membrane Proteins.
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- Phosphorylation of Adult Type Sept5 (CDCrel-1) by Cyclin-dependent Kinase 5 Inhibits Interaction with Syntaxin-1.
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- Disruption of Sept6, a Fusion Partner Gene of MLL, Does Not Affect Ontogeny, Leukemogenesis Induced by MLL-SEPT6, or Phenotype Induced by the Loss of Sept4.
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