Sec13 induces genomic instability in U2OS cells.
- Author:
Choong Ryoul SIHN
1
;
Eun Jung SUH
;
Kee Ho LEE
;
Sang Hoon KIM
Author Information
1. Department of Biology, College of Sciences, Kyung Hee University, Seoul 130-701, Korea. shkim@khu.ac.kr
- Publication Type:Brief Communication ; Research Support, Non-U.S. Gov't
- Keywords:
Sec13;
mitosis;
genomic instability;
U2OS cells;
nuclear pore complex
- MeSH:
Anaphase;
Antineoplastic Agents/pharmacology;
Cell Line, Tumor/drug effects/metabolism/pathology;
*G1 Phase;
*Genomic Instability;
Green Fluorescent Proteins/metabolism;
Humans;
Kinetochores/metabolism;
Membrane Proteins/*genetics/metabolism;
Metaphase;
Mitosis/*physiology;
*Mitotic Spindle Apparatus;
Nocodazole/pharmacology;
Osteosarcoma/genetics/metabolism/pathology;
Research Support, Non-U.S. Gov't
- From:Experimental & Molecular Medicine
2005;37(3):255-260
- CountryRepublic of Korea
- Language:English
-
Abstract:
Sec13p has been known as an endoplasmic reticulum-Golgi transport protein. Recently, it has also been shown to be required for the formation of septation in the fission yeast Schizosaccharomyces pombe. In the present study, we focused on the role of a human homolog of Saccharomyces cerevisiae SEC13, Sec13 protein during mitosis in U2OS cells. We found that the expression of Sec13 was constant throughout the cell cycle, and localized to the kinetochores at metaphase during mitosis. By using green fluorescent protein technology, we observed that Sec13 is required for evasion of mitotic arrest in response to spindle damage, leading to G1-like phase and apoptotic cell death. In addition, cells expressing exogenous Sec13 showed giant nuclei compared to endogenous ones in the absence of nocodazole. These results demonstrate that Sec13 is involved in the regulation of the metaphase/anaphase transition and may be functionally associated with mitotic machinery to maintain genomic stability during mitosis.
