Mitotic catastrophe induced by overexpression of budding yeast Rad2p

• Published in: Yeast (Chichester, England) Vol. 27; no. 7; pp. 399 - 411
• Main Authors: Kang, Mi-Sun, Yu, Sung-Lim, Lim, Hyun-Sook, Choi, Bohwa, Park, Chang-Shin, Kang, Ju-Hee, Lee, Sung-Keun
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.07.2010
• Subjects: Caspases - genetics; Cell Cycle Proteins - genetics; DNA-Binding Proteins - biosynthesis; DNA-Binding Proteins - genetics; Endodeoxyribonucleases - biosynthesis; Endodeoxyribonucleases - genetics; Gene Deletion; Gene Expression; Mitosis; mitotic catastrophe; nucleotide excision repair; RAD2; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - physiology; Saccharomyces cerevisiae Proteins - biosynthesis; Saccharomyces cerevisiae Proteins - genetics
• ISSN: 0749-503X; 1097-0061; 1097-0061
• DOI: 10.1002/yea.1764

Mitotic catastrophe provokes endopolyploidy, giant cell formation and, eventually, delayed cell death. Mitotic catastrophe is induced by defective cell cycle checkpoints and by some anticancer drugs, ionizing radiation and microtubule-destabilizing agents. RAD2 is a yeast homologue of XPG, which is a human endonuclease involved in nucleotide excision repair. Here we show that Rad2p overexpression alone, in the absence of extrinsic DNA damage, causes cell growth arrest and mitotic catastrophe. Interestingly, Rad2p-induced cell growth arrest is not caused by the catalytic activity of Rad2p but rather by its C-terminal region. Cells growth-arrested by Rad2p induction do not show apoptotic phenotypes and deletion of YCA1, a yeast caspase homologue, does not affect cell growth arrest by Rad2p induction. However, Rad2p-induced cell growth arrest is released by rad9 deletion but is not affected by downstream DNA damage checkpoint genes. These observations suggest that RAD2 has a function in coordinating cell cycle regulation and damaged DNA repair. Copyright © 2010 John Wiley & Sons, Ltd.