Mortalin controls centrosome duplication via modulating centrosomal localization of p53

Oncogene
Z MaK Fukasawa

Abstract

Abnormal amplification of centrosomes, commonly found in human cancer, is the major cause of mitotic defects and chromosome instability in cancer cells. Like DNA, centrosomes duplicate once in each cell cycle, hence the defect in the mechanism that ensures centrosome duplication to occur once and only once in each cell cycle results in abnormal amplification of centrosomes and mitotic defects. Centrosomes are non-membranous organelles, and undergo dynamic changes in its constituents during the centrosome duplication cycle. Through a comparative mass spectrometric analysis of unduplicated and duplicated centrosomes, we identified mortalin, a member of heat shock protein family, as a protein that associates preferentially with duplicated centrosomes. Further analysis revealed that mortalin localized to centrosomes in late G1 before centrosome duplication, remained at centrosomes during S and G2, and dissociated from centrosomes during mitosis. Overexpression of mortalin overrides the p53-dependent suppression of centrosome duplication, and mortalin-driven centrosome duplication requires physical interaction between mortalin and p53. Moreover, mortalin promotes dissociation of p53 from centrosomes through physical interaction. The...Continue Reading

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Citations

Sep 5, 2008·Biogerontology·Custer C DeocarisRenu Wadhwa
Dec 2, 2009·The Journal of Biological Chemistry·Renu WadhwaRobert M Tanguay
Oct 17, 2007·Human Gene Therapy·Maki ShiotaRenu Wadhwa
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