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Autophagy controls centrosome number by degrading Cep63

Centrosome number is associated with the chromosome segregation and genomic stability. The ubiquitin–proteasome system is considered to be the main regulator of centrosome number. However, here we show that autophagy also regulates the number of centrosomes. Autophagy-deficient cells carry extra cen...

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Published in:Nature communications 2016-11, Vol.7 (1), p.13508-13508, Article 13508
Main Authors: Watanabe, Yuichiro, Honda, Shinya, Konishi, Akimitsu, Arakawa, Satoko, Murohashi, Michiko, Yamaguchi, Hirofumi, Torii, Satoru, Tanabe, Minoru, Tanaka, Shinji, Warabi, Eiji, Shimizu, Shigeomi
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Language:English
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Summary:Centrosome number is associated with the chromosome segregation and genomic stability. The ubiquitin–proteasome system is considered to be the main regulator of centrosome number. However, here we show that autophagy also regulates the number of centrosomes. Autophagy-deficient cells carry extra centrosomes. The autophagic regulation of centrosome number is dependent on a centrosomal protein of 63 (Cep63) given that cells lacking autophagy contain multiple Cep63 dots that are engulfed and digested by autophagy in wild-type cells, and that the upregulation of Cep63 increases centrosome number. Cep63 is recruited to autophagosomes via interaction with p62, a molecule crucial for selective autophagy. In vivo , hematopoietic cells from autophagy-deficient and p62 −/− mice also contained multiple centrosomes. These results indicate that autophagy controls centrosome number by degrading Cep63. The ubiquitin-proteasome system is thought to be the primary regulator of centrosome number. Here, Watanabe et al . show that selective autophagy also plays a role in regulating centrosome number via p62-dependent recruitment of centrosomal protein 63 to autophagosomes.
ISSN:2041-1723
2041-1723
DOI:10.1038/ncomms13508