Skip to Content
Merck

Autophagy controls centrosome number by degrading Cep63.

Nature communications (2016-11-22)
Yuichiro Watanabe, Shinya Honda, Akimitsu Konishi, Satoko Arakawa, Michiko Murohashi, Hirofumi Yamaguchi, Satoru Torii, Minoru Tanabe, Shinji Tanaka, Eiji Warabi, Shigeomi Shimizu
ABSTRACT

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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-γ-Tubulin antibody, Mouse monoclonal, clone GTU-88, ascites fluid
Sigma-Aldrich
3-Methyladenine, autophagy inhibitor
Sigma-Aldrich
Anti-Atg1/ULK1 antibody produced in rabbit, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
ANTI-FLAG® M2 antibody, Mouse monoclonal, 1 mg/mL, clone M2, affinity isolated antibody, buffered aqueous solution (50% glycerol, 10 mM sodium phosphate, and 150 mM NaCl, pH 7.4)