4.8 Article

Autophagy controls centrosome number by degrading Cep63

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NATURE COMMUNICATIONS
卷 7, 期 -, 页码 -

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NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms13508

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资金

  1. MEXT of Japan [22229002, 16K15230, 15H01554, 26110001, 26110005, 15K19004]
  2. Japan Agency for Medical Research and development, AMED
  3. Scientific Technique Research Promotion Program for Agriculture, Forestry, Fisheries and Food Industry
  4. Secom Science and Technology Foundation
  5. Takeda Science Foundation
  6. Grants-in-Aid for Scientific Research [15K08420, 15K19004, 16K15230, 22229002, 26430051, 25440080, 15H04926, 26110001, 26110005, 15H01554] Funding Source: KAKEN

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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.

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