期刊
NATURE COMMUNICATIONS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms13508
关键词
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资金
- MEXT of Japan [22229002, 16K15230, 15H01554, 26110001, 26110005, 15K19004]
- Japan Agency for Medical Research and development, AMED
- Scientific Technique Research Promotion Program for Agriculture, Forestry, Fisheries and Food Industry
- Secom Science and Technology Foundation
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [15K08420, 15K19004, 16K15230, 22229002, 26430051, 25440080, 15H04926, 26110001, 26110005, 15H01554] Funding Source: KAKEN
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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