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The Role of Autophagy in Genome Stability through Suppression of Abnormal Mitosis under Starvation
Author(s) -
Aiko Matsui,
Yoshiaki Kamada,
Akira Matsuura
Publication year - 2013
Publication title -
plos genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.587
H-Index - 233
eISSN - 1553-7404
pISSN - 1553-7390
DOI - 10.1371/journal.pgen.1003245
Subject(s) - autophagy , biology , starvation , microbiology and biotechnology , cell cycle , genome instability , mitosis , cell division , saccharomyces cerevisiae , cell cycle checkpoint , cell growth , cell , dna damage , genetics , yeast , dna , apoptosis , endocrinology
The coordination of subcellular processes during adaptation to environmental change is a key feature of biological systems. Starvation of essential nutrients slows cell cycling and ultimately causes G1 arrest, and nitrogen starvation delays G2/M progression. Here, we show that budding yeast cells can be efficiently returned to the G1 phase under starvation conditions in an autophagy-dependent manner. Starvation attenuates TORC1 activity, causing a G2/M delay in a Swe1-dependent checkpoint mechanism, and starvation-induced autophagy assists in the recovery from a G2/M delay by supplying amino acids required for cell growth. Persistent delay of the cell cycle by a deficiency in autophagy causes aberrant nuclear division without sufficient cell growth, leading to an increased frequency in aneuploidy after refeeding the nitrogen source. Our data establish the role of autophagy in genome stability through modulation of cell division under conditions that repress cell growth.

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