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DNA base excision repair and nucleotide excision repair synergistically contribute to survival of stationary‐phase cells of the fission yeast Schizosaccharomyces pombe
Author(s) -
Senoo Takanori,
Kawano Shinji,
Ikeda Shogo
Publication year - 2017
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10722
Subject(s) - schizosaccharomyces pombe , base excision repair , nucleotide excision repair , dna repair , biology , dna damage , dna glycosylase , schizosaccharomyces , mutant , proliferating cell nuclear antigen , microbiology and biotechnology , genetics , dna , gene
Defects of genome maintenance may causally contribute to aging. In general, base excision repair (BER) is involved in the repair of subtle base lesions and AP sites, and bulky helix‐distorting lesions are restored by nucleotide excision repair (NER). Here, we measured the chronological lifespan (CLS) of BER‐ and NER‐deficient mutants of the fission yeast Schizosaccharomyces pombe , and observed the aging process of cells. The CLS of the nth1 (gene for DNA glycosylase/AP lyase) mutant and the rad16 (a homolog of human XPF ) mutant were slightly shorter than that of the wild‐type (WT) strain. However, survival of the nth1 Δ rad16 Δ double mutant was significantly reduced after entry into the stationary phase. Deletion of rad16 in an AP endonuclease mutant apn2 Δ also accelerated chronological aging. These results indicate that BER and NER synergistically contribute to genome maintenance in non‐dividing cells. Reactive oxygen species (ROS) accumulated in cells during the stationary phase, and nth1 Δ rad16 Δ cells produced more ROS than WT cells. High mutation frequencies and nuclear DNA fragmentation were observed in nth1 Δ rad16 Δ stationary‐phase cells concurrent with apoptotic‐like cell death. Calorie restriction significantly reduced the level of ROS in the stationary phase and extended the CLS of nth1 Δ rad16 Δ cells. Therefore, ROS production critically affects the survival of the DNA repair mutant during chronological aging.