Open AccessCG8005 Mediates Transit-Amplifying Spermatogonial Divisions via Oxidative Stress in Drosophila Testes
Author(s) -
Wanyin Chen,
Xiaojin Luan,
Yi–Dan Yan,
Min Wang,
Qianwen Zheng,
Xia Chen,
Jun Yu,
Jie Fang
Publication year - 2020
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2020/2846727
Subject(s) - gene knockdown , oxidative stress , keap1 , reactive oxygen species , microbiology and biotechnology , biology , gene silencing , oxidative phosphorylation , stem cell , phenotype , transcription factor , gene , biochemistry
The generation of reactive oxygen species (ROS) widely occurs in metabolic reactions and affects stem cell activity by participating in stem cell self-renewal. However, the mechanisms of transit-amplifying (TA) spermatogonial divisions mediated by oxidative stress are not fully understood. Through genetic manipulation of Drosophila testes, we demonstrated that CG8005 regulated TA spermatogonial divisions and redox homeostasis. Using in vitro approaches, we showed that the knockdown of CG8005 increased ROS levels in S2 cells; the induced ROS generation was inhibited by NAC and exacerbated by H 2 O 2 pretreatments. Furthermore, the silencing of CG8005 increased the mRNA expression of oxidation-promoting factors Keap1, GstD1, and Mal-A6 and decreased the mRNA expression of antioxidant factors cnc, Gclm, maf-S, ND-42, and ND-75. We further investigated the functions of the antioxidant factor cnc, a key factor in the Keap1-cnc signaling pathway, and showed that cnc mimicked the phenotype of CG8005 in both Drosophila testes and S2 cells. Our results indicated that CG8005, together with cnc, controlled TA spermatogonial divisions by regulating oxidative stress in Drosophila .