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COXIV and SIRT2‐mediated G6PD deacetylation modulate ROS homeostasis to extend pupal lifespan
Author(s) -
Geng ShaoLei,
Zhang XiaoShuai,
Xu WeiHua
Publication year - 2021
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.15592
Subject(s) - tfam , sirtuin , biology , reactive oxygen species , sirt2 , microbiology and biotechnology , nrf1 , sod2 , diapause , mitochondrial ros , mitochondrion , acetylation , biochemistry , oxidative stress , mitochondrial biogenesis , superoxide dismutase , gene , larva , botany
Low levels of growth hormone 20E in diapause‐destined pupae inhibit both PKA and sirtuin 2 levels, which fail to improve the c‐Myc/TFAM/cytochrome oxidase subunit IV (COXIV) expression and Glucose‐6‐phosphate dehydrogenase (G6PD) activity, and cause increased reactive oxygen species (ROS) levels in mitochondria and cytoplasm to induce diapause and extend the pupal lifespan. However, in nondiapause‐destined pupal brains, the activated PKA‐TFAM‐COXIV pathway and high G6PD activity respond to high 20E levels, which reduce the ROS levels and thus induce pupal‐adult development.