Abstract：
:Nutrients are not only organic compounds fueling bioenergetics and biosynthesis, but also key chemical signals controlling growth and metabolism. Nutrients enormously impact the production of reactive oxygen species (ROS), which play essential roles in normal physiology and diseases. How nutrient signaling is integrated with redox regulation is an interesting, but not fully understood, question. Herein, we report that superoxide dismutase 1 (SOD1) is a conserved component of the mechanistic target of rapamycin complex 1 (mTORC1) nutrient signaling. mTORC1 regulates SOD1 activity through reversible phosphorylation at S39 in yeast and T40 in humans in response to nutrients, which moderates ROS level and prevents oxidative DNA damage. We further show that SOD1 activation enhances cancer cell survival and tumor formation in the ischemic tumor microenvironment and protects against the chemotherapeutic agent cisplatin. Collectively, these findings identify a conserved mechanism by which eukaryotes dynamically regulate redox homeostasis in response to changing nutrient conditions.
journal_name
Mol Celljournal_title
Molecular cellauthors
Tsang CK,Chen M,Cheng X,Qi Y,Chen Y,Das I,Li X,Vallat B,Fu LW,Qian CN,Wang HY,White E,Burley SK,Zheng XFSdoi
10.1016/j.molcel.2018.03.029subject
Has Abstractpub_date
2018-05-03 00:00:00pages
502-515.e8issue
3eissn
1097-2765issn
1097-4164pii
S1097-2765(18)30232-6journal_volume
70pub_type
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