期刊
CELL REPORTS
卷 14, 期 7, 页码 1684-1697出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.01.039
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资金
- NIH [R01 EY024906, R01 EB016629, P20 EB007076, R01 DE023177, R01 HL118761, P30 EY002520, P30 EY007551]
- Kyle and Josephine Morrow Endowed Chair
- Vivian L. Smith Foundation
- Knights Templar Eye Foundation Career Starter Grant
A fundamental principle governing organ size and function is the fine balance between cell proliferation and cell differentiation. Here, we identify RONIN (THAP11) as a key transcriptional regulator of retinal progenitor cell (RPC) proliferation. RPC-specific loss of Ronin results in a phenotype strikingly similar to that resulting from the G1- to S-phase arrest and photoreceptor degeneration observed in the Cyclin D1 nullmutants. However, we determined that, rather than regulating canonical cell-cycle genes, RONIN regulates a cohort of mitochondrial genes including components of the electron transport chain (ETC), which have been recently implicated as direct regulators of the cell cycle. Coincidentally, with premature cell-cycle exit, Ronin mutants exhibited deficient ETC activity, reduced ATP levels, and increased oxidative stress that we ascribe to specific loss of subunits within complexes I, III, and IV. These data implicate RONIN as a positive regulator of mitochondrial gene expression that coordinates mitochondrial activity and cell-cycle progression.
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