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hyperfused mitochondrial state achieved at G₁-S regulates cyclin E buildup and entry into S phase
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hyperfused mitochondrial state achieved at G₁-S regulates cyclin E buildup and entry into S phase
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Journal Article
hyperfused mitochondrial state achieved at G₁-S regulates cyclin E buildup and entry into S phase
2009
Overview
Mitochondria undergo fission-fusion events that render these organelles highly dynamic in cells. We report a relationship between mitochondrial form and cell cycle control at the G₁-S boundary. Mitochondria convert from isolated, fragmented elements into a hyperfused, giant network at G₁-S transition. The network is electrically continuous and has greater ATP output than mitochondria at any other cell cycle stage. Depolarizing mitochondria at early G₁ to prevent these changes causes cell cycle progression into S phase to be blocked. Inducing mitochondrial hyperfusion by acute inhibition of dynamin-related protein-1 (DRP1) causes quiescent cells maintained without growth factors to begin replicating their DNA and coincides with buildup of cyclin E, the cyclin responsible for G₁-to-S phase progression. Prolonged or untimely formation of hyperfused mitochondria, through chronic inhibition of DRP1, causes defects in mitotic chromosome alignment and S-phase entry characteristic of cyclin E overexpression. These findings suggest a hyperfused mitochondrial system with specialized properties at G₁-S is linked to cyclin E buildup for regulation of G₁-to-S progression.
Publisher
National Academy of Sciences,National Acad Sciences
