Wani, Gulzar A.; Sprenger, Hans-Georg; Ndoci, Kristiano; Chandragiri, Srikanth; Acton, Richard James; Schatton, Desiree; Kochan, Sandra M. V.; Sakthivelu, Vignesh; Jevtic, Milica; Seeger, Jens M.; Mueller, Stefan; Giavalisco, Patrick; Rugarli, Elena I.; Motori, Elisa; Langer, Thomas; Bergami, Matteo published the artcile< Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L>, SDS of cas: 112-63-0, the main research area is mitochondrial protease adult neural stem cell selfrenewal metabolic control; OMA1; YME1L; adult neurogenesis; metabolic rewiring; mitochondria; mitochondrial dynamics; mitochondrial proteome; neural stem cells; proliferation; self-renewal.
The transition between quiescence and activation in neural stem and progenitor cells (NSPCs) is coupled with reversible changes in energy metabolism with key implications for lifelong NSPC self-renewal and neurogenesis. How this metabolic plasticity is ensured between NSPC activity states is unclear. We find that a state-specific rewiring of the mitochondrial proteome by the i-AAA peptidase YME1L is required to preserve NSPC self-renewal. YME1L controls the abundance of numerous mitochondrial substrates in quiescent NSPCs, and its deletion activates a differentiation program characterized by broad metabolic changes causing the irreversible shift away from a fatty-acid-oxidation-dependent state. Conditional Yme1l deletion in adult NSPCs in vivo results in defective self-renewal and premature differentiation, ultimately leading to NSPC pool depletion. Our results disclose an important role for YME1L in coordinating the switch between metabolic states of NSPCs and suggest that NSPC fate is regulated by compartmentalized changes in protein network dynamics.
Cell Reports published new progress about Adult, mammalian. 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, SDS of cas: 112-63-0.
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