Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L

被引：28

作者：

Wani, Gulzar A. ^{[1
]}

Sprenger, Hans-Georg ^{[2
]}

Ndoci, Kristiano ^{[1
]}

Chandragiri, Srikanth ^{[2
]}

Acton, Richard James ^{[1
]}

Schatton, Desiree ^{[1
]}

Kochan, Sandra M. V. ^{[1
]}

Sakthivelu, Vignesh ^{[1
]}

Jevtic, Milica ^{[1
]}

Seeger, Jens M. ^{[3
,4
]}

Mueller, Stefan ^{[1
,5
]}

Giavalisco, Patrick ^{[2
]}

Rugarli, Elena I. ^{[1
,6
]}

Motori, Elisa ^{[1
,2
]}

Langer, Thomas ^{[1
,2
]}

Bergami, Matteo ^{[1
,5
,6
,7
,8
]}

机构：

[1] Univ Cologne, Cologne Excellence Cluster Cellular Stress Respon, Joseph Stelzmann Str 26, D-50931 Cologne, Germany

[2] Max Planck Inst Biol Ageing, Joseph Stelzmann Str 9b, D-50931 Cologne, Germany

[3] CECAD Res Ctr, Inst Mol Immunol, Joseph Stelzmann Str 26, D-50931 Cologne, Germany

[4] Univ Hosp Cologne, Joseph Stelzmann Str 26, D-50931 Cologne, Germany

[5] Ctr Mol Med, Robert Koch Str 21, D-50931 Cologne, Germany

[6] Univ Cologne, Inst Genet, Zueurolpicher Str 47a, D-50674 Cologne, Germany

[7] Univ Cologne, Fac Med, Kerpener Str 62, D-50937 Cologne, Germany

[8] Univ Hosp Cologne, Kerpener Str 62, D-50937 Cologne, Germany

来源：

CELL REPORTS | 2022年 / 38卷 / 07期

基金：

欧洲研究理事会;

关键词：

MASS-SPECTROMETRY; SUBVENTRICULAR ZONE; REVEALS; OPA1; DYNAMICS; FUSION; NEUROGENESIS; QUIESCENCE; PHENOTYPES; ENERGY;

D O I：

10.1016/j.celrep.2022.110370

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页数：25

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