Autophagy collaborates with apoptosis pathways to control oligodendrocyte number.

Autor:	Zhang T; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Bhambri A; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Zhang Y; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Barbosa D; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Bae HG; Department of Cellular and Integrative Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA., Xue J; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Wazir S; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Mulinyawe SB; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA., Kim JH; Department of Cellular and Integrative Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA., Sun LO; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: lu.sun@utsouthwestern.edu.
Jazyk:	angličtina
Zdroj:	Cell reports [Cell Rep] 2023 Aug 29; Vol. 42 (8), pp. 112943. Date of Electronic Publication: 2023 Aug 06.
DOI:	10.1016/j.celrep.2023.112943
Abstrakt:	Oligodendrocytes are the sole myelin-producing cells in the central nervous system. Oligodendrocyte number is tightly controlled across diverse brain regions to match local axon type and number, yet the underlying mechanisms remain unclear. Here, we show that autophagy, an evolutionarily conserved cellular process that promotes cell survival under physiological conditions, elicits premyelinating oligodendrocyte apoptosis during development. Autophagy flux is increased in premyelinating oligodendrocytes, and its genetic blockage causes ectopic oligodendrocyte survival throughout the entire brain. Autophagy functions cell autonomously in the premyelinating oligodendrocyte to trigger cell apoptosis, and it genetically interacts with the TFEB pathway to limit oligodendrocyte number across diverse brain regions. Our results provide in vivo evidence showing that autophagy promotes apoptosis in mammalian cells under physiological conditions and reveal key intrinsic mechanisms governing oligodendrogenesis. Competing Interests: Declaration of interests The authors declare no competing interests. (Published by Elsevier Inc.)
Databáze:	MEDLINE
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