Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells [gene expression]
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ABSTRACT: Autophagy is critical for protecting HSCs from metabolic stress. Here, we used a genetic approach to inactivate autophagy in adult HSCs by deleting the Atg12 gene. We show that loss of autophagy causes accumulation of mitochondria and an oxidative phosphorylation (OXPHOS)-activated metabolic state, which drives accelerated myeloid differentiation likely through epigenetic deregulations rather than transcriptional changes, and impairs HSC self-renewal activity and regenerative potential. To determine how loss of autophagy affects gene expression, we conducted microarray analysis of purified control and Atg12 conditional knockout HSCs.
ORGANISM(S): Mus musculus
PROVIDER: GSE81719 | GEO | 2017/03/03
SECONDARY ACCESSION(S): PRJNA322388
REPOSITORIES: GEO
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