Blocked O-GlcNAc cycling disrupts mouse hematopoeitic stem cell maintenance and early T cell development.

ABSTRACT: Small numbers of hematopoietic stem cells (HSCs) balance self-renewal and differentiation to produce the diversity and abundance of cell types that make up the blood system. How nutrients are recruited to support this massive differentiation and proliferation process remains largely unknown. The unique metabolism of adult HSCs, which rely on glycolysis and glutaminolysis, suggests a potential role for the post-translational modification O-GlcNAc as a critical nutrient signal in these cells. Glutamine, glucose, and other metabolites drive the hexosamine biosynthetic pathway (HBP) ultimately leading to the O-GlcNAc modification of critical intracellular targets. Here, we used a conditional targeted genetic deletion of the enzyme that removes O-GlcNAc, O-GlcNAcase (OGA), to determine the cons

SUBMITTER: Abramowitz LK 

PROVIDER: S-EPMC6715813 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature