Mitochondrial Protein Synthesis Is Essential for Terminal Differentiation of CD45^- TER119^-Erythroid and Lymphoid Progenitors.

ABSTRACT: p32/C1qbp regulates mitochondrial protein synthesis and is essential for oxidative phosphorylation in mitochondria. Although dysfunction of p32/C1qbp impairs fetal development and immune responses, its role in hematopoietic differentiation remains unclear. Here, we found that mitochondrial dysfunction affected terminal differentiation of newly identified erythroid/B-lymphoid progenitors among CD45^- Ter119^- CD31^- triple-negative cells (TNCs) in bone marrow. Hematopoietic cell-specific genetic deletion of p32/C1qbp (p32cKO) in mice caused anemia and B-lymphopenia without reduction of hematopoietic stem/progenitor cells. In addition, p32cKO mice were susceptible to hematopoietic stress with delayed recovery from anemia. p32/C1qbp-deficient CD51^- TNC

SUBMITTER: Gotoh K 

PROVIDER: S-EPMC7578749 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature