Efficient terminal erythroid differentiation requires the APC/C cofactor Cdh1 to limit replicative stress in erythroblasts.

ABSTRACT: The APC/C-Cdh1 ubiquitin ligase complex drives proteosomal degradation of cell cycle regulators and other cellular proteins during the G1 phase of the cycle. The complex serves as an important modulator of the G1/S transition and prevents premature entry into S phase, genomic instability, and tumor development. Additionally, mounting evidence supports a role for this complex in cell differentiation, but its relevance in erythropoiesis has not been addressed so far. Here we show, using mouse models of Cdh1 deletion, that APC/C-Cdh1 activity is required for efficient terminal erythroid differentiation during fetal development as well as postnatally. Consistently, Cdh1 ablation leads to mild but persistent anemia from birth to adulthood. Interestingly, loss of Cdh1 seems to affect both, stead

SUBMITTER: Cuadrado M 

PROVIDER: S-EPMC9213546 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature