Cep55 regulation of PI3K/Akt signaling is required for neocortical development and ciliogenesis.

ABSTRACT: Homozygous nonsense mutations in CEP55 are associated with several congenital malformations that lead to perinatal lethality suggesting that it plays a critical role in regulation of embryonic development. CEP55 has previously been studied as a crucial regulator of cytokinesis, predominantly in transformed cells, and its dysregulation is linked to carcinogenesis. However, its molecular functions during embryonic development in mammals require further investigation. We have generated a Cep55 knockout (Cep55-/-) mouse model which demonstrated preweaning lethality associated with a wide range of neural defects. Focusing our analysis on the neocortex, we show that Cep55-/- embryos exhibited depleted neural stem/progenitor cells in the ventricular zone as a result of significantly increased cel

SUBMITTER: Rashidieh B 

PROVIDER: S-EPMC8577787 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature