Dosage-dependent requirements of Magoh for cortical interneuron generation and survival.

ABSTRACT: Embryonic interneuron development underlies cortical function and its disruption contributes to neurological disease. Yet the mechanisms by which viable interneurons are produced from progenitors remain poorly understood. Here, we demonstrate dosage-dependent requirements of the exon junction complex component Magoh for interneuron genesis in mouse. Conditional Magoh ablation from interneuron progenitors, but not post-mitotic neurons, depletes cortical interneuron number through adulthood, with increased severity in homozygotes. Using live imaging, we discover that Magoh deficiency delays progenitor mitotic progression in a dosage-sensitive fashion, with 40% of homozygous progenitors failing to divide. This shows that Magoh is required in progenitors for both ge

SUBMITTER: Sheehan CJ 

PROVIDER: S-EPMC6983725 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature