Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

We examined the effect of Myt1l deficiency in the cortices of mice during developement. Homozygous Myt1l deficiency resulted in postnatal lethality, and mutant mice presented gene expression changes associated with developmental delays and resembled changes observed in autism spectrum disorder patients. Overall design: Bulk RNA sequencing of Myt1l (+/+; WT), Myt1l (+/-; HET), and Myt1l (-/-; HOM) mouse cortices at E18.5, P0, and of Myt1l (+/+; WT), Myt1l (+/-; HET) at P22, and adult (3-month-old).