Fig. 4: Loss of MYT1L disrupts proportions of excitatory neurons at P1.
From: MYT1L deficiency impairs excitatory neuron trajectory during cortical development
A UMAP projection showing 98,797 nuclei in 36 clusters from the forebrain of P1 MYT1L WT (n = 8) and Het (n = 4) animals. B From left to right: summary plot showing the numbers of nuclei and genes detected in each cluster; bar plot displaying the mean ± SEM relative proportions of nuclei in each annotated cell cluster for MYT1L WT and Het genotypes; mean ± SEM proportions of Het normalized to WT; and number of differentially expressed genes (DEGs) per cell type that are upregulated in WT (light blue; n = 8 biological replicates) and upregulated in Het (medium blue, n = 4 biological replicates) (*FDR adjusted p < 0.05, moderated t-test). Dot plots showing enriched GO biological processes terms in (C) MYT1L-activated (decreased expression in Het) and (D) MYT1L-repressed (increased expression in Het) DEGs. Overrepresentation of genes within GO terms was determined using a one-sided hypergeometric test, with p values adjusted for multiple testing using the Benjamini-Hochberg method. E UMAP visualization of excitatory neuron clusters colored by pseudotime. The arrow indicates the inferred developmental trajectory from early (blue) to late (yellow) pseudotime. F Distribution of excitatory neuron subtypes along the pseudotime axis for WT (light blue; n = 8 biological replicates) and Het (blue; n = 4 biological replicates). Box plots show median (center line), interquartile range (box), and whiskers extending to 1.5 times the interquartile range. Asterisks indicate statistically significant differences between WT and Het distributions (*FDR adjusted p < 0.05, two-sided Kolmogorov-Smirnov test). G Percentage change in cell proportion along pseudotime in Het samples normalized to WT for two excitatory neuron subtypes: Im L2-4 ExN (top) and Im ExN_1 (bottom).
