Topic: cortical excitatory neurons

Prader-Willi syndrome (PWS) is a neurodevelopmental disorder, characterized by hyperphagia, developmental delay and cognitive deficits. The PWS genomic locus (15q11-q13) is maternally imprinted and the pathology arises when the paternal genome copy is deleted, with maternal uniparental disomy of chromosome 15 or imprinting defects. This genomic locus harbors different C/D box small nucleolar RNAs (SNORDs) that feature short transcripts usually involved in post-transcriptional modifications of rRNA. In particular, SNORD116 is included in the majority of the disease-causing chromosomal deletions

The cerebral cortex is composed of an extraordinary number of neuronal and glial cell types assembling into cortical circuits that account for cognitive abilities. Remarkable heterogeneity in the spectrum of cortical cell types has been described on the basis of global transcriptome analysis. How cell-type diversity is generated by radial glia progenitor (RGP) cells during development is however still poorly understood. Here we focus on the Rptor/mTORC1 signaling pathway and its role in RGP cell lineage progression and cortical neurogenesis. By using Mosaic Analysis with Double Markers (MADM)