PLX289067

GSE86479: Pseudotemporal ordering of single cells reveals metabolic control of postnatal beta cell proliferation

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

Maintenance of blood glucose homeostasis depends on appropriate pancreatic beta cell mass, which is established during early postnatal life through expansion of beta cell numbers. Postnatally, the proliferative capacity of beta cells declines rapidly but the cell extrinsic cues and intracellular signals that cause this decline remain unknown. Here we generated single-cell RNA-seq data of beta cells from multiple postnatal time points and ordered cells based on transcriptional similarity along a linear trajectory. This analysis increased the resolution of transcriptome dynamics during postnatal beta cell development and revealed decreasing mRNA levels of a network of transcription factors, mitochondrial genes and regulators of amino acid metabolism. Through experimental validation we show that these transcription factors and metabolic pathways drive neonatal beta cell proliferation and mass expansion, suggesting a causal role for their regulation in the postnatal decline of beta growth. SOURCE: Maike Sander (masander@ucsd.edu) - UC San Diego