C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.

Leptin acts cell autonomously on brainstem neurons that express GLP-1 to suppress development of excitatory viscerosensory inputs to the hypothalamus.

Experimental results suggest a previously unknown regulatory mechanism for GLP-1 production in L cells, which could offer new insights into diabetes treatments.

Non-native synthetic short-chain glycosphingolipids fused to GLP-1 enable intestinal absorption with high bioavailability in vivo.

Analyzing the readout of Notch signaling with single RNA precision reveals that active transcription sites are the most accurate measure of Notch-dependent transcriptional activation.

A genetically encoded sensor and a photocaged peptide together enable precise investigation of human glucagon-like peptide-1 receptor activation with high spatiotemporal resolution.

Autophagic flux assays in the nematode Caenorhabditis elegans suggest that autophagy decreases during normal aging, whereas long-lived daf-2 and glp-1 mutants maintain autophagic capacity in distinct spatiotemporal-specific manners to extend lifespan.

Increased Notch signaling enhances germ cell reprograming in C. elegans by antagonizing PRC2-mediated repression, which results in the activation of UTX-1 and other reprograming-promoting genes.

Class 1 histone deacetylase (HDAC) inhibitor MS-275 enhances the efficacy of glucagon-like peptide 1 receptor (GLP-1R) therapy for glycemic control and reduction of obesity.

Somatic aging and germline RNAi pathways promote inheritance of ancestral starvation memory through reallocation of fat storage in Caenorhabditis elegans.