Michael M. Francis

Transcriptional responses to chronic oxidative stress require cholinergic activation of G-protein-coupled receptor signaling

This study shows that cholinergic activation of G-protein-coupled receptor signaling is essential for transcriptional responses to chronic oxidative stress in C. elegans, linking cholinergic signaling to antioxidant defenses and neurodegenerative disease.

Genome-wide analysis reveals pathways important for the development and maturation of excitatory synaptic connections to GABAergic neurons

The paper identifies three C. elegans genes critical for synapse formation and maturation with GABAergic neurons through genetic screening.

Cell non-autonomous signaling through the conserved C. elegans glycopeptide hormone receptor FSHR-1 regulates cholinergic neurotransmission

This study identifies FSHR-1 as a key receptor mediating cell non-autonomous regulation of synaptic transmission in C. elegans through inter-tissue signaling.

The homeodomain transcriptional regulator DVE-1 directs a program for synapse elimination during circuit remodeling

This paper identifies DVE-1 as a transcriptional regulator that directs synapse elimination during GABAergic circuit remodeling in C. elegans by controlling the ubiquitin-proteasome system.

Kinesin-3 mediated axonal delivery of presynaptic neurexin stabilizes dendritic spines and postsynaptic components

The paper shows that kinesin-3 delivers neurexin to presynaptic terminals, stabilizing dendritic spines and postsynaptic components in C. elegans motor neurons.

A conserved neuropeptide system links head and body motor circuits to enable adaptive behavior

The paper shows that the NLP-12 neuropeptide system in C. elegans modulates head and body motor circuits through CKR-1 and CKR-2 GPCRs to regulate food search behavior.

Gain-of-function mutations in the UNC-2/CaV2α channel lead to hyperactivity and excitation-dominant synaptic transmission in Caenorhabditis elegans

This study identifies a gain-of-function mutation in the UNC-2/CaV2α channel in C. elegans that causes hyperactivity and excitation-dominant synaptic transmission by altering cholinergic and GABAergic transmission.