Khursheed Alam Wani

The paper identifies oleate depletion as a metabolic signal sensed by C. elegans to activate innate immunity against bacterial infection.

This study identifies kri-1/KRIT1 as a regulator that limits skn-1/NRF2 activity to control immune responses and lipid homeostasis in C. elegans, supporting reproductive health.

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.

This study shows that S. aureus infection causes degeneration of nociceptive neurons in C. elegans, leading to impaired behavior and reduced neuronal function.

The paper identifies lysosomal TIR-1/SARM1 as a sensor for oxidative stress induced by pathogenic bacteria, activating intestinal immunity in C. elegans.

This study shows that a glucose-fed microbiota in C. elegans reduces lifespan and healthspan, increases intestinal permeability, and raises susceptibility to bacterial pathogens.

The paper shows that the C. elegans neuron RIM both promotes and suppresses locomotion behavior to fine tune motor output through dual neurotransmission mechanisms.