Bin Qi

This study identifies bacterial peptidoglycan as a conserved activator of lysosomal function that extends lifespan in C. elegans and mice by enhancing V-ATPase activity and lysosomal acidification.

This study shows that pathogen-induced neuronal signaling disrupts lysosomal function and collagen homeostasis in C. elegans, identifying NSIF-1 and ELT-3 as key regulators.

This study identifies how bacterial tryptophan metabolism activates lysosomal function to promote lipid breakdown and reduce hepatic steatosis in both C. elegans and mice.

This study identifies microbial peptidoglycan as a mitophagy inducer that protects against hepatocyte death and liver fibrosis by interacting with p62.

The paper identifies a bacterial sensing mechanism in neurons that activates intestinal mitochondrial surveillance to protect against infections.

This study shows that neurons detect harmful food sources and trigger systemic digestive shutdown to avoid harm.

The paper shows PAR-5 mediates host-pathogen co-evolution in C. elegans by enhancing embryo development and reducing pathogen virulence, while pathogens exploit PAR-5 to evade immunity.

The paper identifies the UPRER-immunity axis as a physiological system that evaluates food quality and promotes aversion to low-quality food.