BioProject

Mitochondrial functions across different tissues are regulated in a coordinated fashion to optimize fitness of the organism. More...

Mitochondrial functions across different tissues are regulated in a coordinated fashion to optimize fitness of the organism. Mitochondrial unfolded protein response (UPRmt) can be non-autonomously elicited by mitochondrial perturbation in neurons, but neuronal signals that propagate such response and its physiological significance remains incompletely understood. Here we show that in C. elegans, loss of neuronal fzo-1/Mitofusin induces non-autonomous UPRmt through multiple neurotransmitters and neurohormones, including acetylcholine, serotonin, glutamate, tyramine and insulin-like peptides. Neuronal fzo-1 depletion also triggers non-autonomous mitochondrial fragmentation, which requires autophagy and mitophagy genes. Systemic activation of UPRmt and mitochondrial fragmentation in C. elegans via perturbing neuronal mitochondrial dynamics improves resistance to pathogenic Pseudomonas infection, which is supported by transcriptomic signatures of immunity and stress response genes. We propose that C. elegans surveils neuronal mitochondrial dynamics that coordinate systemic UPRmt and mitochondrial connectivity for pathogen defense and optimized survival under bacterial infection. Overall design: Total RNA profiles of zcIs13 and zcIs13; Punc-119_ds-fzo-1 RNAi Caenorhabditis elegans were generated by deep sequencing using Illumina Solexa technology. Less...