Your browser doesn't support javascript.
loading
Neuronal mitochondrial dynamics coordinate systemic mitochondrial morphology and stress response to confer pathogen resistance in C. elegans.
Chen, Li-Tzu; Lin, Chih-Ta; Lin, Liang-Yi; Hsu, Jiun-Min; Wu, Yu-Chun; Pan, Chun-Liang.
Afiliación
  • Chen LT; Institute of Molecular Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan; Center of Precision Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan.
  • Lin CT; Institute of Molecular Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan.
  • Lin LY; Institute of Molecular Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan.
  • Hsu JM; Institute of Molecular Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan.
  • Wu YC; Institute of Molecular Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan; Center of Precision Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan.
  • Pan CL; Institute of Molecular Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan; Center of Precision Medicine, College of Medicine, National Taiwan University, No.7 Chung-Shan South Road, Taipei 10002, Taiwan. Electronic address: chunliangpan@gmail.
Dev Cell ; 56(12): 1770-1785.e12, 2021 06 21.
Article en En | MEDLINE | ID: mdl-33984269
Mitochondrial functions across different tissues are regulated in a coordinated fashion to optimize the fitness of an organism. Mitochondrial unfolded protein response (UPRmt) can be nonautonomously elicited by mitochondrial perturbation in neurons, but neuronal signals that propagate such response and its physiological significance remain incompletely understood. Here, we show that in C. elegans, loss of neuronal fzo-1/mitofusin induces nonautonomous UPRmt through multiple neurotransmitters and neurohormones, including acetylcholine, serotonin, glutamate, tyramine, and insulin-like peptides. Neuronal fzo-1 depletion also triggers nonautonomous 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 to coordinate systemic UPRmt and mitochondrial connectivity for pathogen defense and optimized survival under bacterial infection.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Caenorhabditis elegans / Proteínas de Caenorhabditis elegans / GTP Fosfohidrolasas / Mitocondrias / Neuronas Límite: Animals Idioma: En Revista: Dev Cell Asunto de la revista: EMBRIOLOGIA Año: 2021 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Caenorhabditis elegans / Proteínas de Caenorhabditis elegans / GTP Fosfohidrolasas / Mitocondrias / Neuronas Límite: Animals Idioma: En Revista: Dev Cell Asunto de la revista: EMBRIOLOGIA Año: 2021 Tipo del documento: Article País de afiliación: Taiwán Pais de publicación: Estados Unidos