Our paper entitled "Disruption of mitochondrial dynamics affects behaviour and lifespan in Caenorhabditis elegans" has been accepted by Cellular and Molecular Life Sciences!!
Fundamental to the function of mitochondria is their ability to divide and fuse. Mutations in the genes that control these events are associated with neurodegenerative disease, including Charcot-Marie Tooth type 2A. We mutated these genes in C. elegans to define their roles in animal behaviour and lifespan. Our results demonstrate the vital importance of mitochondrial dynamics for normal behaviour and lifespan, and highlight differing roles for fusion and fission over an animals’ lifespan, with fusion required throughout life and fission more important later in life, likely to combat ageing-associated stressors.
Our paper describes new methods for quantifying mitochondrial morphology in C. elegans tissues, and identifies surprising tissue-specific differences in morphology in the absence of fusion or fission proteins. We show that loss of the mitochondrial fusion or fission proteins induces age-dependent and progressive deficits in animal movement, and in neuronal and muscle function. From ultrastructural analysis, we reveal a novel role for the fusion protein FZO-1 / Mitofusin 2 in regulating the structure of the inner mitochondrial membrane. Furthermore, we find that loss of the individual fusion/fission proteins all significantly reduce median lifespan, but maximal lifespan remains unchanged.
Congratulations to all involved!
Fundamental to the function of mitochondria is their ability to divide and fuse. Mutations in the genes that control these events are associated with neurodegenerative disease, including Charcot-Marie Tooth type 2A. We mutated these genes in C. elegans to define their roles in animal behaviour and lifespan. Our results demonstrate the vital importance of mitochondrial dynamics for normal behaviour and lifespan, and highlight differing roles for fusion and fission over an animals’ lifespan, with fusion required throughout life and fission more important later in life, likely to combat ageing-associated stressors.
Our paper describes new methods for quantifying mitochondrial morphology in C. elegans tissues, and identifies surprising tissue-specific differences in morphology in the absence of fusion or fission proteins. We show that loss of the mitochondrial fusion or fission proteins induces age-dependent and progressive deficits in animal movement, and in neuronal and muscle function. From ultrastructural analysis, we reveal a novel role for the fusion protein FZO-1 / Mitofusin 2 in regulating the structure of the inner mitochondrial membrane. Furthermore, we find that loss of the individual fusion/fission proteins all significantly reduce median lifespan, but maximal lifespan remains unchanged.
Congratulations to all involved!
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