![]() The fluorescence of MitoGFP was observed along ventral cord neurites of (A,B,C) wild-type animals, (D,E,F) egl-9(sa307) mutants, (G,H,I) hif-1(ia4) mutants, (J,K,L) egl-9(sa307) hif-1(ia4) double mutants, and (M,N,O) egl-9 mutants with a transgene expressing the wild-type EGL-9A cDNA from the glr-1 promoter. Our results suggest the existence of a conserved anoxic stress response involving changes in mitochondrial fission and fusion. In response to anoxia, SKN-1 promotes the expression of the mitochondrial resident protein Stomatin-like 1 (STL-1), which helps facilitate mitochondrial dynamics following anoxia. ![]() Anoxia results in mitochondrial oxidative stress, and the oxidative response factor SKN-1/Nrf is required for both rapid mitochondrial refusion and rapid behavioral recovery during reoxygenation. Mitochondria are significantly larger in egl-9 mutants after reoxygenation, a phenotype similar to stress-induced mitochondria hyperfusion (SIMH). Mutants for egl-9 exhibit a rapid refusion of mitochondria and a rapid behavioral recovery from suspended animation during reoxygenation both phenotypes require HIF-1. The hypoxia response pathway, including EGL-9 and HIF-1, is not required for anoxia-induced fission, but does regulate mitochondrial reconstitution during reoxygenation. We show that neuronal mitochondria undergo DRP-1-dependent fission in response to anoxia and undergo refusion upon reoxygenation. elegans, which adapt to extreme oxygen deprivation (anoxia, less than 0.1% oxygen) by entering into a reversible suspended animation state of locomotory arrest. Here we examine mitochondrial stress response in C. ![]() It is important to understand how mitochondria respond to oxygen deprivation given the critical role they play in using oxygen to generate cellular energy. Many aerobic organisms encounter oxygen-deprived environments and thus must have adaptive mechanisms to survive such stress.
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