Caenorhabditis elegans ATPase inhibitor factor 1 (IF1) MAI-2 preserves the mitochondrial membrane potential (Δψm) and is important to induce germ cell apoptosis

Inhibitor protein
DOI: 10.1371/journal.pone.0181984 Publication Date: 2017-08-22T17:37:55Z
ABSTRACT
When the electrochemical proton gradient is disrupted in mitochondria, IF1 (Inhibitor Factor-1) inhibits reverse hydrolytic activity of F1Fo-ATP synthase, thereby allowing cells to conserve ATP at expense losing mitochondrial membrane potential (Δψm). The function has been studied mainly different cell lines, but these studies have generated contrasting results, which not helpful understand real role this protein a whole organism. In work, we Caenorhabditis elegans IF1´s vivo. C. two inhibitor proteins F1Fo-ATPase, MAI-1 and MAI-2. To determine their localization elegans, translational reporters found that MAI-2 expressed ubiquitously mitochondria; conversely, was cytoplasm nuclei certain tissues. By CRISPR/Cas9 genome editing, mai-2 mutant alleles. Here, showed animals normal progeny, embryonic development lifespan. Contrasting with results previously obtained no evident defects network, dimer/monomer synthase ratio, concentration or respiration. Our suggest some roles attributed lines could reflect organism be specific methods used silence, knockout overexpress protein. However, did observe lacking had an enhanced Δψm lower physiological germ apoptosis. Importantly, must under stress IF1. Accordingly, observed were more sensitive heat shock, oxidative electron transport chain blockade. Furthermore, important induce apoptosis types stress. propose might play by regulating Δψm. Additionally, that, conditions, does essential role.
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