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Metalloprotease OMA1 is involved in fine‐tuning of mitochondrial bioenergetic function in embryonic development (756.4)
Author(s) -
Khalimonchuk Oleh,
Zahayko Nataliya,
Rahn Jennifer,
Fernandez Mario,
Lewis Robert,
Chan Sherine
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.756.4
Subject(s) - microbiology and biotechnology , bioenergetics , biology , mitochondrion , zebrafish , mitochondrial fusion , mitochondrial dna , genetics , gene
Mitochondria are involved in key cellular functions including energy production, metabolic homeostasis and apoptosis. Normal mitochondrial function is preserved by several interrelated mechanisms. One mechanism ‐ intramitochondrial quality control (IMQC) is represented by conserved proteases distributed across mitochondrial compartments. Many aspects of IMQC are unclear. Together with the m‐AAA protease, OMA1 (ATP‐independent protease in the inner membrane (IM)) was implicated in depolarization‐induced cleavage of IM GTPase OPA1 and thus regulation of mitochondrial dynamics in response to stress. Genetic knockout of OMA1 in the mouse altered energy expenditure and thermogenesis. These defects were attributed to the impeded stress processing of OPA1. We investigated the role of OMA1 in embryonic development using the zebrafish model. Analysis of the OMA1 morphant embryos revealed abnormal blood circulation and developmental defects of the heart and eyes. Surprisingly, the levels and processing of OPA1 were not significantly altered. In vivo evaluation of respiratory function in OMA1‐/‐ MEFs indicated loss of OMA1 leads to bioenergetic deficits without impairing basal mitochondrial efficiency. These results point to the importance of OMA1 in vertebrate development and indicate a role of this protease in the fine‐tuning of respiratory function that may extend beyond stress processing of OPA1. Grant Funding Source : NIH‐NIGMS P30 GM103335