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Mitochondrial OPA1 cleavage is reversibly activated by differentiation of H9c2 cardiomyoblasts by Iraselia Garcia; Fredy Calderon; Patrick De la Torre; Shaynah St. Vallier; Cristobal Rodriguez; Divya Agarwala; Megan Keniry; Wendy Innis-Whitehouse; Robert Gilkerson is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is Mitochondrial OPA1 cleavage is reversibly activated by differentiation of H9c2 cardiomyoblasts about?

Optic atrophy-1 (OPA1) is a dynamin-like GTPase localized to the mitochondrial inner membrane, playing key roles in inner membrane fusion and cristae maintenance. OPA1 is regulated by the mitochondrial transmembrane potential (Δψ): when Δψ is intact, long OPA1 isoforms (L-OPA1) carry out inner membrane fusion. Upon loss of Δψ, L-OPA1 isoforms are proteolytically cleaved to short (S-OPA1) isoforms by the stress-inducible OMA1 metalloprotease, causing collapse of the mitochondrial network and promoting apoptosis. Here, we show that L-OPA1 isoforms of H9c2 cardiomyoblasts are retained under loss of Δψ, despite the presence of OMA1. However, when H9c2s are differentiated to a more cardiac-like phenotype via treatment with retinoic acid (RA) in low serum media, loss of Δ ψ induces robust, and reversible, cleavage of L-OPA1 and subsequent OMA1 degradation. These findings indicate that a potent developmental switch regulates Δ ψ-sensitive OPA1 cleavage, suggesting novel developmental and regulatory mechanisms for OPA1 homeostasis.

Who reads Mitochondrial OPA1 cleavage is reversibly activated by differentiation of H9c2 cardiomyoblasts?

Author

Iraselia Garcia; Fredy Calderon; Patrick De la Torre; Shaynah St. Vallier; Cristobal Rodriguez; Divya Agarwala; Megan Keniry; Wendy Innis-Whitehouse; Robert Gilkerson

Publisher

Elsevier BV

Published

2020

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)