Opa1 and Drp1 reciprocally regulate cristae morphology, ETC function, and NAD+ regeneration in KRas-mutant lung adenocarcinoma
Dane Sessions, Kee‐Beom Kim, Jennifer A. Kashatus, Nikolas Churchill, Kwon-Sik Park, Marty W. Mayo, Hiromi Sesaki, David F. Kashatus
Abstract
regeneration. Simultaneous inactivation of Drp1 and Opa1 restores cristae morphology, ETC activity, and cell proliferation indicating that mitochondrial fission activity drives ETC dysfunction induced by Opa1 knockout. Our results support a model in which mitochondrial fission events disrupt cristae structure, and tumor cells with hyperactive fission activity require Opa1 activity to maintain ETC function.
Topics & Concepts
Cell biologyRegeneration (biology)MutantNAD+ kinaseKRASFunction (biology)BiologyLungAdenocarcinomaCancer researchMutationGeneticsCancerInternal medicineMedicineBiochemistryGeneEnzymeRNA modifications and cancerMitochondrial Function and PathologyATP Synthase and ATPases Research