Abstract
Background: Mitochondrial dynamics are tightly coupled with cellular redox homeostasis; however, the underlying regulatory mechanisms remain poorly defined. Methods: We constructed yeast mutants and evaluated mitochondrial function, morphology, and redox states using growth assays, fluorescence imaging, and flow cytometry. RNA sequencing, RIP assays, and RT-qPCR were applied to identify Ecm19p target genes. Results: Deletion of ECM19 alone had no evident impact on mitochondrial morphology or respiratory function. In contrast, double deletion of ECM19 with the fusion gene FZO1 (ecm19D fzo1D) rescued mitochondrial function and morphology and reduced ROS and malondialdehyde levels relative to fzo1D. Conversely, combining ecm19D with fission genes MDV1 or CAF4 resulted in hyperfused mitochondria, dependent on the division factor Dnm1p. RNA-seq revealed that ecm19D upregulates redox processes, including catalase (CTA1) and thiol peroxidase (TSA2). RIP-PCR confirmed Ecm19p binds directly to CTA1 and TSA2 transcripts and reduces their mRNA stability. Under H₂O₂ stress, ecm19D cta1D and ecm19D tsa2D double mutants exhibited improved growth, elevated antioxidant capacity, and lower ROS and malondialdehyde than single mutants. Conclusion: Ecm19 collaborates with Mdv1 and Caf4 to promote mitochondrial fission and post-transcriptionally represses CTA1 and TSA2 expression to regulate cellular redox, thereby coordinating mitochondrial fission with redox homeostasis.