Mitochondrial stress induces transcription of cytosolic and mitochondrial protein synthesis components via NHR-180.

Inhibition of NHR-180 enhances mitochondrial function and development in atfs-1(null) C. elegans under mitochondrial stress.

• Why it matters: Understanding how mitochondrial stress responses are regulated can reveal targets for improving mitochondrial health and function, especially when key regulators like ATFS-1 are impaired.
• What they did: Researchers performed an RNAi suppressor screen in C. elegans and found that reducing NHR-180 activity increases mitochondrial function and development, with NHR-180 levels rising during mitochondrial dysfunction and promoting gene transcription for protein synthesis.
• The result: NHR-180 inhibition, along with S6 kinase suppression, improves mitochondrial respiration, mtDNA content, and function in both worms and mammalian models, suggesting potential strategies to mitigate mitochondrial deficiencies.