Inhibition of scheggia/SLC25A1 citrate transporter alleviates XPD deficits.

ABSTRACT: XPD is an evolutionarily conserved protein critical for DNA repair, transcription, cell cycle, and chromosome segregation. XPD mutations result in complex genetic diseases, including xeroderma pigmentosum (XP). XPD is also implicated in protecting cells from oxidative stress but has not been linked to specific metabolic gene functions. Here, we report an intriguing genetic interaction between Drosophila Xpd and the scheggia (sea) gene encoding the mitochondrial citrate transporter. We show that the reduced eye size by Xpd RNAi in Drosophila is partially restored by the knockdown of sea. sea RNAi suppresses ectopic cell death and DNA damages resulting from Xpd knockdown. To test whether this negative relationship between Xpd and sea can be recapitulated in human cells, we examined the effec

SUBMITTER: Cho DG 

PROVIDER: S-EPMC12669715 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature