EGD1 facilitates nascent polypeptide chain binding to ribosomes and coordinates protein targeting to mitochondria. Key findings include:
Mitophagy Regulation: EGD1 interacts with Atg32, a pro-mitophagic protein, to enable mitochondrial degradation. Deletion of EGD1 reduces Atg32 phosphorylation and mitophagy efficiency, whereas BTT1 (a paralogous β-subunit) deletion has minimal impact .
Protein Folding: NAC disruption alters chaperone balance, rescuing polyglutamine-induced toxicity in yeast. EGD1Δ strains show partial rescue of htt-103Q toxicity, unlike EGD2Δ or BTT1Δ strains .
EGD1 influences transcriptional activation in galactose-regulated genes. Disruption of EGD1 delays GAL1/10 induction during carbon source shifts, suggesting a role in modulating Gal4p activity .
Mitochondrial Degradation: EGD1Δ yeast exhibit impaired mitophagy and reduced Atg32 phosphorylation .
Transcriptional Defects: EGD1 disruption delays GAL1/10 RNA accumulation during galactose induction .
EGD1 and BTT1 are paralogous β-subunits with distinct roles:
EGD1’s role in mitochondrial quality control and transcriptional regulation positions it as a potential therapeutic target for diseases involving protein misfolding or metabolic dysfunction. Further studies could explore:
Antifungal Strategies: Leveraging EGD1’s interaction with Atg32 to enhance antifungal efficacy.
Neurodegenerative Diseases: Investigating EGD1’s role in mitigating polyglutamine toxicity in mammalian models.
KEGG: cgr:CAGL0L12540g
STRING: 284593.XP_449313.1