Abstract
In yeast, the endoplasmic reticulum (ER)-mitochondria encounter structure (ERMES) tethers the ER to mitochondria, but its primary function remains unclear. To gain insight into ERMES functions, we screened multi-copy suppressors of the growth-defective phenotype of mmm1∆ cells, which lack a core component of ERMES, and identified MCP1, MGA2, SPT23, and YGR250C (termed RIE1). Spt23 and Mga2 are homologous transcription factors known to activate transcription of the OLE1 gene, which encodes the fatty acid ∆9 desaturase. We found that Ole1 partially relieves the growth defects of ERMES-lacking cells, thus uncovering a relationship between fatty acid metabolism and ERMES functions.
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