High copy Rme1p suppresses iron-induced cell growth defect of Saccharomyces cerevisiae

In the yeast Saccharomyces cerevisiae, iron can be toxic. Because of this phenomenon, its metabolism of iron is strictly regulated. We have constructed a model system in which cell growth is defected during periods of iron overload. When Aft1-1^up protein was overexpressed with Gal10 promoter, a galactose inducible promoter, cell growth was defected and levels of CLN2 transcript decreased. However transcript levels of AFT1 and FET3 genes increased over time in a consistent manner throughout the course of AFT1-1^up overexpression. We have screened to find genes to suppress cell growth defect by iron overload with YEp-derived high copy yeast genomic DNA library and found that high copy of Rme1p suppressed cell growth defects. Rme1p has been known as an activator protein of CLN2 gene expression. Taking these results together, we suggest that the yeast cell cycle is arrested at the G₁ phase by iron overload via Cln2p.