Journal of Microbiology and Biotechnology

The Korean Society for Microbiology and Biotechnology (한국미생물·생명공학회)
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High Copy Rme1p Suppresses Iron-Induced Cell Growth Defect of Saccharomyces cerevisiae

  • Park, Yong-Sung (School of Life Sciences and Biotechnology, Korea University) ;
  • Yun, Cheol-Won (School of Life Sciences and Biotechnology, Korea University) ;
  • Kong, Jae-Yang (Korea Research Institute of Chemical Technology) ;
  • Kim, Tae-Hyoung (Chosun University School of Medicine, Department of Biochemistry ＆ Molecular Biology) ;
  • Sung, Ha-Chin (School of Life Sciences and Biotechnology, Korea University)
  • Published : 2004.06.01
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Abstract

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 over-load. When $Aft1-1^{up}$ protein was overexpressed with Ga110 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 Rmelp 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 $G_1$, phase by iron overload via Cln2p.

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References

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