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Gene Review

MRS4  -  Mrs4p

Saccharomyces cerevisiae S288c

Synonyms: Mitochondrial RNA-splicing protein MRS4, YKR052C
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Disease relevance of MRS4


High impact information on MRS4

  • Mrs3p, mrs4p, and frataxin provide iron for Fe-S cluster synthesis in mitochondria [2].
  • In addition, both proteins regulate MRS4 via a variant FeRE with Aft2p being the stronger activator from this particular element [3].
  • Conversely, a deltaYFH1 strain overexpressing MRS4 has an increased mitochondrial iron content and no mitochondrial genome [4].
  • Overexpression of the MRS3 and MRS4 proteins causes a temperature-dependent petite phenotype; this is consistent with a mitochondrial function of these proteins [5].
  • When present in high copy number plasmids, the nuclear genes MRS3 and MRS4 from Saccharomyces cerevisiae can suppress the mitochondrial RNA splicing defects of several mit- intron mutations [5].

Biological context of MRS4

  • Deletion of the yeast frataxin homolog (YFH1) was combined with deletions of MRS3 and MRS4, mitochondrial carrier proteins implicated in iron homeostasis [6].
  • MRS3 and MRS4, the genes for two mitochondrial-solute carrier proteins, can suppress both phenotypes when present in high-copy-number plasmids [7].
  • In order to search for further multicopy suppressors of the mrs2-1 mutant phenotype, an yeast genomic DNA library, MW90, was constructed in YEp351 from a strain deleted for the MRS2, MRS3 and MRS4 genes [7].
  • Disruption of the yeast mfrn orthologues, MRS3 and MRS4, causes defects in iron metabolism and mitochondrial Fe-S cluster biogenesis [8].

Anatomical context of MRS4


Other interactions of MRS4

  • Frataxin and mitochondrial carrier proteins, Mrs3p and Mrs4p, cooperate in providing iron for heme synthesis [6].


  1. cDNAs from Onchocerca sp. encoding members of the MRS3/MRS4 class of mitochondrial solute carriers. Catmull, J., Miller, D.J. Biochim. Biophys. Acta (1996) [Pubmed]
  2. Mrs3p, mrs4p, and frataxin provide iron for Fe-S cluster synthesis in mitochondria. Zhang, Y., Lyver, E.R., Knight, S.A., Pain, D., Lesuisse, E., Dancis, A. J. Biol. Chem. (2006) [Pubmed]
  3. Aft1p and Aft2p mediate iron-responsive gene expression in yeast through related promoter elements. Rutherford, J.C., Jaron, S., Winge, D.R. J. Biol. Chem. (2003) [Pubmed]
  4. Deletion of the mitochondrial carrier genes MRS3 and MRS4 suppresses mitochondrial iron accumulation in a yeast frataxin-deficient strain. Foury, F., Roganti, T. J. Biol. Chem. (2002) [Pubmed]
  5. MRS3 and MRS4, two suppressors of mtRNA splicing defects in yeast, are new members of the mitochondrial carrier family. Wiesenberger, G., Link, T.A., von Ahsen, U., Waldherr, M., Schweyen, R.J. J. Mol. Biol. (1991) [Pubmed]
  6. Frataxin and mitochondrial carrier proteins, Mrs3p and Mrs4p, cooperate in providing iron for heme synthesis. Zhang, Y., Lyver, E.R., Knight, S.A., Lesuisse, E., Dancis, A. J. Biol. Chem. (2005) [Pubmed]
  7. A multitude of suppressors of group II intron-splicing defects in yeast. Waldherr, M., Ragnini, A., Jank, B., Teply, R., Wiesenberger, G., Schweyen, R.J. Curr. Genet. (1993) [Pubmed]
  8. Mitoferrin is essential for erythroid iron assimilation. Shaw, G.C., Cope, J.J., Li, L., Corson, K., Hersey, C., Ackermann, G.E., Gwynn, B., Lambert, A.J., Wingert, R.A., Traver, D., Trede, N.S., Barut, B.A., Zhou, Y., Minet, E., Donovan, A., Brownlie, A., Balzan, R., Weiss, M.J., Peters, L.L., Kaplan, J., Zon, L.I., Paw, B.H. Nature (2006) [Pubmed]
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