Disease relevance of MRS4

• cDNA clones from the parasitic nematodes Onchocerca volvulus and Onchocerca gibsoni encode homologs of the yeast proteins MRS3 and MRS4 [1].

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

• The function of MRS4 in iron import into mitochondria is discussed [4].

Other interactions of MRS4

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

References