Has a role in both calcium and manganese homeostasis. Involved in the transfer of iron and Mn(2+) from the cytosol to the vacuole for storage of these metals. Down-regulated under iron starvation by TIS11. Transcriptionally up-regulated by YAP5 in response to increased cytosolic iron. Deletion causes an increase in metal sensitivity at 15 mM manganese, but does not affect invertase glycosylation. Deletion shows increased sensitivity to external iron, which is suppressed by MRS3 or MRS4 overexpression requiring oxygen but not respiration, and exacerbated by ectopic expression of the iron transporter FET4. Deletion also results in decreased vacuolar iron content and decreased iron stores, which affect cytosolic iron levels and cell growth. Deletion together with MRS3 and MRS4 restores cellular and mitochondrial iron homeostasis to near normal level, corrects the MRS3 and MRS4 double deletion phenotype (which shows increased resistance to cobalt but decreased resistance to copper and cadmium), and has near normal levels of aconitase activity. When overexpressed, maintains respiratory function in a YFH1 deletion mutant regardless of extracellular iron concentration, activates the iron-dependent transcription factor AFT1 resulting in an increase in iron uptake, cytosolic iron accumulation and a change in copper metabolism. Overexpression prevents excessive mitochondrial iron accumulation by limiting mitochondrial iron uptake and results in increased expression of the high affinity iron transport system composed of FET3 and FTR1. Overexpression also suppresses the rapamycin-resistant phenotype of PMR1 deletion mutant. Present with 2840 molecules/cell in log phase SD medium. Belongs to the CCC1 family.