AIM14/YGL160W Summary Help

AIM14 BASIC INFORMATION

Standard Name AIM14 1
Systematic Name YGL160W
Feature Type ORF, Verified
Description Putative protein of with similarity to iron/copper reductases (FRE1-8), possibly involved in iron homeostasis; may interact with ribosomes; null mutant displays elevated frequency of mitochondrial genome loss (1, 2, 3 and see Summary Paragraph)
Name Description Altered Inheritance rate of Mitochondria 1
GO Annotations All AIM14 GO evidence and references
    View Computational GO annotations for AIM14
Molecular Function
Manually curated
Biological Process
Manually curated
Cellular Component
Manually curated
High-throughput
Mutant Phenotype All AIM14 Phenotype details and references
Large-scale survey
null
overexpression
Interactions AIM14 All interactions details and references
4 total interaction(s) for 4 unique genes/features.
Physical Interactions
  • Affinity Capture-MS: 1
  • Affinity Capture-RNA: 2

Genetic Interactions
  • Synthetic Haploinsufficiency: 1

Sequence Information
ChrVII:200567 to 202279 | ORF Map | GBrowse
Gbrowse
Last Update Coordinates: 2004-07-20 | Sequence: 1996-07-31
Subfeature details
Relative
Coordinates
Chromosomal
Coordinates
Most Recent Updates
Coordinates Sequence
CDS 1..1713 200567..202279 2004-07-20 1996-07-31
External Links All Associated Seq | Entrez Gene | Entrez RefSeq Protein | MIPS | UniProtKB
Primary SGDIDS000003128

AIM14 RESOURCES

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Click on histogram for expression summary
Expression Summary histogram

SUMMARY PARAGRAPH for AIM14

YGL160W is part of a family of nine homologous genes involved or predicted to be involved in iron uptake that can be roughly grouped into three classes based on sequence similarity and transcriptional regulation: FRE1 and FRE7; FRE2 through FRE6; and FRE8 and YGL160W (2, 4). FRE8 and YGL160W transcription is not affected by either iron or copper (2). Mutants lacking FRE8 are unable to grow in low iron and are respiration deficient (5).

Fre1p and Fre2p are the major cell-surface iron reductases and together account for 90-98% of cell-surface reductase activity (6, 7, 8). Fre1p and Fre2p are homologous to the human gp91phox protein (OMIM), the large subunit of human cytochrome b558 (8, 9, 10), which reduces oxygen to bactericidal superoxide (O2-) on the surface of phagocytic leukocytes. Deficiency of gp91phox causes X-linked chronic granulomatous disease (OMIM).

Last updated: 2005-08-17

REFERENCES CITED ON THIS PAGE [View Complete Literature Guide for AIM14]

1) Hess DC, et al.  (2009) Computationally driven, quantitative experiments discover genes required for mitochondrial biogenesis. PLoS Genet 5(3):e1000407
2) Georgatsou E and Alexandraki D  (1999) Regulated expression of the Saccharomyces cerevisiae Fre1p/Fre2p Fe/Cu reductase related genes. Yeast 15(7):573-84
3) Fleischer TC, et al.  (2006) Systematic identification and functional screens of uncharacterized proteins associated with eukaryotic ribosomal complexes. Genes Dev 20(10):1294-307
4) Martins LJ, et al.  (1998) Metalloregulation of FRE1 and FRE2 homologs in Saccharomyces cerevisiae. J Biol Chem 273(37):23716-21
5) De Freitas JM, et al.  (2004) Exploratory and confirmatory gene expression profiling of mac1Delta. J Biol Chem 279(6):4450-8
6) Dancis A, et al.  (1990) Genetic evidence that ferric reductase is required for iron uptake in Saccharomyces cerevisiae. Mol Cell Biol 10(5):2294-301
7) Anderson GJ, et al.  (1992) Ferric iron reduction and iron assimilation in Saccharomyces cerevisiae. J Inorg Biochem 47(3-4):249-55
8) Georgatsou E and Alexandraki D  (1994) Two distinctly regulated genes are required for ferric reduction, the first step of iron uptake in Saccharomyces cerevisiae. Mol Cell Biol 14(5):3065-73
9) Dancis A, et al.  (1992) Ferric reductase of Saccharomyces cerevisiae: molecular characterization, role in iron uptake, and transcriptional control by iron. Proc Natl Acad Sci U S A 89(9):3869-73
10) Shatwell KP, et al.  (1996) The FRE1 ferric reductase of Saccharomyces cerevisiae is a cytochrome b similar to that of NADPH oxidase. J Biol Chem 271(24):14240-4