ATX1 / YNL259C Overview

Standard Name
ATX1 1
Systematic Name
Feature Type
ORF , Verified
Cytosolic copper metallochaperone; transports copper to the secretory vesicle copper transporter Ccc2p for eventual insertion into Fet3p, which is a multicopper oxidase required for high-affinity iron uptake; human homolog ATOX1 can complement yeast atx1 mutant; overexpression of human ATOX1 suppresses lysine auxotrophy of the yeast sod1 null mutant, as does overexpression of yeast ATX1 1 2 3
Name Description
AnTioXidant 1
Comparative Info
Sequence Details


The S. cerevisiae Reference Genome sequence is derived from laboratory strain S288C. Download DNA or protein sequence, view genomic context and coordinates. Click "Sequence Details" to view all sequence information for this locus, including that for other strains.

Protein Details


Basic sequence-derived (length, molecular weight, isoelectric point) and experimentally-determined (median abundance, median absolute deviation) protein information. Click "Protein Details" for further information about the protein such as half-life, abundance, domains, domains shared with other proteins, protein sequence retrieval for various strains, physico-chemical properties, protein modification sites, and external identifiers for the protein.

Length (a.a.)
Mol. Weight (Da)
Isoelectric Point
Median Abundance (molecules/cell)
7617 +/- 5887
Half-life (hr)


Curated mutant alleles for the specified gene, listed alphabetically. Click on the allele name to open the allele page. Click "SGD search" to view all alleles in search results. Click "YeastMine" to view all alleles in YeastMine.

View all ATX1 alleles in SGD search | YeastMine

Gene Ontology Details

Gene Ontology

GO Annotations consist of four mandatory components: a gene product, a term from one of the three Gene Ontology (GO) controlled vocabularies (Molecular Function, Biological Process, and Cellular Component), a reference, and an evidence code. SGD has manually curated and high-throughput GO Annotations, both derived from the literature, as well as computational, or predicted, annotations. Click "Gene Ontology Details" to view all GO information and evidence for this locus as well as biological processes it shares with other genes.

Copper chaperone involved in cellular response to oxidative stress and iron ion homeostasis; localizes to the cytosol

View computational annotations

Molecular Function

Manually Curated

Biological Process

Manually Curated

Cellular Component

Manually Curated
Phenotype Details


Phenotype annotations for a gene are curated single mutant phenotypes that require an observable (e.g., "cell shape"), a qualifier (e.g., "abnormal"), a mutant type (e.g., null), strain background, and a reference. In addition, annotations are classified as classical genetics or high-throughput (e.g., large scale survey, systematic mutation set). Whenever possible, allele information and additional details are provided. Click "Phenotype Details" to view all phenotype annotations and evidence for this locus as well as phenotypes it shares with other genes.

Non-essential gene; null mutants show decreased competitive fitness, poor anoxic growth, are impaired in respiration, sensitive to cycloheximide, curcumin, antifungal ciclopirox olamine, and cardiovascular drug amiodarone; heterozygous diploid nulls are sensitive to starvation
Interaction Details


Interaction annotations are curated by BioGRID and include physical or genetic interactions observed between at least two genes. An interaction annotation is composed of the interaction type, name of the interactor, assay type (e.g., Two-Hybrid), annotation type (e.g., manual or high-throughput), and a reference, as well as other experimental details. Click "Interaction Details" to view all interaction annotations and evidence for this locus, including an interaction visualization.

87 total interactions for 80 unique genes

Physical Interactions

  • Affinity Capture-RNA: 5
  • Co-crystal Structure: 1
  • PCA: 4
  • Reconstituted Complex: 3
  • Two-hybrid: 3

Genetic Interactions

  • Dosage Rescue: 1
  • Negative Genetic: 63
  • Positive Genetic: 1
  • Synthetic Growth Defect: 3
  • Synthetic Haploinsufficiency: 1
  • Synthetic Lethality: 2
Regulation Details


The number of putative Regulators (genes that regulate it) and Targets (genes it regulates) for the given locus, based on experimental evidence. This evidence includes data generated through high-throughput techniques. Click "Regulation Details" to view all regulation annotations, shared GO enrichment among regulation Targets, and a regulator/target diagram for the locus.

ATX1 encodes a cytoplasmic metallochaperone that delivers intracellular copper cations to Ccc2p, a Cu(2+)-transporting P-type ATPase in the Golgi membrane. Copper is an essential metal component of enzymes performing electron transfer reactions. At the same time, copper is redox-active and potentially highly cytotoxic. Cells must therefore avoid accumulating free intracellular copper and control its delivery from the sites of uptake to the final destinations. The primary destinations for copper are the cytochrome c oxidase in the mitochondria, a component of the electron transport chain, the copper-zinc superoxide dismutase Sod1p in the cytoplasm, a protein involved in protection against oxidative stress, and the high affinity iron transporter Fet3p in the plasma membrane. Atx1p is a part of the Atx1p-Ccc2p relay system that delivers copper to the Golgi for incorporation into Fet3p before Fet3p is delivered to the plasma membrane via the secretory pathway. Thus, the three proteins, Atx1p, Ccc2p and Fet3p, link both copper and iron homeostasis. Expression of all three genes is known to be regulated by Aft1p, a transcriptional activator that relocates to the nucleus under low-iron conditions. ATX1 has also been shown to be induced by oxygen but the mechanisms have not been studied. A similar copper relay system exists in human cells: human Atox1/HAH10, homolog of ATX1, encodes a copper chaperone, and ATP7A and ATP7B, homologs of CCC2, encode copper-transporting ATPases in the Golgi. The human proteins can complement the respective yeast mutations. Defects in this system, caused by mutations in ATP7A or ATP7B, result in Menkes or Wilson diseases, respectively.
Expression Details


Expression data are derived from records contained in the Gene Expression Omnibus (GEO), and are first log2 transformed and normalized. Referenced datasets may contain one or more condition(s), and as a result there may be a greater number of conditions than datasets represented in a single clickable histogram bar. The histogram division at 0.0 separates the down-regulated (green) conditions and datasets from those that are up-regulated (red). Click "Expression Details" to view all expression annotations and details for this locus, including a visualization of genes that share a similar expression pattern.

Summary Paragraph

A summary of the locus, written by SGD Biocurators following a thorough review of the literature. Links to gene names and curated GO terms are included within the Summary Paragraphs.

Last Updated: 2005-07-18

Literature Details


All manually curated literature for the specified gene, organized into topics according to their relevance to the gene (Primary Literature, Additional Literature, or Review). Click "Literature Details" to view all literature information for this locus, including shared literature between genes.