The Saccharomyces cerevisiae ire15 mutant has a defect in the expression of the IN01 gene, showing an inositol auxotrophic phenotype. The growth defect of this mutant is suppressed by human cDNAs such as for the TGF-beta receptor-encoding gene (TGFR) [Nikawa, Gene 149 (1994) 367-372]. Here, we isolated a new human cDNA, HCP1, which suppresses the ire15 mutation by genetic complementation. Sequencing analysis revealed that HCP1 encodes 360 amino acid residues (40,515 Da). The product of HCP1 is highly conserved among species and the yeast homolog was also found to suppress the ire15 mutation. Northern blot analysis revealed that multicopies of the yeast and human HCP1, as well as TGFR, resulted in an increase in the IN01 mRNA level in the yeast mutant. These results clearly indicate that the products of human and yeast HCP1 are structural and functional homologs, and are involved in expression of genes such as of IN01.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Reference||Annotation Extension|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Conditions||Strain||Source||Reference|