1998 Fiscal Year Final Research Report Summary

Inositol/TGFbeta receptor signal transduction in yeast

Research Project

Project/Area Number	09680627
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Functional biochemistry
Research Institution	Kyushu Institute of Technology
Principal Investigator	NIKAWA Junichi Kyushu Institute of Technology Faculty of Computer Science and Systems Engineering, Associate Professor, 情報工学部, 助教授 (00134271)
Project Period (FY)	1997 – 1998
Keywords	Yeast / Inositol / TGFbeta receptor
Research Abstract	We previously reported that thc Saccharomyces cerevisiae irel5 mutation results in an inositol-auxotiophic phenotype, and that human cDNAs, such as TGF^<beta> receptor-encoding cDNA, can suppress the irel5 mutation. In this study, we found that the gene responsible for the irel5 mutation is HAG 1, which encodes a transcription factor for KAR2, obtained by isolating a yeast single-copy suppressor gene and by performing complementation analysis. Sequencing analysis revealed that the mutant HAG I gene obtained from We ire 15 mutant contained an AAA codon at position 50 instead of the AGA coin observed in the wild-type gene, resulting in the altearition of the amino acid horn Aug to Lys. All human cDNAs and yeast multicopy suppressors, which had been isolated -as suppressors for the irel5 mutation, were able to suppress the inositol-auxotrophic phenotype but not the defect in KA R2 induction of the hac I-disrupted strain

(2 results)