Taxonomic group: fungi / Ascomycota
(Phylum: Ascomycota)
Organ / tissue: cell wall
NCBI PubMed ID: 8026578Journal NLM ID: 0155157Publisher: Elsevier
Institutions: Department of Mycology and Molecular Genetics, Nippon Roche Research Center, Kanagawa, Japan
HM-1 killer toxin secreted from Hansenula mrakii inhibits the growth of Saccharomyces cerevisiae cells by interfering with β-1,3-glucan synthesis. We found that HM-1 killer toxin killed intact cells but not protoplasts. In addition, cells lacking the functional KRE6 allele (kre6 delta) became resistant to higher concentration of HM-1 killer toxin. As reported by Roemer and Bussey [(1991) Proc. Natl. Acad. Sci. 88 11295-11299], cells lacking functional KRE6 had a reduced level of the cell wall β-1,6-glucan compared to that in cells harboring the normal KRE6. These results suggest that the cell wall β-glucan is involved in the action of HM-1 killer toxin. Addition of HM-1 killer toxin with several kinds of oligosaccharides revealed that either β-1,3- or β-1,6-glucan blocked the cytocidal action of HM-1 killer toxin whereas α-1,4-glucan and chitin did not. Mannan also interfered with HM-1 killer toxin action, but this inhibitory effect was much weaker than that observed with β-1,3- or β-1,6-glucans. Thus, it appears that the cell wall β-glucan interacts with HM-1 killer toxin, and that this toxin-β-glucan commitment is required for the action of HM-1 killer toxin.
Structure type: homopolymer ; n=20
Trivial name: pachyman
Contained glycoepitopes: IEDB_1397514,IEDB_142488,IEDB_146664,IEDB_153543,IEDB_158555,IEDB_161166,IEDB_558869,IEDB_857743,IEDB_983931,SB_192
Methods: GLC, Southern blotting, cloning, toxin resistance assay, single-step gene disruption, methylation assay. acid hydrolysis
Biosynthesis and genetic data: genetic data
Related record ID(s): 125818
NCBI Taxonomy refs (TaxIDs): 4932Reference(s) to other database(s): GTC:G51056AN, CCSD:
33804, CBank-STR:4225
Show glycosyltransferases
There is only one chemically distinct structure:
Found 
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