The KNH1 gene from Saccharomyces cerevisiae was identified as an open
reading frame on the right arm of chromosome IV. The product encoded b
y the KNH1 gene, Knh1p, shares 46% overall identity with Kre9p, a prot
ein required for cell surface beta 1,6-glucan synthesis. While disrupt
ion of the KNH1 locus had no effect on cell growth, killer toxin sensi
tivity or beta 1,6-glucan levels, overexpression of KNH1 was found to
suppress the severe growth defect of a kre9 Delta mutant and restored
the level of alkali-insoluble beta 1,6-glucan to almost wild-type leve
ls. Knh1p, like Kre9p, can be found in the extracellular culture mediu
m as an O-glycoprotein, with a molecular mass of 45-61 kDa. Disruption
of both KNH1 and KRE9 is lethal, and unlike single kre9 Delta mutants
, could not be rescued by overproducing SKN7, a putative transcription
factor involved in the regulation of extracellular matrix assembly. T
ranscription of KNH1 was found to be carbon-source and kre9 Delta depe
ndent, but SKN7 independent, suggesting that KNH1 is subject to altern
ative transcriptional control. The KNH1 sequence has been deposited in
GenBank under Accession Number U31538.