The KNH1 gene of Saccharomyces cerevisiae is a functional homolog of KRE9.

The KNH1 gene from Saccharomyces cerevisiae was identified as an open reading frame on the right arm of chromosome IV. The product encoded by the KNH1 gene, Knhlp, shares 46% overall identity with Kre9p, a protein required for cell surface beta 1,6-glucan synthesis. While disruption of the KNH1 locus had no effect on cell growth, killer toxin sensitivity 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 levels. Knhlp, like Kre9p, can be found in the extracellular culture medium 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. Transcription of KNH1 was found to be carbon-source and kre9 delta dependent, but SKN7 independent, suggesting that KNH1 is subject to alternative transcriptional control.