High impact information on KRE9

• Using this screen, we were surprised to identify two KRE genes (KRE5 and KRE9) that are involved in the biosynthesis of the cell wall beta1,6-glucan [1].
• The Candida albicans KRE9 gene is required for cell wall beta-1, 6-glucan synthesis and is essential for growth on glucose [2].
• The yeast KRE9 gene encodes an O glycoprotein involved in cell surface beta-glucan assembly [3].
• Analysis of the glucan material remaining in a kre9 delta null mutant indicated a polymer with a reduced average molecular mass. kre9 delta null mutants also displayed several additional cell-wall-related phenotypes, including an aberrant multiply budded morphology, a mating defect, and a failure to form projections in the presence of alpha-factor [3].
• Recessive mutations leading to killer resistance identify the KRE9, KRE10 and KRE11 genes [4].

Biological context of KRE9

• 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 [5].

Anatomical context of KRE9

• Disruption of KRE9 leads to serious growth impairment and an altered cell wall containing less than 20% of the wild-type amount of (1-->6)-beta-glucan [3].

Associations of KRE9 with chemical compounds

• The Candida glabrata KRE9 (CgKRE9) and KNH1 (CgKNH1) genes have been isolated as multicopy suppressors of the tetracycline-sensitive growth of a Saccharomyces cerevisiae mutant with the disrupted KNH1 locus and the KRE9 gene placed under the control of a tetracycline-responsive promoter [6].

Other interactions of KRE9

• The KNH1 gene of Saccharomyces cerevisiae is a functional homolog of KRE9 [5].
• A search for genes which, at elevated copy number, could suppress the growth defect in a strain disrupted at the KRE9 locus has identified the SKN7 gene [7].

References