High impact information on KRE6

• KRE6 and SKN1 are predicted to encode homologous proteins that participate in assembly of the cell wall polymer (1-->6)-beta-glucan [1].
• Kre6p when even mildly overproduced, can suppress this pkc1 lysis defect [1].
• Mutations in two other loci, KRE5 and KRE6 also lead to a defect in cell wall (1----6)-beta-glucan production and appear to be epistatic to KRE1 [2].
• The KRE6 gene product is required for synthesis of the major beta-glucans of the yeast cell wall, as mutations in this gene confer reduced levels of both the (1----6)- and (1----3)-beta-D-glucan polymers [3].
• Yeast beta-glucan synthesis: KRE6 encodes a predicted type II membrane protein required for glucan synthesis in vivo and for glucan synthase activity in vitro [3].

Biological context of KRE6

• The phenotype and structure of the KRE6 product, Kre6p, suggest that Kre6p may be a beta-glucan synthase, and if so, it implies that beta-glucan synthases are functionally redundant in yeast [3].
• Determination of DNA sequence in the KRE6 region of the Saccharomyces cerevisiae genome completes a 10.4 kbp section on the extreme right arm of chromosome XVI [4].
• We have reinvestigated the role of Kre6 and Skn1 in the biogenesis of beta1,6-glucan [5].

Anatomical context of KRE6

• It has been postulated that the synthesis of beta1,6-glucan begins in the endoplasmic reticulum with the formation of protein-bound primer structures and that these primer structures are extended in the Golgi complex by two putative glucosyltransferases that are functionally redundant, Kre6 and Skn1 [5].

Associations of KRE6 with chemical compounds

• Synthetic defects for growth are also observed with mutation in KRE6, a gene coding for a glucan synthase, required for cell wall construction [6].

Regulatory relationships of KRE6

• The results of Northern blot analysis revealed that C. albicans KRE6 was expressed at a higher level than SKN1 in the yeast phase, while SKN1 expression was strongly induced upon induction of hyphal formation [7].
• When KRE6 transcription was suppressed by using the HEX1 promoter, C. albicans cells exhibited the partial defect in cell separation and increased susceptibility to Calcofluor White [7].

Other interactions of KRE6

• CWH41 also displays strong genetic interactions with KRE1 and KRE6, two genes known to be involved in the beta 1,6-glucan biosynthetic pathway [8].
• Successful incorporation of HA-tagged Sed1p into the cell wall involves KRE6 [9].
• The indispensability of BIG1 and KRE6 for the viability of gas1Delta cells confirmed the important role of beta-1,6-glucan in cells that are defective in the processing of beta-1,3-glucan [10].
• KRE6, encoding a glucanase-like protein, was identified as a multicopy suppressor of a temperature-sensitive kre5 allele, suggesting that these proteins may participate in a common beta-1,6-biosynthetic pathway [11].
• Kre6p showed extensive co-localization with Och1p-containing cis-Golgi vesicles [12].

References