Reference: Frydlova I, et al. (2009) Deregulation of DSE1 gene expression results in aberrant budding within the birth scar and cell wall integrity pathway activation in Saccharomyces cerevisiae. Eukaryot Cell 8(4):586-94

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Abstract

Strains of Saccharomyces cerevisiae lacking Isw2, the catalytic subunit of the Isw2 chromatin remodeling complex, show the mating type independent activation of the cell wall integrity (CWI) signaling pathway. Since the CWI pathway activation usually reflects cell wall defects, we searched for the cell wall-related genes changed in expression. The genes DSE1, CTS1 and CHS1 were upregulated as a result of the Isw2 absence, according to previously published gene expression profiles (Frydlova, I., M. Basler, P. Vasicova, I. Malcova, and J. Hasek. 2007. Curr Genet 52:87-95). Western blot analyses of double deletion mutants, however, did not indicate contribution of the chitin metabolism-related genes CTS1 and CHS1 to the CWI pathway activation. Nevertheless, deletion of the DSE1 gene encoding a daughter cell-specific protein with unknown function suppressed the CWI pathway activation in isw2Delta cells. In addition, deletion of DSE1 also abolished the budding-within-the-birth-scar phenotype of isw2Delta cells. Plasmid-driven overexpression proved that deregulation of the Dse1 synthesis was also responsible for the CWI pathway activation and manifestation of the budding-within-the-birth-scar phenotype in wild-type cells. The overproduced Dse1-GFP localized to both sides of the septum and persisted in unbudded cells. Although the exact cellular role of this daughter cell-specific protein has to be elucidated, our data point to involvement of Dse1 in bud site selection in haploid cells.

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Journal Article
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Frydlova I, Malcova I, Vasicova P, Hasek J
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