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Eukaryotic Cell, April 2009, p. 586-594, Vol. 8, No. 4
1535-9778/09/$08.00+0 doi:10.1128/EC.00376-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

dlová,
Ivana Malcová,
Pavla Va
icová, and
Ji
í Ha
ek*
Institute of Microbiology, Academy of Sciences of the Czech Republic, v.v.i., Prague, Czech Republic
Received 28 November 2008/ Accepted 11 February 2009
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 absence of Isw2, according to previously published gene expression profiles (I. Frydlova, M. Basler, P. Vasicova, I. Malcova, and J. Hasek, Curr. Genet. 52:87-95, 2007). Western blot analyses of double deletion mutants, however, did not indicate the contribution of the chitin metabolism-related genes CTS1 and CHS1 to the CWI pathway activation. Nevertheless, the deletion of the DSE1 gene encoding a daughter cell-specific protein with unknown function suppressed CWI pathway activation in isw2
cells. In addition, the deletion of DSE1 also abolished the budding-within-the-birth-scar phenotype of isw2
cells. The plasmid-driven overexpression proved that the deregulation of Dse1 synthesis was also responsible for CWI pathway activation and manifestation of the budding-within-the-birth-scar phenotype in wild-type cells. The overproduced Dse1-green fluorescent protein 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 the involvement of Dse1 in bud site selection in haploid cells.
ská 1083, 142 20 Prague 4, Czech Republic. Phone: 420-241062503. Fax: 420-241062501. E-mail: hasek{at}biomed.cas.cz
Published ahead of print on 27 February 2009.
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