Up-regulation of genes encoding glycosylphosphatidylinositol (GPI)-attached proteins in response to cell wall damage caused by disruption of FKS1 in Saccharomyces cerevisiae

Citation
H. Terashima et al., Up-regulation of genes encoding glycosylphosphatidylinositol (GPI)-attached proteins in response to cell wall damage caused by disruption of FKS1 in Saccharomyces cerevisiae, MOL G GENET, 264(1-2), 2000, pp. 64-74
Citations number
75
Categorie Soggetti
Molecular Biology & Genetics
Journal title
MOLECULAR AND GENERAL GENETICS
ISSN journal
00268925 → ACNP
Volume
264
Issue
1-2
Year of publication
2000
Pages
64 - 74
Database
ISI
SICI code
0026-8925(200009)264:1-2<64:UOGEG(>2.0.ZU;2-0
Abstract
FKS1 and FKS2 encode alternative catalytic subunits of the glucan synthases that are responsible for synthesis of beta-1,3-glucan in the Saccharomyces cerevisiae cell wall. Disruption of FKS1 reduces the glucan content of the cell wall. increases chitin content and activates the expression of CWP1, which encodes a glycosylphosphatidylinositol (GPI)-dependent cell wall prot ein. These cellular responses have been regarded as compensating for cell w all damage in order to maintain cell wall integrity. Here. we report the id entification, by genome-wide screening, of 22 genes that are transcriptiona lly up-regulated in fks1 Delta cells. Among them, five genes were found to encode GPI-attached proteins, three of which are covalently associated with the cell wall. Deletion and replacement analysis of the promoter regions i dentified Rlm1-binding sequences as being responsible for the up-regulation following disruption of FKS1. Using the rlm1 Delta tetOp-FKS1 strain, in w hich the expression of FKS1 can be repressed by doxycycline, we examined th e requirement for Rlm1 for the transcriptional up-regulation of these five genes. Three of the five genes were not up-regulated by doxycycline, indica ting that Rlm1 mediates their up-regulation when FKS1 is inactivated. The r emaining two genes were up-regulated by doxycycline, suggesting that a tran scription factor other than Rlm1 is involved in their response to disruptio n of FKS1.