THE CELL-SURFACE FLOCCULIN FLO11 IS REQUIRED FOR PSEUDOHYPHAE FORMATION AND INVASION BY SACCHAROMYCES-CEREVISIAE

Citation
Ws. Lo et Am. Dranginis, THE CELL-SURFACE FLOCCULIN FLO11 IS REQUIRED FOR PSEUDOHYPHAE FORMATION AND INVASION BY SACCHAROMYCES-CEREVISIAE, Molecular biology of the cell, 9(1), 1998, pp. 161-171
Citations number
34
Categorie Soggetti
Cell Biology",Biology
ISSN journal
10591524
Volume
9
Issue
1
Year of publication
1998
Pages
161 - 171
Database
ISI
SICI code
1059-1524(1998)9:1<161:TCFFIR>2.0.ZU;2-5
Abstract
Diploid yeast develop pseudohyphae in response to nitrogen starvation, while haploid yeast produce invasive filaments which penetrate the ag ar in rich medium. We have identified a gene, FLO11, that-encodes a ce ll wall protein which is critically required for both invasion and pse udohyphae formation in response to nitrogen starvation. FLO11 encodes a cell surface flocculin with a structure similar to the class of yeas t serine/threonine-rich GPI-anchored cell wall proteins. Cells of the Saccharomyces cerevisiae strain Sigma 1278b with deletions of FLO11 do not form pseudohyphae as diploids nor invade agar as haploids. In ric h media, FLO11 is regulated by mating type; it is expressed in haploid cells but not in diploids. Upon transfer to nitrogen starvation media , however, FLO11 transcripts accumulate in diploid cells, but not in h aploids. Overexpression of FLO11 in diploid cells, which are otherwise not invasive, enables them to invade agar. Thus, the mating type repr ession of FLO11 in diploids grown in rich media suffices to explain th e inability of these cells to invade. The promoter of FLO11 contains a consensus binding sequence for Ste12p and Tec1p, proteins known to co operatively activate transcription of Ty1 elements and the TEC1 gene d uring development of pseudohyphae. Yeast with a deletion of STE12 does not express FLO11 transcripts, indicating that STE12 is required for FLO11 expression. These ste12-deletion strains also do not invade agar . However, the ability to invade can be restored by overexpressing FLO 11. Activation of FLO11 may thus be the primary means by which Ste12p and Tec1p cause invasive growth.