Transcriptional coregulation by the cell integrity mitogen-activated protein kinase Slt2 and the cell cycle regulator Swi4

Citation
K. Baetz et al., Transcriptional coregulation by the cell integrity mitogen-activated protein kinase Slt2 and the cell cycle regulator Swi4, MOL CELL B, 21(19), 2001, pp. 6515-6528
Citations number
59
Categorie Soggetti
Molecular Biology & Genetics
Journal title
MOLECULAR AND CELLULAR BIOLOGY
ISSN journal
02707306 → ACNP
Volume
21
Issue
19
Year of publication
2001
Pages
6515 - 6528
Database
ISI
SICI code
0270-7306(200110)21:19<6515:TCBTCI>2.0.ZU;2-F
Abstract
In Saccharomyces cerevisiae, the heterodimeric transcription factor SBF (fo r SCB binding factor) is composed of Swi4 and Swi6 and activates gene expre ssion at the G(1)/S-phase transition of the mitotic cell cycle. Cell cycle commitment is associated not only with major alterations in gene expression but also with highly polarized cell growth; the mitogen-activated protein kinase (MAPK) Slt2 is required to maintain cell wall integrity during perio ds of polarized growth and cell wall stress. We describe experiments aimed at defining the regulatory pathway involving the cell cycle transcription f actor SBF and Slt2-MAPK. Gene expression assays and chromatin immunoprecipi tation experiments revealed Slt2-dependent recruitment of SBF to the promot ers of the G(1) cyclins PCL1 and PCL2 after activation of the Slt2-MAPK pat hway. We performed DNA microarray analysis and identified other genes whose expression was reduced in both SLT2 and SWI4 deletion strains. Genes that are sensitive to both Slt2 and Swi4 appear to be uniquely regulated and rev eal a role for Swi4, the DNA-binding component of SBF, which is independent of the regulatory subunit Swi6. Some of the Swi4- and Slt2-dependent genes do not require Swi6 for either their expression or for Swi4 localization t o their promoters. Consistent with these results, we found a direct interac tion between Swi4 and Slt2. Our results establish a new Slt2-dependent mode of Swi4 regulation and suggest roles for Swi4 beyond its prominent role in controlling cell cycle transcription.