Saccharomyces cerevisiae Heat Shock Transcription Factor Regulates Cell Wall Remodeling in Response to Heat Shock

American Society for Microbiology - Tập 4 Số 6 - Trang 1050-1056 - 2005
Hiromi Imazu1, Hiroshi Sakurai1
1School of Health Sciences, Faculty of Medicine, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa 920-0942, Japan

Tóm tắt

ABSTRACT The heat shock transcription factor Hsf1 of the yeast Saccharomyces cerevisiae regulates expression of genes encoding heat shock proteins and a variety of other proteins as well. To better understand the cellular roles of Hsf1, we screened multicopy suppressor genes of a temperature-sensitive hsf1 mutation. The RIM15 gene, encoding a protein kinase that is negatively regulated by the cyclic AMP-dependent protein kinase, was identified as a suppressor, but Rim15-regulated stress-responsive transcription factors, such as Msn2, Msn4, and Gis1, were unable to rescue the temperature-sensitive growth phenotype of the hsf1 mutant. Another class of suppressors encoded cell wall stress sensors, Wsc1, Wsc2, and Mid2, and the GDP/GTP exchange factor Rom2 that interacts with these cell wall sensors. Activation of a protein kinase, Pkc1, which is induced by these cell wall sensor proteins upon heat shock, but not activation of the Pkc1-regulated mitogen-activated protein kinase cascade, was necessary for the hsf1 suppression. Like Wsc-Pkc1 pathway mutants, hsf1 cells exhibited an osmotic remedial cell lysis phenotype at elevated temperatures. Several of the other suppressors were found to encode proteins functioning in cell wall organization. These results suggest that Hsf1 in concert with Pkc1 regulates cell wall remodeling in response to heat shock.

Từ khóa


Tài liệu tham khảo

10.1128/mcb.8.9.3761-3769.1988

10.1128/MCB.21.19.6515-6528.2001

10.1128/MCB.16.10.5264

10.1046/j.1365-2958.1999.01467.x

10.4161/cc.3.4.791

10.1002/cfg.85

10.1083/jcb.147.1.163

10.1083/jcb.200104057

10.1093/genetics/142.4.1083

10.1126/science.1059497

10.1074/jbc.M312954200

10.1093/emboj/16.16.4924

10.1074/jbc.M210691200

10.1128/MMBR.62.4.1264-1300.1998

10.1128/MCB.24.12.5249-5256.2004

10.1128/MCB.24.9.3648-3659.2004

10.1046/j.1365-2958.1999.01375.x

10.1007/s004380050717

10.1002/j.1460-2075.1991.tb07958.x

10.1046/j.1365-2958.1999.01667.x

10.1101/gad.9.13.1559

10.1128/JB.181.11.3330-3340.1999

10.1111/j.1574-6976.2002.tb00613.x

10.1111/j.1574-6968.1995.tb07347.x

10.1083/jcb.116.5.1221

10.1128/MCB.20.11.3843-3851.2000

10.1128/MCB.19.1.402

10.1101/gad.12.24.3788

10.1128/JB.181.24.7414-7420.1999

10.1091/mbc.12.6.1835

10.1074/jbc.274.19.13235

10.1016/0092-8674(90)90124-W

10.1002/j.1460-2075.1996.tb00573.x

10.1128/mcb.12.11.4896-4905.1992

10.1093/emboj/19.11.2569

10.1128/MCB.21.1.271-280.2001

10.1096/fj00-0294rev

10.1128/MCB.19.6.3969

10.1101/gad.12.18.2943

10.1091/mbc.e02-04-0201

10.1073/pnas.88.24.11295

10.1083/jcb.127.2.567

10.1007/s004120050364

10.1006/bbrc.2001.5234

10.1093/genetics/162.2.663

10.1128/MCB.15.10.5618

10.1016/0092-8674(90)90123-V

10.1046/j.1365-2958.1999.01538.x

10.1099/00221287-146-9-2133

10.1074/jbc.273.41.26875

10.1073/pnas.94.25.13804

10.1128/MCB.17.5.2688

10.1074/jbc.M411256200

10.1128/MCB.16.10.5254

10.1242/jcs.110.16.1879

Thông tin
Thông tin xuất bản

American Society for Microbiology

Tập 4 Số 6

1050-1056

Thông tin tác giả