Mösch H U, Kübler E, Krappmann S, Fink G R, Braus G H
Institute for Microbiology and Genetics, Georg-August-University, D-37077 Göttingen, Germany.
Mol Biol Cell. 1999 May;10(5):1325-35. doi: 10.1091/mbc.10.5.1325.
The two highly conserved RAS genes of the budding yeast Saccharomyces cerevisiae are redundant for viability. Here we show that haploid invasive growth development depends on RAS2 but not RAS1. Ras1p is not sufficiently expressed to induce invasive growth. Ras2p activates invasive growth using either of two downstream signaling pathways, the filamentation MAPK (Cdc42p/Ste20p/MAPK) cascade or the cAMP-dependent protein kinase (Cyr1p/cAMP/PKA) pathway. This signal branch point can be uncoupled in cells expressing Ras2p mutant proteins that carry amino acid substitutions in the adenylyl cyclase interaction domain and therefore activate invasive growth solely dependent on the MAPK cascade. Both Ras2p-controlled signaling pathways stimulate expression of the filamentation response element-driven reporter gene depending on the transcription factors Ste12p and Tec1p, indicating a crosstalk between the MAPK and the cAMP signaling pathways in haploid cells during invasive growth.
芽殖酵母酿酒酵母的两个高度保守的RAS基因对细胞活力而言是冗余的。在此我们表明，单倍体侵袭性生长发育依赖于RAS2而非RAS1。Ras1p表达量不足以诱导侵袭性生长。Ras2p利用两条下游信号通路中的任意一条激活侵袭性生长，即丝状化丝裂原活化蛋白激酶（Cdc42p/Ste20p/丝裂原活化蛋白激酶）级联反应或环磷酸腺苷依赖性蛋白激酶（Cyr1p/环磷酸腺苷/蛋白激酶A）通路。在表达Ras2p突变蛋白的细胞中，该信号分支点可被解开，这些突变蛋白在腺苷酸环化酶相互作用结构域中携带氨基酸替换，因此激活仅依赖于丝裂原活化蛋白激酶级联反应的侵袭性生长。Ras2p控制的两条信号通路均依赖转录因子Ste12p和Tec1p刺激丝状化反应元件驱动的报告基因的表达，这表明在单倍体细胞侵袭性生长过程中，丝裂原活化蛋白激酶和环磷酸腺苷信号通路之间存在串扰。
