Boy-Marcotte E, Perrot M, Bussereau F, Boucherie H, Jacquet M
Institut de Génétique et Microbiologie, Unité de Recherche Associée CNRS 2225, Université Paris-Sud, Orsay, France.
J Bacteriol. 1998 Mar;180(5):1044-52. doi: 10.1128/JB.180.5.1044-1052.1998.
The multicopy suppressors of the snf1 defect, Msn2p and Msn4p transcription factors (Msn2/4p), activate genes through the stress-responsive cis element (CCCCT) in response to various stresses. This cis element is also the target for repression by the cyclic AMP (cAMP)-signaling pathway. We analyzed the two-dimensional gel electrophoresis pattern of protein synthesis of the msn2 msn4 double mutant and compared it with that of the wild-type strain during exponential growth phase and at the diauxic transition. Thirty-nine gene products (including those of ALD3, GDH3, GLK1, GPP2, HSP104, HXK1, PGM2, SOD2, SSA3, SSA4, TKL2, TPS1, and YBR149W) are dependent upon Msn2/4p for their induction at the diauxic transition. The expression of all these genes is repressed by cAMP. Thirty other genes identified during this study are still inducible in the mutant. A subset of these genes were found to be superinduced at the diauxic transition, and others were subject to cAMP repression (including ACH1, ADH2, ALD6, ATP2, GPD1, ICL1, and KGD2). We conclude from this analysis that Msn2/4p control a large number of genes induced at the diauxic transition but that other, as-yet-uncharacterized regulators, also contribute to this response. In addition, we show here that cAMP repression applies to both Msn2/4p-dependent and -independent control of gene expression at the diauxic shift. Furthermore, the fact that all the Msn2/4p gene targets are subject to cAMP repression suggests that these regulators could be targets for the cAMP-signaling pathway.
snf1缺陷的多拷贝抑制因子Msn2p和Msn4p转录因子(Msn2/4p),通过应激反应顺式元件(CCCCT)激活基因以应对各种应激。该顺式元件也是环磷酸腺苷(cAMP)信号通路的抑制靶点。我们分析了msn2 msn4双突变体在指数生长期和双相转变期的蛋白质合成二维凝胶电泳图谱,并将其与野生型菌株的图谱进行比较。39种基因产物(包括ALD3、GDH3、GLK1、GPP2、HSP104、HXK1、PGM2、SOD2、SSA3、SSA4、TKL2、TPS1和YBR149W的基因产物)在双相转变期的诱导依赖于Msn2/4p。所有这些基因的表达都受到cAMP的抑制。在本研究中鉴定出的另外30种基因在突变体中仍可诱导。其中一部分基因在双相转变期被超诱导,其他基因则受到cAMP的抑制(包括ACH1、ADH2、ALD�、ATP2、GPD1、ICL1和KGD2)。我们从该分析得出结论,Msn2/4p控制大量在双相转变期诱导的基因,但其他尚未鉴定的调节因子也参与了这一反应。此外,我们在此表明,cAMP抑制适用于双相转变期基因表达的Msn2/4p依赖性和非依赖性控制。此外,所有Msn2/4p基因靶点都受到cAMP抑制这一事实表明,这些调节因子可能是cAMP信号通路的靶点。