Ng L C, O'Neill E, Shingler V
Department of Cell and Molecular Biology, Umeâ University, S-901 87 Umeâ, Sweden.
J Biol Chem. 1996 Jul 19;271(29):17281-6. doi: 10.1074/jbc.271.29.17281.
The final sigma54-dependent DmpR activator regulates transcription of the dmp operon that encodes the enzymes for catabolism of (methyl)phenols. DmpR is expressed constitutively, but its transcriptional promoting activity is controlled positively in direct response to the presence of aromatic pathway substrates (effectors). DmpR has a distinct domain structure with the amino-terminal A-domain controlling the specificity of activation of the regulator by aromatic effectors (signal reception), a central C-domain mediating an ATPase activity essential for transcriptional activation, and a carboxyl-terminal D-domain involved in DNA binding. Deletion of the A-domain has been shown previously to result in an effector-independent transcriptional activator with constitutive ATPase activity. These results, in conjunction with the location of mutations within the A- and C-domains which exhibit an effector-independent (semiconstitutive) property, have led to a working model in which the A-domain serves to mask the ATPase and transcriptional promoting activity of the C-domain in the absence of effectors. To investigate the mechanism by which the A-domain exerts its repressive effect, we developed a genetic system to select positively for intramolecular second site revertants of DmpR. The results demonstrate (i) that mutations within the A-domain can suppress the semiconstitutive activity of C-domain located mutations and vice versa; (ii) that the C-domain located mutations do not influence the intrinsic ATPase and transcriptional promoting property of the C-domain in the absence of the A-domain; and (iii) that semiconstitutive mutations of the A- and C-domain have an additive effect. Taken together these results support a model in which the A-domain represses the function(s) of the C-domain by direct interactions between residues of the two domains.
最终的依赖σ54的DmpR激活剂调控dmp操纵子的转录,该操纵子编码用于(甲基)苯酚分解代谢的酶。DmpR组成型表达,但其转录促进活性直接响应芳香族途径底物(效应物)的存在而受到正向调控。DmpR具有独特的结构域结构,其氨基末端的A结构域控制芳香族效应物(信号接收)对调节因子激活的特异性,中央的C结构域介导转录激活所必需的ATP酶活性,以及羧基末端的D结构域参与DNA结合。先前已表明,缺失A结构域会导致产生具有组成型ATP酶活性的效应物非依赖性转录激活剂。这些结果,连同在A和C结构域内表现出效应物非依赖性(半组成型)特性的突变位置,导致了一个工作模型,即在没有效应物的情况下,A结构域用于掩盖C结构域的ATP酶和转录促进活性。为了研究A结构域发挥其抑制作用的机制,我们开发了一种遗传系统,用于正向选择DmpR的分子内第二位点回复突变体。结果表明:(i)A结构域内的突变可以抑制位于C结构域的突变的半组成型活性,反之亦然;(ii)位于C结构域的突变在没有A结构域的情况下不影响C结构域固有的ATP酶和转录促进特性;(iii)A和C结构域的半组成型突变具有累加效应。综合这些结果支持了一个模型,即A结构域通过两个结构域的残基之间的直接相互作用来抑制C结构域的功能。