Garges S, Adhya S
Developmental Genetics Section, National Cancer Institute, Bethesda, Maryland 20892.
J Bacteriol. 1988 Apr;170(4):1417-22. doi: 10.1128/jb.170.4.1417-1422.1988.
We isolated and characterized crp mutations in Escherichia coli that allow cyclic AMP (cAMP) receptor protein to function without cAMP. These mutants defined a region involved in the cAMP-induced allosteric change of cAMP receptor protein that is necessary for activation of the protein. Currently, we have isolated intragenic suppressors of the crp mutations. These crp (Sup) mutants require cAMP for activity. The crp (Sup) mutations map in regions which define new sites of changes involved in cAMP receptor protein activation. From these results, we suggest that to activate cAMP receptor protein cAMP brings about (i) a hinge reorientation to eject the DNA-binding F alpha-helices, (ii) proper alignment between the two subunits, and (iii) an adjustment between the position of the two domains. Cyclic GMP fails to effect the last step.
我们在大肠杆菌中分离并鉴定了一些crp突变,这些突变使环腺苷酸(cAMP)受体蛋白在没有cAMP的情况下仍能发挥功能。这些突变体定义了一个与cAMP诱导的cAMP受体蛋白变构变化相关的区域,而这种变构变化是该蛋白激活所必需的。目前,我们已经分离出了crp突变的基因内抑制子。这些crp(Sup)突变体的活性需要cAMP。crp(Sup)突变位于定义cAMP受体蛋白激活过程中涉及新变化位点的区域。从这些结果来看,我们认为为了激活cAMP受体蛋白,cAMP会引发:(i)一个铰链重新定向以排出DNA结合Fα螺旋;(ii)两个亚基之间的正确排列;以及(iii)两个结构域位置之间的调整。环鸟苷酸(cGMP)无法影响最后一步。