Gentry D R, Cashel M
Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda 20892-2785, Maryland, USA.
Mol Microbiol. 1996 Mar;19(6):1373-84. doi: 10.1111/j.1365-2958.1996.tb02480.x.
The spoT gene of Escherichia coli encodes a guanosine 3',5'-bis(diphosphate) 3'-pyrophosphohydrolase (ppGppase) as well as an apparent guanosine 3',5'-bis(diphosphate) synthetase (designated PSII). To determine the regions of the SpoT protein that are required for these two competing activities, we analysed plasmid-borne deletion mutations for their ability to complement chromosomal mutations defective in each activity. We found that a region containing the first 203 amino acids of the 702-amino-acid SpoT protein was sufficient for ppGppase activity while an overlapping region containing residues 67-374 was sufficient for PSII activity. These data indicate that the catalytic sites involved in the two activities are separate but closely linked in the primary sequence of the SpoT protein. A ppGppase-defective delta 1-58 deletion mutant strain failed to synthesize ppGpp in response to nutrient limitation, also supporting the notion that PSII activity from wild-type SpoT does not increase in response to nutrient limitation. Using a strain lacking PSII activity but retaining ppGppase activity, we determined the contribution of the RelA protein (ppGpp synthetase I, PSI) to ppGpp synthesis following glucose starvation. We found that the RelA protein activity accounts for the initial burst of ppGpp synthesis at the onset of glucose starvation but that this source of synthesis is absent when amino acids are present during glucose starvation.
大肠杆菌的spoT基因编码一种鸟苷3',5'-双(二磷酸)3'-焦磷酸水解酶(ppGpp酶)以及一种明显的鸟苷3',5'-双(二磷酸)合成酶(称为PSII)。为了确定SpoT蛋白中这两种相互竞争活性所需的区域,我们分析了质粒携带的缺失突变体对每种活性有缺陷的染色体突变进行互补的能力。我们发现,包含702个氨基酸的SpoT蛋白前203个氨基酸的区域足以支持ppGpp酶活性,而包含67 - 374位残基的重叠区域足以支持PSII活性。这些数据表明,参与这两种活性的催化位点是分开的,但在SpoT蛋白的一级序列中紧密相连。一个ppGpp酶缺陷的Δ1 - 58缺失突变体菌株在营养限制时无法合成ppGpp,这也支持了野生型SpoT的PSII活性不会因营养限制而增加的观点。利用一个缺乏PSII活性但保留ppGpp酶活性的菌株,我们确定了RelA蛋白(ppGpp合成酶I,PSI)在葡萄糖饥饿后对ppGpp合成的贡献。我们发现,RelA蛋白活性解释了葡萄糖饥饿开始时ppGpp合成的初始爆发,但当葡萄糖饥饿期间存在氨基酸时,这种合成来源就不存在了。