DksA affects ppGpp induction of RpoS at a translational level
DksA affects ppGpp induction of RpoS at a translational level
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DOI：
10.1128/jb.184.16.4455-4465.2002
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发表时间：
2002-08-01
影响因子：
3.2
通讯作者：
Cashel, M
中科院分区：
文献类型：
--
作者：
Brown, L;Gentry, D;Cashel, M
已知 RpoS sigma 因子（也称为 sigma(S) 或 sigma(38)）可调节至少 50 个基因，以响应环境压力源或进入稳定期。 RpoS 丰度和活性的调节很复杂，有许多因素在多个层面上参与。其中一个因素是营养应激信号 ppGpp。 ppGpp 的缺失会阻止或延迟进入稳定期期间 rpoS 的诱导。已知在不饥饿的情况下人工诱导 ppGpp 可在对数生长期诱导 25 至 50 倍的 rpoS。发现 ppGpp 的诱导对 rpoS 转录物丰度或 RpoS 蛋白稳定性只有很小的影响；相反，根据 RpoS 脉冲标记和启动子独立对 lacZ 融合的影响判断，ppGpp 提高了 rpoS mRNA 翻译的效率。发现 DksA 以与 ppGpp 相关的方式影响 RpoS 丰度。删除 dksA 会阻止 ppGpp 诱导 rpoS。 DksA 的过量产生会诱导 rpoS，但不会诱导 ppGpp。删除 dksA 既不会改变 ppGpp 响应氨基酸饥饿的调节，也不会消除 ppGpp 对稳定 RNA 合成的抑制作用。尽管这表明 dksA 对 ppGpp 具有上位性，但诱导 ppGpp 不会诱导 DksA。 dksA 缺失确实显示出与 ppGpp(0) 突变体相同的多氨基酸要求的子集，但过量产生的 DksA 不能满足 ppGpp(0) 要求。 dksA 多营养缺陷型的测序自发外源抑制因子通常与抑制 ppGpp(0) 表型的 T563P rpoB 等位基因相同。我们认为 DksA 在 ppGpp 下游发挥作用，但间接调节 rpoS 诱导。
The RpoS sigma factor (also called sigma(S) or sigma(38)) is known to regulate at least 50 genes in response to environmental sources of stress or during entry into stationary phase. Regulation of RpoS abundance and activity is complex, with many factors participating at multiple levels. One factor is the nutritional stress signal ppGpp. The absence of ppGpp blocks or delays the induction of rpoS during entry into stationary phase. Artificially inducing ppGpp, without starvation, is known to induce rpoS during the log phase 25- to 50-fold. Induction of ppGpp is found to have only minor effects on rpoS transcript abundance or on RpoS protein stability; instead, the efficiency of rpoS mRNA translation is increased by ppGpp as judged by both RpoS pulse-labeling and promoter-independent effects on lacZ fusions. DksA is found to affect RpoS abundance in a manner related to ppGpp. Deleting dksA blocks rpoS induction by ppGpp. Overproduction of DksA induces rpoS but not ppGpp. Deleting dksA neither alters regulation of ppGpp in response to amino acid starvation nor nullifies the inhibitory effects of ppGpp on stable RNA synthesis. Although this suggests that dksA is epistatic to ppGpp, inducing ppGpp does not induce DksA. A dksA deletion does display a subset of the same multiple-amino-acid requirements found for ppGpp(0) mutants, but overproducing DksA does not satisfy ppGpp(0) requirements. Sequenced spontaneous extragenic suppressors of dksA polyauxotrophy are frequently the same T563P rpoB allele that suppresses a ppGpp(0) phenotype. We propose that DksA functions downstream of ppGpp but indirectly regulates rpoS induction.