The PTS(Ntr) system globally regulates ATP-dependent transporters in Rhizobium leguminosarum.
The PTS(Ntr) system globally regulates ATP-dependent transporters in Rhizobium leguminosarum.
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PTS(NTr) 系统全局调节豆根瘤菌中 ATP 依赖性转运蛋白。
DOI：
10.1111/j.1365-2958.2012.08014.x
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发表时间：
2012
影响因子：
3.6
通讯作者：
Prell J
中科院分区：
文献类型：
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作者：
Prell J
豆科根瘤菌菌株 Rlv3841 中 PTSNtr 系统的 ptsPencoding EINtro 突变引起了在许多细菌中观察到的多效性表型。突变体形成干燥的菌落，并且在有机氮或二羧酸盐上生长不良。最引人注目的是，ptsP 突变体的多种 ATP 依赖性 ABC 转运蛋白活性较低。这种翻译后发生的激活缺乏可以解释许多多效性效应。相比之下，质子耦合转运系统在 aptsPmutant 中没有受到抑制。 PtsP 的调节还涉及编码 EIIANtr 的两个 ptsN 拷贝，从而导致磷酸化级联反应。与大肠杆菌一样，Rlv3841 PTSNtr 系统也通过高亲和力 ATP 依赖性 K+ 转运蛋白 KdpABC 的转录激活来调节 K+ 稳态。这涉及双组分传感器调节器对 KdpDE 与未磷酸化 EIIANtr 的直接相互作用。至关重要的是，ptsP 突变体不能磷酸化 PtsN1 或 PtsN2，但具有完全激活的 KdpABC 转运蛋白。这与 ABC 转运蛋白观察到的模式相反，后者显然需要 PtsN 磷酸化。这些结果表明，ATP 依赖性运输可能通过响应细胞能量电荷的 PTSNtr 进行调节。 ABC 运输可能会在低能量状态下失活，从而为包括 K+ 稳态在内的重要过程保存 ATP。
Mutation ofptsPencoding EINtrof the PTSNtrsystem inRhizobium leguminosarumstrain Rlv3841 caused a pleiotropic phenotype as observed with many bacteria. The mutant formed dry colonies and grew poorly on organic nitrogen or dicarboxylates. Most strikingly theptsPmutant had low activity of a broad range of ATP‐dependent ABC transporters. This lack of activation, which occurred post‐translationally, may explain many of the pleiotropic effects. In contrast proton‐coupled transport systems were not inhibited in aptsPmutant. Regulation by PtsP also involves two copies ofptsNthat code for EIIANtr, resulting in a phosphorylation cascade. As inEscherichia coli, the Rlv3841 PTSNtrsystem also regulates K+homeostasis by transcriptional activation of the high‐affinity ATP‐dependent K+transporter KdpABC. This involves direct interaction of a two‐component sensor regulator pair KdpDE with unphosphorylated EIIANtr. Critically,ptsPmutants, which cannot phosphorylate PtsN1 or PtsN2, had a fully activated KdpABC transporter. This is the opposite pattern from that observed with ABC transporters which apparently require phosphorylation of PtsN. These results suggest that ATP‐dependent transport might be regulated via PTSNtrresponding to the cellular energy charge. ABC transport may be inactivated at low energy charge, conserving ATP for essential processes including K+homeostasis.