A Mn-sensing riboswitch activates expression of a Mn2+/Ca2+ ATPase transporter in Streptococcus.
A Mn-sensing riboswitch activates expression of a Mn2+/Ca2+ ATPase transporter in Streptococcus.
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Mn 感应核糖开关可激活链球菌中 Mn2/Ca2 ATP 酶转运蛋白的表达。
DOI:
10.1093/nar/gkz494
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发表时间:
2019
影响因子:
14.9
通讯作者:
Giedroc,DavidP
中科院分区:
文献类型:
--
作者:
Martin,JuliaE;Le,MyT;Bhattarai,Nabin;Capdevila,DaianaA;Shen,Jiangchuan;Winkler,MalcolmE;Giedroc,DavidP
Maintaining manganese (Mn) homeostasis is important for the virulence of numerous bacteria. In the human respiratory pathogenStreptococcus pneumoniae, the Mn-specific importer PsaBCA, exporter MntE, and transcriptional regulator PsaR establish Mn homeostasis. In other bacteria, Mn homeostasis is controlled byyybP-ykoYfamily riboswitches. Here, we characterize ayybP-ykoYfamily riboswitch upstream of themgtAgene encoding a PII-type ATPase inS. pneumoniae, suggested previously to function in Ca2+efflux. We show that themgtAriboswitch aptamer domain adopts a canonicalyybP-ykoYstructure containing a three-way junction that is compacted in the presence of Ca2+or Mn2+at a physiological Mg2+concentration. Although Ca2+binds to the RNA aptamer with higher affinity than Mn2+,in vitroactivation of transcription read-through ofmgtAby Mn2+is much greater than by Ca2+. Consistent with this result,mgtAmRNA and protein levels increase ≈5-fold during cellular Mn stress, but only in genetic backgrounds ofS. pneumoniaeandBacillus subtilisthat exhibit Mn2+sensitivity, revealing that this riboswitch functions as a failsafe ‘on’ signal to prevent Mn2+toxicity in the presence of high cellular Mn2+. In addition, our results suggest that theS. pneumoniae yybP-ykoYriboswitch functions to regulate Ca2+efflux under these conditions.