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首页> 外文期刊>The FEBS journal >Target DNA stabilizes Mycobacterium tuberculosis DevR/DosR phosphorylation by the full-length oxygen sensors DevS/DosS and DosT
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Target DNA stabilizes Mycobacterium tuberculosis DevR/DosR phosphorylation by the full-length oxygen sensors DevS/DosS and DosT

机译：目标DNA通过全长氧传感器开发/ DOS和DOST稳定结核分枝杆菌DEVR / DOSR磷酸化

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摘要

Mycobacterium tuberculosis strongly relies on a latency, or nonreplicating persistence, to escape a human host's immune system. The DevR (DosR), DevS (DosS), and DosT proteins are key components of this process. Like the rhizobial FixL oxygen sensor, DevS and DosT are histidine protein kinases with a heme-binding domain. Like the FixJ partner and substrate of FixL, DevR is a classical response regulator of the two-component class. When activated by DevS or DosT during hypoxia in vivo, DevR induces a dormancy regulon of more than 40 genes. To investigate the contributions of DevS, DosT, and target DNA to the phosphorylation of DevR, we developed an in vitro assay in which the full-length, sensing, DevS and DosT proteins were used to phosphorylate DevR with ATP, in the presence of target DNAs that were introduced as oligonucleotides linked to magnetic nanoparticles. We found that the DevR phosphorylations proceeded only for the deoxy states of the sensors. The reaction was strongly inhibited by O-2, but not CO or NO. The production of phospho-DevR was enhanced sixfold by target consensus DNA or acr-DNA. The phospho-DevR bound tightly to that DNA (K-d similar to 0.8 nm toward acr-DNA), and it was only slightly displaced by a 200-fold excess of unphosphorylated DevR or of a truncated DevR with only a DNA-binding domain. To our knowledge, this represents the first in vitro study of the ligand regulation of DevR phosphorylation by full-length DevS and DosT, and demonstration of a positive effect of DNA on this reaction.
机译：结核分枝杆菌强烈依赖于延迟或非重种持续性，以逃避人类宿主的免疫系统。 Devr（DOSR），DEVS（DOSS）和DOST蛋白是该过程的关键部件。与Rhizobial FixL氧传感器一样，DEVS和DOST是具有血红素结合结构域的组氨酸蛋白激酶。与FixJ合作伙伴和FixL的基板一样，Devr是双组分类的经典响应调节器。当在体内缺氧期间由DEVS或DOST激活时，DEVR诱导超过40个基因的休眠状态。探讨DEVS，DORT和靶DNA对DEVR磷酸化的贡献，我们开发了一种体外测定，其中全长，感测，DEVS和DOST蛋白用于靶向靶标的DEVR，在靶标存在下作为与磁性纳米颗粒连接的寡核苷酸引入的DNA。我们发现Devr磷酸化仅用于传感器的脱氧状态。通过O-2强烈抑制反应，但不具有CO或NO。通过目标共识DNA或ACR-DNA产生磷酸-Devr的生产增强了六倍。将磷磷缺乏紧密地绑定到该DNA（K-D类似于0.8nm朝向ACR-DNA），并且仅通过仅具有DNA结合结构域的多磷酸化Devr或截短的Devr略微移位。据我们所知，这代表了全长DEVS和DORT的DEVR磷酸化配体调节的第一个体外研究，并证明DNA对该反应的积极作用。

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