Restoration of flagellar biosynthesis by varied mutational events in Campylobacter jejuni.
Restoration of flagellar biosynthesis by varied mutational events in Campylobacter jejuni.
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DOI：
10.1111/j.1365-2958.2008.06428.x
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发表时间：
2008-10
影响因子：
3.6
通讯作者：
Hendrixson, David R.
中科院分区：
文献类型：
--
作者：
Hendrixson, David R.
在空肠弯曲菌中，涉及FlgSR双组分系统的复杂调节级联和相位变化都控制σ54依赖性鞭毛基因的表达。在这项研究中，突变机制影响生产的FlgS组氨酸激酶被发现。随机的非运动的、非鞭毛化的flgS变体在鸡肠道中的生长受损。通过体内和体外研究鉴定的鞭毛生物合成、基因表达和运动性恢复的自发回复突变体相对于flgS经历了不同的基因内和基因外突变事件。恢复性基因内事件包括真相位变异、第二位点基因内回复以及flgS内短DNA片段的插入和缺失。在体内分离的能动回复突变体具有相同的，单一的基因外突变，以创建一个部分组成型活性的FlgR蛋白在FlgS的情况下。考虑到FlgR的产生也受到相位变化的影响，这些新发现表明FlgSR双组分系统是独特的，因为每个蛋白质都受到相位变化和磷酸化的控制。此外，本研究还强调了C. jejuni，并表明细菌可能拥有一套突变机制，以克服遗传病变，损害生产的毒力和定植决定因素，同时缺乏正常的错配修复系统。
Both a complex regulatory cascade involving the FlgSR two-component system and phase variation control expression of σ54-dependent flagellar genes in Campylobacter jejuni. In this study, mutational mechanisms influencing production of the FlgS histidine kinase were discovered. Random non-motile, non-flagellated flgS variants were impaired for growth in the chick intestinal tract. Spontaneous revertants restored for flagellar biosynthesis, gene expression, and motility identified by in vivo and in vitro studies had undergone diverse intragenic and extragenic mutational events relative to flgS. Restorative intragenic events included true phase variation, second-site intragenic reversion, and insertion and deletion of short DNA segments within flgS. In vivo-isolated motile revertants possessed an identical, single extragenic mutation to create a partially constitutively-active FlgR protein in the absence of FlgS. Considering that FlgR production is also influenced by phase variation, these new findings suggest that the FlgSR two-component system is a unique in that each protein is controlled by phase variation and phosphorylation. In addition, this study highlights the mutational activities of C. jejuni and suggests that the bacterium may possess a repertoire of mutational mechanisms to overcome genetic lesions that impair production of virulence and colonization determinants while lacking a normal mismatch repair system.
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影响因子：
3.6
作者：
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通讯作者：
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作者：
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