细菌趋化系统是促进细菌成功的众所周知的信号通路。趋化性系统包括化学感受器和CheA激酶,由CheW或CheV支架蛋白连接。支架蛋白提供化学感受器和CheA之间以及化学感受器之间的连接以创建大分子阵列。趋化性是许多微生物定植宿主所必需的,包括胃病原体幽门螺杆菌。这种细菌与两种不同的支架蛋白建立化学感受器-CheA接触,CheW和CheV1.幽门螺杆菌cheW或cheV1缺失突变体都失去化学感受器阵列形成,但表现出不同的半固体琼脂趋化性测定行为:ΔcheW突变体表现出完全迁移失败,而ΔcheV1::猫突变体显示50%的减少。在调查这些不同的反应时,我们发现这两种突变体最初都在迁徙中挣扎。然而,随着时间的推移,÷cheV1::猫突变体发展出稳定的,增强的迁移能力,称为“可迁移”(Mig+)。对四个不同ΔcheV1::catMig菌株的全基因组测序分析鉴定了hpg27_252(hp0273)中的单核苷酸多态性(SNP),这些多态性被预测为截短编码的蛋白质。对hpg27_252编码的蛋白质的计算分析表明,它编码了一种假设的蛋白质,该蛋白质是PilOIV型丝膜比对复合蛋白的远程同源物。尽管幽门螺杆菌缺乏IV型细丝,我们的分析表明它保留了PilO同源基因的操纵子,PilN,和PilM。在÷cheV1::cat或野生型菌株中删除hpg27_252导致半固体琼脂中的迁移增强。因此,我们的研究表明,虽然cheV1突变体最初具有显著的迁移缺陷,它们可以通过基因抑制因子恢复迁移能力,强调了细菌迁移中复杂的调节机制。
目的:趋化运动性,存在于超过一半的细菌中,依赖于包含受体的趋化性信号系统,激酶,和支架蛋白。在幽门螺杆菌中,胃病原体,趋化性对于定殖至关重要,以CheV1和CheW为关键支架蛋白。虽然这两种支架对于构建化学感受器复合物至关重要,它们的作用在其他测定中有所不同。我们的研究重新检查了cheV1突变体在半固体琼脂中的行为,标准的趋化性测试。最初,cheV1突变体表现出与cheW突变体相似的缺陷,但是他们进化出了基因抑制基因,增强了迁移能力。这些抑制因子涉及以前未表征的基因的突变,未知的运动行为。我们的发现强调了cheV1突变体中的显着趋化性缺陷,并确定了影响细菌运动性的新元素。
The bacterial chemotaxis system is a well-understood signaling pathway that promotes bacterial success. Chemotaxis systems comprise chemoreceptors and the CheA kinase, linked by CheW or CheV scaffold proteins. Scaffold proteins provide connections between chemoreceptors and CheA and also between chemoreceptors to create macromolecular arrays. Chemotaxis is required for host colonization by many microbes, including the stomach pathogen Helicobacter pylori. This bacterium builds chemoreceptor-CheA contacts with two distinct scaffold proteins, CheW and CheV1. H. pylori cheW or cheV1 deletion mutants both lose chemoreceptor array formation, but show differing semisolid agar chemotaxis assay behaviors: ∆cheW mutants exhibit total migration failure, whereas ∆cheV1::cat mutants display a 50% reduction. On investigating these varied responses, we found that both mutants initially struggle with migration. However, over time, ∆cheV1::cat mutants develop a stable, enhanced migration capability, termed \"migration-able\" (Mig+). Whole-genome sequencing analysis of four distinct ∆cheV1::cat Mig+ strains identified single-nucleotide polymorphisms (SNPs) in hpg27_252 (hp0273) that were predicted to truncate the encoded protein. Computational analysis of the hpg27_252-encoded protein revealed it encoded a hypothetical protein that was a remote homolog of the PilO Type IV filament membrane alignment complex protein. Although H. pylori lacks Type IV filaments, our analysis showed it retains an operon of genes for homologs of PilO, PilN, and PilM. Deleting hpg27_252 in the ∆cheV1::cat or wild type strain resulted in enhanced migration in semisolid agar. Our study thus reveals that while cheV1 mutants initially have significant migration defects, they can recover the migration ability through genetic suppressors, highlighting a complex regulatory mechanism in bacterial migration.
Chemotactic motility, present in over half of bacteria, depends on chemotaxis signaling systems comprising receptors, kinases, and scaffold proteins. In Helicobacter pylori, a stomach pathogen, chemotaxis is crucial for colonization, with CheV1 and CheW as key scaffold proteins. While both scaffolds are essential for building chemoreceptor complexes, their roles vary in other assays. Our research reexamines cheV1 mutants\' behavior in semisolid agar, a standard chemotaxis test. Initially, cheV1 mutants exhibited defects similar to those of cheW mutants, but they evolved genetic suppressors that enhanced migration. These suppressors involve mutations in a previously uncharacterized gene, unknown in motility behavior. Our findings highlight the significant chemotaxis defects in cheV1 mutants and identify new elements influencing bacterial motility.