RgpF是维持变形链球菌的压力耐受性和毒力所必需的。,Journal of Bacteriology

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RgpF是维持变形链球菌的压力耐受性和毒力所必需的。
Journal of Bacteriology ( IF 2.7 ) Pub Date : 2017-09-20 , DOI: 10.1128/jb.00497-17
C J Kovacs ₁ , R C Faustoferri ₂ , R G Quivey _{2,

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细菌细胞壁动力学已被认为是细胞生理，压力耐受性和毒力的重要决定因素。在变形链球菌中，细胞壁主要由与肽聚糖连接的鼠李糖-葡萄糖多糖（RGP）组成。尽管进行了大量研究描述了其形成和组成，但尚未充分研究RGP在变形链球菌生物学中的潜在作用。本研究的特征是rgpF缺失导致的RGP破坏的影响，rgpF是编码鼠李糖基转移酶的基因，参与了RGP核心多鼠李糖主链的构建。与野生型相比，ΔrgpF突变菌株显示出总体适应性降低，对各种胁迫诱导培养条件的敏感性增强，并且无法耐受酸攻击。rgpF的损失引起了与膜相关的功能的扰动，而这种功能对酸度至关重要，这是变形链球菌耐酸性的标志。跨膜的质子梯度被破坏，并且ΔrgpF突变株无法诱导在低pH条件下培养的培养物中F1Fo ATPase的活性。此外，在rgpF缺失后，变形链球菌的毒性潜能也大大降低。ΔrgpF突变株产生的生物膜明显不足，表明其粘附于羟基磷灰石表面的能力受到损害。此外，ΔrgpF突变体失去了针对口服过氧化物原性链球菌的竞争能力，并且在体内加勒梅隆菌感染模型中显示出明显的减毒力。总的来说，这些结果突显了RGP在维持变形链球菌的整体抗逆性和毒力性状中的关键作用。虽然这些结构与变形链球菌在抗原上是不同的，但是在链球菌中，它们的形成过程和导致其构建的酶是非常保守的。本研究描述了RgpF丢失的后果，RgpF是参与RGP构建的鼠李糖基转移酶。rgpF的缺失导致生物体的整体适应能力严重降低，最终导致毒力显着减弱。我们的数据证明了RGP和变形链球菌细胞壁生理之间的重要联系，

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RgpF Is Required for Maintenance of Stress Tolerance and Virulence in Streptococcus mutans.

Bacterial cell wall dynamics have been implicated as important determinants of cellular physiology, stress tolerance, and virulence. In Streptococcus mutans, the cell wall is composed primarily of a rhamnose-glucose polysaccharide (RGP) linked to the peptidoglycan. Despite extensive studies describing its formation and composition, the potential roles for RGP in S. mutans biology have not been well investigated. The present study characterizes the impact of RGP disruption as a result of the deletion of rgpF, the gene encoding a rhamnosyltransferase involved in the construction of the core polyrhamnose backbone of RGP. The ΔrgpF mutant strain displayed an overall reduced fitness compared to the wild type, with heightened sensitivities to various stress-inducing culture conditions and an inability to tolerate acid challenge. The loss of rgpF caused a perturbation of membrane-associated functions known to be critical for aciduricity, a hallmark of S. mutans acid tolerance. The proton gradient across the membrane was disrupted, and the ΔrgpF mutant strain was unable to induce activity of the F1Fo ATPase in cultures grown under low-pH conditions. Further, the virulence potential of S. mutans was also drastically reduced following the deletion of rgpF The ΔrgpF mutant strain produced significantly less robust biofilms, indicating an impairment in its ability to adhere to hydroxyapatite surfaces. Additionally, the ΔrgpF mutant lost competitive fitness against oral peroxigenic streptococci, and it displayed significantly attenuated virulence in an in vivoGalleria mellonella infection model. Collectively, these results highlight a critical function of the RGP in the maintenance of overall stress tolerance and virulence traits in S. mutansIMPORTANCE The cell wall of Streptococcus mutans, the bacterium most commonly associated with tooth decay, is abundant in rhamnose-glucose polysaccharides (RGP). While these structures are antigenically distinct to S. mutans, the process by which they are formed and the enzymes leading to their construction are well conserved among streptococci. The present study describes the consequences of the loss of RgpF, a rhamnosyltransferase involved in RGP construction. The deletion of rgpF resulted in severe ablation of the organism's overall fitness, culminating in significantly attenuated virulence. Our data demonstrate an important link between the RGP and cell wall physiology of S. mutans, affecting critical features used by the organism to cause disease and providing a potential novel target for inhibiting the pathogenesis of S. mutans.

更新日期：2019-11-01

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