Department of Plant Pathology, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Department of Plant Pathology, University of Minnesota, Minneapolis, Minnesota, USA.
Appl Environ Microbiol. 2023 Feb 28;89(2):e0156522. doi: 10.1128/aem.01565-22. Epub 2023 Jan 23.
Adhesins (ive prote) help bacteria stick to and colonize diverse surfaces and often contribute to virulence. The genome of the bacterial wilt pathogen Ralstonia solanacearum () encodes dozens of putative adhesins, some of which are upregulated during plant pathogenesis. Little is known about the role of these proteins in bacterial wilt disease. During tomato colonization, three putative adhesin genes were upregulated in a Δ quorum-sensing mutant that cannot respond to high cell densities: (alstonia hesin ), (alstonia ollagen-like rotein ), and . Based on this differential gene expression, we hypothesized that adhesins repressed by PhcA contribute to early disease stages when experiences a low cell density. During root colonization, upregulated and , but not , relative to bacteria in the stem at mid-disease. Root attachment assays and confocal microscopy with Δ and Δ revealed that all three adhesins help attach to tomato seedling roots. Biofilm assays on abiotic surfaces found that does not require RadA, RcpA, or RcpB for interbacterial attachment (cohesion), but these proteins are essential for anchoring aggregates to a surface (adhesion). However, did not require the adhesins for later disease stages , including colonization of the root endosphere and stems. Interestingly, all three adhesins were essential for full competitive fitness . Together, these infection stage-specific assays identified three proteins that contribute to adhesion and the critical first host-pathogen interaction in bacterial wilt disease. Every microbe must balance its need to attach to surfaces with the biological imperative to move and spread. The high-impact plant-pathogenic bacterium Ralstonia solanacearum can stick to biotic and abiotic substrates, presumably using some of the dozens of putative adhesins encoded in its genome. We confirmed the functions and identified the biological roles of multiple afimbrial adhesins. By assaying the competitive fitness and the success of adhesin mutants in three different plant compartments, we identified the specific disease stages and host tissues where three previously cryptic adhesins contribute to success in plants. Combined with tissue-specific regulatory data, this work indicates that R. solanacearum deploys distinct adhesins that help it succeed at different stages of plant pathogenesis.
黏附素(ive prote)帮助细菌黏附和定殖于各种表面,通常有助于毒力。细菌萎蔫病原体 Ralstonia solanacearum 的基因组编码数十种假定的黏附素,其中一些在植物发病过程中上调。这些蛋白质在细菌性萎蔫病中的作用知之甚少。在番茄定殖过程中,一个不能响应高细胞密度的群体感应突变体中上调了三个假定的黏附素基因:(alstonia hesin)、(alstonia ollagen-like rotein)和。基于这种差异基因表达,我们假设受 PhcA 抑制的黏附素有助于当经历低细胞密度时早期发病阶段。在根定殖过程中,与茎中细菌相比,和上调,但上调。根附着试验和带有和的共聚焦显微镜显示,这三种黏附素都有助于附着在番茄幼苗根部。在非生物表面的生物膜试验发现,对于细菌之间的附着(内聚力),不需要 RadA、RcpA 或 RcpB,但这些蛋白质对于将聚集体锚定到表面(附着)是必不可少的。然而,在稍后的发病阶段,不需要这些黏附素,包括根内圈和茎的定殖。有趣的是,所有三种黏附素对于完全竞争适应性都是必不可少的。这些感染阶段特异性试验共同确定了三种有助于粘附和细菌性萎蔫病中关键的初次宿主-病原体相互作用的蛋白质。每个微生物都必须平衡其附着表面的需要与移动和传播的生物学必要性。高影响力的植物病原细菌 Ralstonia solanacearum 可以附着于生物和非生物基质,推测是使用其基因组中编码的数十种假定黏附素之一。我们证实了这些功能并确定了多种无纤毛黏附素的生物学作用。通过测定三种不同植物隔室中竞争适应性和黏附素突变体的成功,我们确定了三个以前隐蔽的黏附素有助于植物成功的特定疾病阶段和宿主组织。结合组织特异性调节数据,这项工作表明,R. solanacearum 部署了不同的黏附素,这些黏附素有助于它在植物发病过程的不同阶段取得成功。