Liu Yang, Gates Alexandra D, Liu Zhexian, Duque Quinn, Chen Melissa Y, Hamilton Corri D, O'Toole George A, Haney Cara H
Department of Microbiology and Immunology, The University of British Columbia, Vancouver, Canada.
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, USA.
bioRxiv. 2024 Dec 17:2024.12.17.628960. doi: 10.1101/2024.12.17.628960.
Plant roots form associations with both beneficial and pathogenic soil microorganisms. While members of the rhizosphere microbiome can protect against pathogens, the mechanisms are poorly understood. We hypothesized that the ability to form a robust biofilm on the root surface is necessary for the exclusion of pathogens; however, it is not known if the same biofilm formation components required are necessary WCS365 is a beneficial strain that is phylogenetically closely related to an opportunistic pathogen N2C3 and confers robust protection against N2C3 in the rhizosphere. We used this plant-mutualist-pathogen model to screen collections of WCS365 increased attachment mutants () and surface attachment defective () transposon insertion mutants that form increased or decreased levels of biofilm on an abiotic surface, respectively. We found that while the WCS365 mutants had altered biofilm formation , only a subset of these mutants, including those involved in large adhesion protein (Lap) biosynthesis, flagellin biosynthesis and O-antigen biosynthesis, lost protection against N2C3. We found that the inability of WCS365 mutants to grow , and the inability to suppress pathogen growth, both partially contributed to loss of plant protection. We did not find a correlation between the extent of biofilm formed and pathogen protection indicating that biofilm formation on abiotic surfaces may not fully predict pathogen exclusion . Collectively, our work provides insights into mechanisms of biofilm formation and host colonization that shape the outcomes of host-microbe-pathogen interactions.
植物根系与有益和致病的土壤微生物都能形成共生关系。虽然根际微生物群落的成员可以抵御病原体,但其机制尚不清楚。我们推测在根表面形成强大生物膜的能力是排除病原体所必需的;然而,尚不清楚所需的相同生物膜形成成分对于WCS365是否必要。WCS365是一种有益菌株,在系统发育上与机会致病菌N2C3密切相关,并能在根际对N2C3提供强大的保护作用。我们利用这种植物-共生菌-病原体模型,筛选了WCS365附着增加突变体()和表面附着缺陷()转座子插入突变体的集合,这些突变体分别在非生物表面形成增加或减少的生物膜水平。我们发现,虽然WCS365突变体的生物膜形成发生了改变,但只有这些突变体的一个子集,包括那些参与大粘附蛋白(Lap)生物合成、鞭毛蛋白生物合成和O抗原生物合成的突变体,失去了对N2C3的保护作用。我们发现WCS365突变体无法生长,以及无法抑制病原体生长,都部分导致了植物保护作用的丧失。我们没有发现形成的生物膜程度与病原体保护之间的相关性,这表明在非生物表面形成生物膜可能无法完全预测病原体的排除。总的来说,我们的工作为生物膜形成和宿主定殖机制提供了见解,这些机制塑造了宿主-微生物-病原体相互作用的结果。