Sinorhizobium fredii HH103 Invades Lotus burttii by Crack Entry in a Nod Factor-and Surface Polysaccharide-Dependent Manner
Sinorhizobium fredii HH103 Invades Lotus burttii by Crack Entry in a Nod Factor-and Surface Polysaccharide-Dependent Manner
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DOI：
10.1094/mpmi-09-16-0195-r
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发表时间：
2016-12-01
影响因子：
3.5
通讯作者：
Ruiz-Sainz, Jose E.
中科院分区：
文献类型：
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作者：
Acosta-Jurado, Sebastian;Rodriguez-Navarro, Dulce-Nombre;Ruiz-Sainz, Jose E.
fredii Sinorhizobium HH103-Ri(r)是一种寄主范围较广的根瘤菌，能在荷花中诱导固氮结瘤，但在枇杷中不能诱导结瘤。共聚焦显微镜研究发现，中根瘤菌loll MAFF303099和S. fredii HH103-Rif(r)分别通过感染线和表皮裂缝侵入布氏乳杆菌根部。接种弗雷迪沙门氏菌HH103-Rif(r)后，棉铃虫根毛未见感染丝。fredii HH103-Rif(r) nodA突变体未能形成L. burth结瘤，表明Nod因子对于这种裂缝进入模式是严格必要的，而noeL突变体在L. burtii结瘤中也严重受损，表明Nod因子中focusyl残基的存在是共生相关的。然而，由于没有甲基化或乙酰化的聚焦基残基，没有检测到显著的共生影响。相比之下，fredii HH103-Rif(r)突变体显示脂多糖改变，其共生能力降低，而影响外多糖、荚膜多糖或两者生产的突变体在结瘤过程中未受到损害。不能产生环葡聚糖的突变体和嘌呤或嘧啶的营养不良突变体与布氏乳杆菌形成无效结节。鞭毛蛋白依赖的细菌移动性不需要裂纹感染，因为HH103-Rif(r) fla突变体使L. burtii结瘤。fredii HH103-Rif(r)表面多糖突变体均未与日本乳杆菌有效结瘤。
Sinorhizobium fredii HH103-Ri(r), a broad host range rhizobial strain, induces nitrogen-fixing nodules in Lotus burttii but ineffective nodules in L. japonicus. Confocal microscopy studies showed that Mesorhizobium loll MAFF303099 and S. fredii HH103-Rif(r) invade L. burttii roots through infection threads or epidermal cracks, respectively. Infection threads in root hairs were not observed in L. burttii plants inoculated with S. fredii HH103-Rif(r). A S. fredii HH103-Rif(r) nodA mutant failed to nodulate L. burtth, demonstrating that Nod factors are strictly necessary for this crack-entry mode, and a noeL mutant was also severely impaired in L. burttii nodulation, indicating that the presence of fucosyl residues in the Nod factor is symbiotically relevant. However, significant symbiotic impacts due to the absence of methylation or to acetylation of the fucosyl residue were not detected. In contrast S. fredii HH103-Rif(r) mutants showing lipopolysaccharide alterations had reduced symbiotic capacity, while mutants affected in production of either exopolysaccharides, capsular polysaccharides, or both were not impaired in nodulation. Mutants unable to produce cyclic glucans and purine or pyrimidine auxotrophic mutants formed ineffective nodules with L. burttii. Flagellin-dependent bacterial mobility was not required for crack infection, since HH103-Rif(r) fla mutants nodulated L. burttii. None of the S. fredii HH103-Rif(r) surface-polysaccharide mutants gained effective nodulation with L. japonicus.