Roles for azorhizobial nod factors and surface polysaccharides in intercellular invasion and nodule penetration, respectively
Roles for azorhizobial nod factors and surface polysaccharides in intercellular invasion and nodule penetration, respectively
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DOI：
10.1094/mpmi.1998.11.10.999
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发表时间：
1998-10-01
影响因子：
3.5
通讯作者：
Holsters, M
中科院分区：
文献类型：
--
作者：
D'Haeze, W;Gao, MS;Holsters, M
在根瘤菌和田菁之间的共生相互作用中，形成根瘤和茎生根瘤。细菌通过侧根或不定根基部的细胞间隙进入宿主，并在外皮层形成感染袋。感染线引导细菌到达侵入植物细胞的根瘤原基。为了确定这种感染过程所需的细菌功能，研究了两种结瘤缺陷的突变体；一种不产生Nod因子（nodA突变体），另一种改变了表面多糖（SPS）并诱导假结节的形成，借助在结节发育和类菌体中起作用的nodA-uidA报告基因融合体的帮助，细菌被可视化。与 SPS 突变体相反，nodA 突变体无法定植于外皮质区域。在两种突变体的混合接种中，形成了功能性结节，其中央组织被nodA突变体占据。这些观察结果表明，SPS 在更深的入侵中发挥作用，并且 Nod 因子是进入所必需的。同时应用纯化的 Nod 因子和 nodA 突变细菌恢复了外皮质感染袋的形成，得出这样的结论：细胞间感染是一个依赖于细菌 Nod 因子信号传导的主动过程。
In the symbiotic interaction between Azorhizobium caulinodans and Sesbania rostrata root and stem-borne nodules are formed. The bacteria enter the host via intercellular spaces at lateral or adventitious root bases and form infection pockets in outer cortical layers. Infection threads guide the bacteria to nodule primordia where plant cells are invaded. To identify bacterial functions that are required for this infection process, two mutants defective in nodulation were studied; one produced no Nod factors (nodA mutant), the other had altered surface polysaccharides (SPS) and induced the formation of pseudo-nodules, Bacteria were visualized with the help of a nodA-uidA reporter fusion that was functional during nodule development and in bacteroids. In contrast to the SPS mutant, nodA mutants were unable to colonize outer cortical regions. In mixed inoculations with both mutants, functional nodules were formed, the central tissue of which was occupied by the nodA mutant. These observations suggest that SPS play a role in deeper invasion and that Nod factors are necessary for entry. Simultaneous application of purified Nod factors and nodA mutant bacteria restored the formation of outer cortical infection pockets leading to the conclusion that intercellular infection is an active process that is dependent on bacterial Nod factor signaling.