Suzuki Reira, Kanno Yuri, Abril-Urias Patricia, Seo Mitsunori, Escobar Carolina, Tsai Allen Yi-Lun, Sawa Shinichiro
Faculty of Advanced Science and Technology, Kumamoto University, Kumamoto, Japan.
International Research Organization for Advanced Science and Technology (IROAST), Kumamoto University, Kumamoto, Japan.
Front Plant Sci. 2022 Nov 16;13:1019427. doi: 10.3389/fpls.2022.1019427. eCollection 2022.
Parasites and pathogens are known to manipulate the host's endogenous signaling pathways to facilitate the infection process. In particular, plant-parasitic root-knot nematodes (RKN) are known to elicit auxin response at the infection sites, to aid the development of root galls as feeding sites for the parasites. Here we describe the role of local auxin synthesis induced during RKN infection. Exogenous application of auxin synthesis inhibitors decreased RKN gall formation rates, gall size and auxin response in galls, while auxin and auxin analogues produced the opposite effects, re-enforcing the notion that auxin positively regulates RKN gall formation. Among the auxin biosynthesis enzymes, () was found to be dramatically up-regulated during RKN infection, suggesting it may be a major contributor to the auxin accumulation during gall formation. However, showed only very transient decrease in gall auxin levels and did not show significant changes in RKN infection rates, implying the loss of is likely compensated by other auxin sources. Nevertheless, plants produced significantly smaller galls with fewer mature females and egg masses, confirming that auxin synthesized by is required for proper gall formation and RKN development within. Interestingly, promoter was also activated during cyst nematode infection. These lines of evidence imply auxin biosynthesis from multiple sources, one of them being YUC4, is induced upon plant endoparasitic nematode invasion and likely contribute to their infections. The coordination of these different auxins adds another layer of complexity of hormonal regulations during plant parasitic nematode interaction.
已知寄生虫和病原体可操纵宿主的内源性信号通路以促进感染过程。特别是，植物寄生的根结线虫（RKN）已知会在感染部位引发生长素反应，以帮助形成根瘤作为寄生虫的取食部位。在此我们描述了RKN感染期间诱导的局部生长素合成的作用。外源施加生长素合成抑制剂可降低RKN根瘤形成率、根瘤大小以及根瘤中的生长素反应，而生长素和生长素类似物则产生相反的效果，这强化了生长素正向调节RKN根瘤形成的观点。在生长素生物合成酶中，（）被发现在RKN感染期间显著上调，表明它可能是根瘤形成过程中生长素积累的主要贡献者。然而，显示根瘤生长素水平仅非常短暂地下降，并且RKN感染率没有显著变化，这意味着的缺失可能由其他生长素来源补偿。尽管如此，植物产生的根瘤明显更小，成熟雌虫和卵块数量更少，证实了由合成的生长素是根瘤正常形成和其中RKN发育所必需的。有趣的是，在胞囊线虫感染期间启动子也被激活。这些证据表明，植物内寄生线虫入侵时会诱导多种来源的生长素生物合成，其中之一是YUC4，并且可能有助于它们的感染。这些不同生长素之间的协调增加了植物寄生线虫相互作用期间激素调节的另一层复杂性。
