INRA, Université Côte d'Azur, CNRS, ISA, 400 route des Chappes, BP167, 06903, Sophia Antipolis, France.
UCA Genomix, Institut de Pharmacologie Moléculaire et Cellulaire, CNRS UMR6097, Sophia Antipolis, France.
New Phytol. 2017 Nov;216(3):882-896. doi: 10.1111/nph.14717. Epub 2017 Sep 14.
Root knot nematodes (RKN) are root parasites that induce the genetic reprogramming of vascular cells into giant feeding cells and the development of root galls. MicroRNAs (miRNAs) regulate gene expression during development and plant responses to various stresses. Disruption of post-transcriptional gene silencing in Arabidopsis ago1 or ago2 mutants decrease the infection rate of RKN suggesting a role for this mechanism in the plant-nematode interaction. By sequencing small RNAs from uninfected Arabidopsis roots and from galls 7 and 14 d post infection with Meloidogyne incognita, we identified 24 miRNAs differentially expressed in gall as putative regulators of gall development. Moreover, strong activity within galls was detected for five miRNA promoters. Analyses of nematode development in an Arabidopsis miR159abc mutant had a lower susceptibility to RKN, suggesting a role for the miR159 family in the plant response to M. incognita. Localization of mature miR159 within the giant and surrounding cells suggested a role in giant cell and gall. Finally, overexpression of miR159 in galls at 14 d post inoculation was associated with the repression of the miR159 target MYB33 which expression is restricted to the early stages of infection. Overall, these results implicate the miR159 in plant responses to RKN.
根结线虫(RKN)是一种寄生在根部的线虫,它能诱导血管细胞发生遗传重编程,变成巨型取食细胞,并形成根瘤。microRNAs(miRNAs)在发育过程中以及植物对各种胁迫的反应中调节基因表达。在拟南芥 ago1 或 ago2 突变体中,转录后基因沉默的破坏会降低 RKN 的感染率,这表明该机制在植物-线虫相互作用中起作用。通过对未感染的拟南芥根部和感染 7 天和 14 天后的南方根结线虫 Meloidogyne incognita 根瘤进行小 RNA 测序,我们鉴定出 24 种在根瘤中差异表达的 miRNA,它们可能是根瘤发育的调控因子。此外,在根瘤中检测到五个 miRNA 启动子的强烈活性。在拟南芥 miR159abc 突变体中对线虫发育的分析表明,miR159 家族在植物对 M. incognita 的反应中起作用。成熟的 miR159 在巨型细胞及其周围细胞中的定位表明其在巨型细胞和根瘤形成中起作用。最后,在接种后 14 天根瘤中过表达 miR159 与 miR159 靶标 MYB33 的表达受到抑制有关,而 MYB33 的表达仅限于感染的早期阶段。总的来说,这些结果表明 miR159 参与了植物对 RKN 的反应。