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漆酶基因在小麦 NILs 中对 QTL-Fhb1 抗性的作用,该 QTL 对赤霉病具有抗性。

Role of laccase gene in wheat NILs differing at QTL-Fhb1 for resistance against Fusarium head blight.

机构信息

Plant Science Department, McGill University, Ste.-Anne-de-Bellevue, QC, Canada.

University of Oslo, Norway.

出版信息

Plant Sci. 2020 Sep;298:110574. doi: 10.1016/j.plantsci.2020.110574. Epub 2020 Jun 23.

Abstract

Fusarium head blight (FHB), caused mainly by Fusarium graminearum (Fg), is one of the most severe diseases of wheat. It affects grain yield and quality due to mycotoxin contamination, which is harmful for both human and livestock consumption. Cell wall lignification, following pathogen invasion, is one of the innate defense responses. Plant laccases are known to lignify the secondary cell walls. A metabolo-genomics study identified laccase as one of the candidate genes in QTL-Fhb1 of wheat NILs derived from Sumai 3*5/Thatcher cross. Based on phylogenetics, it was named as TaLAC4. Real-time qPCR revealed a strongly induced expression of TaLAC4 in NIL-R. The VIGS based transient silencing of TaLAC4 in NIL-R resulted in an increased susceptibility leading to Fg spread within the entire spike in 15dpi, contrasting to non-silenced where the infection was limited to inoculated spikelets. Histopathology revealed thickened cell walls, mainly due to G-lignin, in non-silenced NIL-R, relative to silenced, in conjunction with higher total lignin content. Metabolic profiling of TaLAC4 silenced NILs identified the accumulation of several precursor metabolites higher in abundances upstream TaLAC4. These results confirm that the resistance function of TaLAC4 in NIL-R is due to pathogen-induced lignification of secondary cell walls in the rachis.

摘要

镰刀菌穗腐病(FHB)主要由禾谷镰刀菌(Fg)引起,是小麦最严重的病害之一。由于真菌毒素污染,它会影响谷物的产量和质量,对人类和牲畜的食用都有害。细胞壁木质化是病原体入侵后的一种先天防御反应。已知植物漆酶能使次生细胞壁木质化。代谢组学研究在来自苏麦 3*5/撒切尔杂交的小麦近等基因系 QTL-Fhb1 中鉴定出漆酶作为候选基因之一。根据系统发育,它被命名为 TaLAC4。实时 qPCR 显示 TaLAC4 在 NIL-R 中强烈诱导表达。在 NIL-R 中基于 VIGS 的 TaLAC4 瞬时沉默导致易感性增加,导致在 15dpi 时整个穗部的 Fg 扩散,与未沉默的情况形成对比,未沉默的情况感染仅限于接种的小穗。组织病理学显示,与沉默相比,非沉默的 NIL-R 中细胞壁增厚,主要是由于 G-木质素,同时总木质素含量更高。对 TaLAC4 沉默的 NILs 的代谢组学分析确定了几种前体代谢物的积累,这些代谢物在前体代谢物中含量更高。这些结果证实,TaLAC4 在 NIL-R 中的抗性功能是由于次生细胞壁在穗轴中的病原体诱导木质化。

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