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

Copyright © 2020. Published by Elsevier B.V.

Bibliographische Detailangaben
Veröffentlicht in:Plant science : an international journal of experimental plant biology. - 1985. - 298(2020) vom: 08. Sept., Seite 110574
1. Verfasser: Soni, Nancy (VerfasserIn)
Weitere Verfasser: Hegde, Niranjan, Dhariwal, Achal, Kushalappa, Ajjamada C
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2020
Zugriff auf das übergeordnete Werk:Plant science : an international journal of experimental plant biology
Schlagworte:Journal Article Disease resistance Fusarium head blight Laccase Metabolomics VIGS Wheat Plant Proteins EC 1.10.3.2
Beschreibung
Zusammenfassung:Copyright © 2020. Published by Elsevier B.V.
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
Beschreibung:Date Completed 02.03.2021
Date Revised 02.03.2021
published: Print-Electronic
Citation Status MEDLINE
ISSN:1873-2259
DOI:10.1016/j.plantsci.2020.110574