Lookup NU author(s): Tahsin Shoala,
Dr Martin Edwards,
Professor Angharad MR Gatehouse
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Plants have co-evolved with a diverse array of pathogens and insect herbivores and so have evolved an extensive repertoire of constitutive and induced defence mechanisms activated through complex signalling pathways. OXI1 kinase is required for activation of mitogen-activated protein kinases (MAPKs) and is an essential part of the signal transduction pathway linking oxidative burst signals to diverse downstream responses. Furthermore, changes in the levels of OXI1 appear to be crucial for appropriate signalling. Callose deposition also plays a key role in defence. Here we demonstrate, for the first time, that OXI1plays an important role in defence against aphids. The Arabidopsis mutant, oxi1-2, showed significant resistance both in terms of population build-up (p<0.001) and the rate of build-up (p<0.001). Arabidopsis mutants for β-1,3-glucanase, gns2and gns3,showed partial aphid resistance, significantly delaying developmental rate, taking two-fold longer to reach adulthood. Whilst β-1,3-glucanase genes GNS1, GNS2, GNS3and GNS5were not induced in oxi1-2 in response to aphid feeding, GNS2was expressed to high levels in the corresponding WT (Col-0) in response to aphid feeding. Callose synthase GSL5 was up-regulated in oxi1-2in response to aphids. The results suggest that resistance in oxi1-2mutants is through induction of callose deposition via MAPKs resulting in ROS induction as an early response. Furthermore, the results suggest that the β-1,3-glucanase genes, especially GNS2,play an important role in host plant susceptibility to aphids. Better understanding of signalling cascades underpinning tolerance to biotic stress will help inform future breeding programmes for enhancing crop resilience.
Author(s): Shoala T, Edwards MG, Knight MR, Gatehouse AMR
Publication type: Article
Publication status: Published
Journal: Transgenic Research
Print publication date: 01/08/2018
Online publication date: 17/05/2018
Acceptance date: 25/04/2018
ISSN (print): 0962-8819
ISSN (electronic): 1573-9368
Publisher: Springer Netherlands
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