Understanding the Delicate Balance between Microbial Pathogens and Insect Pests and Optimising Protection in Actinidia chinensis

Kiwifruit (Actinidia species) is a major horticultural crop. Actinidia chinensis var. chinensis ‘Hort16A’ is challenged by various biotic stressors with different lifestyles, including the hemi-biotrophic bacterial pathogen Pseudomonas syringae pv. actinidiae (psa) and the necrotrophic fungal pathogen Sclerotinia sclerotiorum (sclerotinia). In the model plant Arabidopsis thaliana, defence hormones (namely salicylic acid (SA) and jasmonic acid (JA)) regulate networks of functionally linked genes to control the deployment of attacker-specific defence. In contrast, the hormone networks regulating ‘Hort16A’ defence are largely unknown. This project aimed to characterise the genetic components, regulation, and inter-pathway communication between the ‘Hort16A’ SA and JA networks during the response to biotic stressors. Throughout this thesis, methodologies used in the ‘Hort16A’ tissue culture system have been optimised, validating its use as a model plant for other perennial crop species. Using A. thaliana as a model, key SA- and JA-associated genes and their roles in the Actinidia defence response were identified. Genes within the ‘Hort16A’ SA network initially regulated the response to sclerotinia, while the SA and JA networks were activated during the later stages of infection. In contrast, ‘Hort16A’ did not mount a successful response to psa, failing to strongly induce either defence network. Defence induction and disease development were impacted by sequential stress events, wherein the prior infection status of ‘Hort16A’ altered the resistance and/or susceptibility to secondary challenge with a different biotic stressor. Time-series dense transcriptomic profiling further characterised the ‘Hort16A’ SA and JA defence networks. The discovery of novel genes and pathway-specific ‘hubs’ highlighted differences between ‘Hort16A’ and model species. Insights into the temporal regulation of hormone-responsive genes facilitated the generation of a chronological timeline of defence, detailing the components and expression patterns of the SA and JA networks. A surprisingly significant level of synergism was observed between the two defence networks and the response to sclerotinia, resulting in the proposed re-modelling of the ‘Hort16A’ defence response. In this model, the SA and JA defence networks display temporally limited mutual antagonism prior to converging upon a common defence response at the later stages of infection, allowing dynamic response to diverse stressors in the multi-stressor environment.

Name thesis:degree_name

PhD

Level thesis:degree_level

Doctoral

Discipline thesis:degree_discipline

Biological Sciences

Grantor dc:publisher

ResearchSpace@Auckland

Year dc:date.issued

2023

Author dc:creator

• Stroud, Erin A.

Advisors dc:contributor.advisor

• Templeton, Matthew D.
• Rikkerink, Erik H.
• Jayaraman, Jay

Statement dc:rights

• Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Licence dc:rights.uri

• https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm

Handle dc:identifier.uri

https://hdl.handle.net/2292/64203

OAI identifier oai:identifier

oai:researchspace.auckland.ac.nz:2292/64203