Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.784120
Title: Dissecting thermosensory suppression of immunity in Arabidopsis
Author: Gardener, Catherine
ISNI:       0000 0004 7969 6863
Awarding Body: University of East Anglia
Current Institution: University of East Anglia
Date of Award: 2019
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Abstract:
As sessile organisms, plants must modify growth and development to suit their environment and ensure reproductive success. Moderate increases in temperature accelerate plant growth whilst compromising immunity. As yet, the precise mechanism through which plants sense and integrate temperature information and coordinate signalling networks influencing growth and immunity are not fully explored. In this thesis, ambient temperature increases of just 2.5˚C were found to strongly influence pathogen resistance. These increases compromised both Pattern-Triggered Immunity (PTI) as well as Effector-Triggered Immunity (ETI), resulting in overall attenuation of immune outputs. Importantly, modulation of immunity was found to be a reliable thermosensory output. Using PATHOGENESIS RELATED1 (PR1) as a marker, a novel mutant resilient 1 (res1) with temperature-resilient immunity was isolated from a PR1-LUC based forward genetic screen. res1 displays robust and temperature resilient immunity, alongside generally perturbed thermosensory responses, suggesting that RES1 is part of a key thermosensory pathway. RES1 was mapped to the gene encoding the cyclic nucleotide gated calcium channel, NGC2. A missense mutation in res1 resulted in an amino acid substitution (A457T) in CNGC2. This mutation also led to the generation of a novel splice variant of this channel, with an in-frame deletion of 14 amino acids. This novel variant appears to impede function of CNGC2 and affect downstream signalling. These findings implicated CNGC2 and therefore changes in calcium dynamics as coordinating ambient temperature signalling. Despite its temperature-resilient maintenance of SA-Triggered Immunity (SATI), res1 has compromised early PTI responses. This response was found to be common to other mutants with perturbed SATI. The existence of negative feedback between this layer of immunity and early PTI signalling was thus identified as a general phenomenon. Knowledge generated from this study both of the nature of TSI and its underlying molecular control will have many potential implications, including devising strategies for climate-resilient disease resistance in crops.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.784120  DOI: Not available
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