Document Type

Thesis

Degree Name

Master of Science (MSc)

Department

Biology

Program Name/Specialization

Integrative Biology

Faculty/School

Faculty of Science

First Advisor

Christian Danve M. Castroverde

Advisor Role

Supervisor

Abstract

Healthy plant development requires balancing both abiotic (e.g. climate) and biotic (e.g. pathogen) challenges, which intercept important signaling pathways in plants. For example, climate change-associated elevated temperature can negatively modulate various aspects of plant immunity, including the production of central immune signals salicylic acid (SA) and N-hydroxypipecolic acid (NHP). Since SA and NHP signaling both require the master immune co-activator protein NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1), it is important to investigate NPR1 as a potentially temperature-regulated molecular hub. Although the NPR1 gene is not transcriptionally downregulated at elevated temperatures (28° C vs. 23° C), little is known about the translational and/or post-translational regulation of NPR1 by NHP and/or its precursor pipecolic acid (Pip) under warmer temperature conditions. In this thesis, I have investigated the effect of exogenous Pip treatment on NPR1 protein levels, nuclear localization and phosphorylation under changing temperatures in the model species Arabidopsis thaliana. Immunoblot analyses revealed that Pip could induce NPR1 total protein levels at 23° C, but struggled to induce NPR1 protein levels at 28° C. Laser confocal microscopy of Arabidopsis leaves was then conducted to observe Pip mediated NPR1 nucleocytoplasmic dynamics at both ambient and warm temperatures. Optimal NPR1-eYFP nuclear localization was observed at 23° C, 8-hours post Pip treatment, but this Pip effect was not maintained at 28° C. Lastly, Phos-tag™ gel electrophoresis and immunoblotting suggested increased NPR1 phosphorylation after immune elicitation with Pip, at both normal (23° C) and elevated temperature (28° C). Increased NPR1 phosphorylation under mock conditions at 28° C suggest NPR1 phosphorylation may also play a role in warm temperature signaling, potentially limiting pathogen-induced NPR1 signaling under similar conditions. Evaluation of NPR1 serine 11 and serine 15 phosphomimic mutant plants suggested the two phosphorylation events were not sufficient to improve the immune priming response at either temperature under both pathogenic Pst AvrRpt2 DC3000 and chemical Pip immune elicitation. Together these findings provide insights into how plants deal with the stressful combination of climate warming and pathogen attack, while also demonstrating the temperature modulation of Pip-induced NPR1-mediated immunity.

Convocation Year

2025

Convocation Season

Spring

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Available for download on Tuesday, January 27, 2026

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