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

Significant crop losses are caused by pathogenic infections annually, which are exacerbated by increasing global temperatures due to climate change. One way by which plants respond to pathogenic attacks is through the activation of pattern-triggered immunity (PTI), effector-triggered immunity (ETI), and systemic acquired resistance (SAR), which lead to production of the central defence phytohormone salicylic acid (SA). Accompanying SA release is the putative mobilization of pipecolic acid (Pip), which acts as an immune regulatory plant metabolite that works with and independently from SA. As demonstrated in the model plant Arabidopsis thaliana following infection with the model bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000, Pip and its hydroxylated derivative N-hydroxypipecolic acid (NHP) accumulate in local and distal tissues to amplify the plant immune response and prime the plant for future infections. Previous studies have only shown that increased temperature negatively impact PTI, ETI and SA production in the local/primary sites of infection. However, how temperature affects plant systemic immunity has not been fully explored. In this thesis, I showed that systemic immunity in Arabidopsis to Pst DC3000 was significantly reduced at elevated temperatures. Elevated temperature decreased expression of the SAR-associated Pip-NHP biosynthetic genes AGD2-LIKE DEFENSE RESPONSE PROTEIN 1 (ALD1) and FLAVIN-DEPENDENT MONOOXYGENASE 1 (FMO1) in systemically primed leaf tissues. Remarkably, exogenous Pip application via local leaf infiltration or root-drench restored immunity to Pst DC3000 at elevated temperature; however, local leaf infiltration did not restore immunity in systemic leaves. I have also shown how Pip-induced gene expression locally and systemically were affected by temperature. Finally, because of the interlinked regulation between SA and Pip/NHP by the master transcription factor CAM-BINDING PROTEIN 60-LIKE G (CBP60g), I have shown that Arabidopsis plants constitutively expressing CBP60g (35S:CBP60g) exhibited SAR at both normal and elevated temperatures. My results suggest that CBP60g controls the temperature-sensitivity of plant systemic immunity by modulating NHP biosynthesis. Overall, this thesis contributes to understanding the signaling pathways regulating local and systemic plant immune responses in our warming climate.

Convocation Year

2023

Convocation Season

Spring

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