From uptake to primed cell wall defence: molecular mechanisms controlling beta-amino acid-induced immune priming in Arabidopsis

Besides innate immunity, plants have acquired immunity, which is based on immune memory from prior stress exposures. This memory enables plants to respond more effectively and rapidly to subsequent pathogen attacks, forming a resistant phenotype, known as induced resistance (IR) response. Two β-amino acids, (R)-β-homoserine (RBH) and β-aminobutyric acid (BABA), act as the stress stimulus triggering IR responses. The molecular mechanisms of RBH- and BABA-IR are still not fully understood, especially in the case of RBH, whose IR potential was only recently discovered. This PhD study aims to address this knowledge gap and enhance our comprehension of β-amino acid-induced resistance.
This work first looked into the mechanisms of RBH-IR by using a forward genetic screen with Arabidopsis (Arabidopsis thaliana) T-DNA insertion collection for mutants impaired in RBH-induced immunity (iri). An amino acid transporter, LYSINE HISTIDINE TRANSPORTER 1 (LHT1), was identified from the screen. Quantifying RBH and BABA content in the LHT1 mutant and overexpression lines and an uptake experiment with yeast expressing LHT1 revealed it acts as the primary transporter of RBH and BABA.
Next, FATTY ACID HYDROXYLASE 2 (FAH2), an interactor of the BABA receptor, IMPAIRED IN BABA-INDUCED IMMUNITY 1 (IBI1) was investigated. Induced resistance and growth response assays showed FAH2 regulates BABA-IR and BABA-induced stress. Furthermore, sphingolipid profiling of wildtype, ibi1-1 and fah2-1, singled out a glycosyl inositol phosphorylceramide which might be a potential negative regulator of BABA-IR.
Finally, this work showed that RBH-IR and BABA-IR employ different regulatory mechanisms in relation to callose-associated penetration resistance, a shared IR response between these two chemicals. While BABA relies on PLASMODESMATA-LOCATED PROTEINs (PDLPs) and the callose synthase POWDERY MILDEW RESISTANT 4 (PMR4) to enhance callose-associated resistance, RBH-induced callose augmentation involves other callose synthases beyond PMR4, and independent from PDLPs. In summary, this thesis advances the understanding of molecular mechanisms underpinning RBH-IR and BABA-IR and provides candidate genes for future breeding programs.