Figure 4.

Effect of β‐aminobutyric acid (BABA) treatments on the Arabidopsis pattern‐triggered immunity (PTI) response. (A) BABA potentiates the expression of FLG22‐INDUCED RECEPTOR‐LIKE KINASE 1 (FRK1), ARABIDOPSIS NON‐RACE SPECIFIC DISEASE RESISTANCE GENE (NDR1)/HAIRPIN‐INDUCED GENE (HIN1)‐LIKE 10 (NHL10) and CYTOCHROME P450, FAMILY 81 (CYP81F2) on Pectobacterium carotovorum ssp. carotovorum (Pcc) WPP17 infection. Transcript levels were analysed at 2 h post‐inoculation (hpi) with 1 × 10⁸ colony‐forming units (cfu)/mL Pcc WPP17. (B,C) Potentiated expression of PTI‐responsive genes 30 min after infiltration with 1 μM flg22 (B) or elf26 (C). For (A–C), transcript levels were determined by quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR) and normalized to both UBQ10 and EF‐1. Relative gene expression levels were compared with water controls (defined value of one). Data represent the means and standard deviation (SD) of three independent biological replicates (n = 9). (D–I) BABA primes callose deposition upon Pcc WPP17 infection (D,E), flg22 (F,G) and elf26 (H,I). Leaves were syringe infiltrated with Pcc WPP17 (1 × 10⁸ cfu/mL), 1 μM flg22 or elf26, and samples were collected 6 h later for aniline blue staining. Graph represents the average number of deposits observed per square millimetre. Biological triplicates were averaged ± SD (n = 27). For A, B, C, E, G and I, asterisks indicate a significant difference from water controls based on Student's t‐test (P < 0.01). White bars, 200 μm. B, BABA treated; W, water treated.