SEARCH

SEARCH BY CITATION

FilenameFormatSizeDescription
mpp827-sup-0001-si.doc6937K

Fig. S1 β-Aminobutyric acid (BABA)-mediated enhanced resistance at 48 h post-inoculation (hpi) with Pectobacterium carotovorum ssp. carotovorum (Pcc) SCC1. Arabidopsis plants were treated with water (A) or BABA (B) and challenged 48 h later with Pcc SCC1 at a concentration of 5 × 106 colony-forming units (cfu)/mL. Photographs were taken 2 days later. White arrows indicate Pcc SCC1-mediated water-soaked lesions.

mpp827-sup-0001-si.doc6937K

Fig. S2 Defective PATHOGENESIS RELATED 1 (PR1) up-regulation in salicylic acid (SA)-defective mutants. Arabidopsis plants were treated with water or BABA and challenged 48 h later with Pectobacterium carotovorum ssp. carotovorum (Pcc) SCC1 at a concentration of 5 × 106 colony-forming units (cfu)/mL. RNAs were harvested at 18 h post-inoculation (hpi). 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). Asterisks indicate a significant difference from the water controls based on Student's t-test (P < 0.01).

mpp827-sup-0001-si.doc6937K

Fig. S3 The Pectobacterium carotovorum ssp. carotovorum (Pcc) hypersensitive response and pathogenicity (hrp)- and hrp conserved (hrc)-deficient mutant strain WPP17 is less virulent than the wild-type Pcc SCC1 strain. Five-week-old Col-0 plants were dip inoculated with 5 × 106 colony-forming units (cfu)/mL Pcc SCC1 (A) or Pcc WPP17 (B) and photographs were taken 1 day later. White arrows indicate Pcc-mediated water-soaked lesions.

mpp827-sup-0001-si.doc6937K

Fig. S4 β-Aminobutyric acid (BABA) primes the pattern-triggered immunity (PTI) response upon infection with wild-type Pectobacterium carotovorum ssp. carotovorum (Pcc) SCC1 bacteria. (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) upon Pcc SCC1 infection. Transcript levels were analysed at 4 h post-inoculation (hpi) with 5 × 106 colony-forming units (cfu)/mL Pcc SCC1. 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). (B) BABA primes callose deposition upon Pcc SCC1 infection. Leaves were syringe infiltrated with Pcc SCC1 (5 × 106 cfu/mL) and samples were collected 12 h later for aniline blue staining. The graph represents the average number of deposits observed per square millimetre. Biological triplicates were the average ± SD (n = 27). Asterisks indicate a significant difference from water controls based on Student's t-test (P < 0.01).

mpp827-sup-0001-si.doc6937K

Fig. S5 β-Aminobutyric acid (BABA)-mediated priming of pattern-triggered immunity (PTI) upon Pectobacterium carotovorum ssp. carotovorum (Pcc) SCC1 infection in salicylic acid (SA)-defective mutants. (A) FLG22-INDUCED RECEPTOR-LIKE KINASE 1 (FRK1) expression is primed in BABA-treated Col-0, SA induction deficient 2-1 (sid2-1) and phytoalexin deficient 4-1 (pad4-1) after inoculation with Pcc SCC1. Transcript levels of FRK1 were analysed at 6 h post-inoculation (hpi) with 5 × 106 colony-forming units (cfu)/mL Pcc SCC1. FRK1 expression 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 Col-0 water controls (defined value of one). Data represent the means and standard deviation (SD) of three independent biological replicates (n = 9). (B) Callose deposition is primed in SA-defective mutants upon Pcc SCC1 infection. Leaves were syringe infiltrated with Pcc SCC1 (5 × 106 cfu/mL), and samples were collected 12 h later for aniline blue staining. Graph represents the average number of deposits observed per square millimetre. Biological triplicates were averaged ± SD (n = 27). Asterisks indicate a significant difference from water controls based on Student's t-test (P < 0.01).

mpp827-sup-0001-si.doc6937K

Fig. S6 Callose deposition in nonbuffer-infiltrated Arabidopsis leaves. Arabidopsis plants were soil drenched with water or β-aminobutyric acid (BABA), and leaves were analysed for callose deposition 2 days later. The graph represents the average number of deposits observed per square millimetre. Biological triplicates were averaged ± standard deviation (SD) (n = 27). Values of BABA-treated plants were not significantly different from those of water-treated controls based on Student's t-test (P < 0.01).

Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.