阿拉伯芥透過誘發反應調控先天性免疫作用抵抗死體寄生型之軟腐病原細菌

Abstract

Boosted responsiveness of plant cells to stress at the onset of pathogen- or chemically-induced resistance is called priming. The chemical beta-aminobutyric acid (BABA) enhances Arabidopsis thaliana resistance to hemi-biotrophic bacteria through priming of the salicylic acid (SA) defence response. Whether BABA increases Arabidopsis resistance to necrotrophic bacteria such as Pectobacterium carotovorum subsp. carotovorum (Pcc) is not clear. Here we show that treatment with BABA protects Arabidopsis against the soft-rot pathogen Pcc. BABA did not prime the expression of the jasmonate/ethylene responsive PDF1.2, which up-regulation is usually associated with resistance to necrotrophic pathogens. Expression of the SA marker gene PR1 upon Pcc infection was primed by BABA treatment, but SA defective mutants demonstrated a wild-type level of BABA-induced resistance against Pcc. BABA primed the expression of the pattern-triggered immunity (PTI)-responsive gene FRK1, NHL10 and CYP81F2 after inoculation with Pcc or after treatment with purified bacterial microbe-associated molecular patterns such as flg22 or elf26. PTI-mediated callose deposition was also potentiated in BABA-treated Arabidopsis and BABA boosted Arabidopsis stomatal immunity to Pcc. BABA treatment primed the PTI response in the SA defective mutants sid2-1 and pad4-1. In addition, BABA-priming was associated with open chromatin configurations in promoter region of PTI marker genes. Our data indicate that BABA primes the PTI responses upon necrotrophic bacteria infection and suggest a role for the PTI responses in BABA-induced resistance. To further investigate the mechanism of BABA induced resistance, the function of AtNUDX25 that is up-regulated by BABA was analyzed. A AtNUDX25 T-DNA insertion knockout line demonstrated increased susceptibility to Pcc and was hyper-sensitive to oxidative stress. These data suggest that AtNUDX25 may play a role in resistance to biotic stress and tolerance to abiotic stress.