bak1-5 mutation uncouples tryptophan-dependent and independent postinvasive immune pathways triggered in Arabidopsis by multiple fungal pathogens

Abstract

20Robust nonhost resistance of Arabidopsis thaliana against the nonadapted 21 hemibiotrophic fungus Colletotrichum tropicale requires PEN2-dependent preinvasive 22Key words: Arabidopsis thaliana, Disease resistance, Metabolism, Plant-pathogen 41 interaction, Plant immunity 42 43The resistance of an entire plant species against all isolates of particular pathogens is 44 called nonhost resistance [1]. Arabidopsis thaliana exhibits nonhost resistance against a 45 nonadapted powdery mildew pathogen Blumeria graminis f. sp. hordei called Bgh. The 46 four PENETRATION genes, PEN1, PEN2, PEN3 and PEN4, have been reported in 47Arabidopsis to control entry of Bgh through activation of vesicle secretion, biosynthesis 48 of putatively antifungal metabolites, and their transport toward pathogen invasion sites, 49 respectively [2,3,4,5,6,7,8,9,10]. 50Colletotrichum tropicale (hereafter Ctro), formally called C. gleosporioides, is a 51 hemibiotrophic fungal pathogen that causes anthracnose on its host mulberry; however, 52 it is not able to infect the nonhost Arabidopsis. Entry control by Arabidopsis against 53Ctro involves PEN2 and PEN3 [11,12], whereas PEN1 is not essential for this unlike 54 the case of Bgh [13]. Nonhost resistance toward Ctro also needs EDR1 (ENHANCED 55 DISEASE RESISTANCE 1) [14], whereas the edr1 mutants exhibit enhanced resistance 56 toward the adapted powdery mildew Golovinomyces cichoracearum (formerly named 57 Erysiphe cichoracearum) [15], suggesting the presence of diverse plant strategies for 58 controlling the entry attempts of pathogens showing distinct infection modes. 59 Importantly, even the pen2 edr1 mutant is still not fully susceptible to Ctro [16], 60 because of strong postinvasive resistance activated once Ctro enters epidermal cells of 61 this mutant, which is defective in the preinvasive resistance that controls pathogen 62 entry. We reported previously that Arabidopsis cyp79B2 cyp79B3 double mutant is fully 63 susceptible to the nonadapted pathogen Ctro [16]. CYP79B2 and CYP79B3 are key 64 enzymes for the biosynthesis of tryptophan (Trp)-derived antimicrobial metabolites. 65 CYP79B2/CYP79B3 convert Trp into indole-3-acetaldoxime (IAOx) [17], and this 66 precursor is then converted into several compounds for antimicrobial immunity, such as 67 4 PEN2 substrates indole-glucosinolates (IGs), PAD3 (PHYTOALEXIN-DEFICIENT3)-68 dependent camalexin, and 4-hydroxy-ICN (4-OH-ICN), whose biosynthesis requires 69 CYP82C2 [18,19,20]. The cyp79B2 cyp79B3 mutant is defective in preinvasive 70 resistance against Ctro because CYP79B2 and CYP79B3 are indispensable for 71 production of IGs, which are substrates metabolized by PEN2 to (unidentified) 72 compounds with presumed antifungal activity [5]. However, contrary with the pen2 73 mutant, the cyp79B2 cyp79B3 plants were also defective in postinvasive resistance to 74Ctro [16]. We have shown that the pen2 pad3 mutant is partially defective in 75 postinvasive resistance to Ctro, indicating that the Arabidopsis phytoalexin, camalexin, 76 is a critical fact...

RLP23 is required for Arabidopsis immunity against the grey mould pathogen Botrytis cinerea

“…The size of the lesions caused by A. brassicicola in the rlp23-1 and rlp23-2 mutants was not significantly different from that of Col-0 ( Fig. 6C), whereas the cyp71A12 cyp71A13 mutant exhibited enhanced susceptibility to the pathogen, consistent with our recent finding 36 . Thus, RLP23 is not essential for the Arabidopsis immunity against A. brassicicola.…”

“…Importantly, AbNLP1 expression was not detected at 4 and 12 hpi. We also found that the A. brassicicola strain Ryo-1 starts to invade Arabidopsis at around 12 hpi 36 . Collectively, these results indicate that AbNLP1 of A. brassicicola is not expressed before/during invasion, in contrast to BcNEP1 of B. cinerea.…”

Plant defensin expression triggered by fungal pathogen invasion depends on EDR1 protein kinase and ORA59 transcription factor in Arabidopsis thaliana

“…At 12 hpi, germinated conidia of Ab started to invade, and from 12 to 24 hpi, the fungal entry rate increased dramatically. 20 We found that the expressions of the two PDF genes tested were not induced at 4 hpi but were significantly induced in WT plants at 12 hpi and further elevated at 24 hpi (Figure 3a and Supplementary Figure 2A). These results suggest that the expressions of PDF genes were triggered by Ab invasion.…”

“…We next tested whether EDR1 and ORA59 might be required for PDF expression triggered upon invasion by a necrotrophic fungus, Alternaria brassicicola strain Ryo-1 (hereafter called Ab), in addition to Ctro. Because our recent study revealed that PEN2 is dispensable for preinvasive resistance against Ab, 20 we used the ora59 mutant instead of the pen2 ora59 mutant for Ab inoculation. Ab was inoculated onto WT (Col-0), edr1 and ora59 mutant plants, and leaf samples were collected at multiple time points (4, 12, 24, 48, 72 and 96 hpi).…”

“…21,22 We recently reported that the expression of PAD3 was induced upon Ab invasion and was involved in postinvasive resistance against Ab. 20 We investigated whether EDR1 and ORA59 are involved in the induced expression of PAD3 upon Ab invasion. The RT-qPCR analysis revealed that PAD3 expression was not detectable at 4 hpi, started to be induced at 12 hpi and was elevated at 24 hpi in WT (Figure 3b), which was consistent with our previous report.…”