Opposing effects of MYZUS PERSICAE-INDUCED LIPASE 1 and jasmonic acid influence the outcome of \u3ci\u3eArabidopsis thaliana–Fusarium graminearum\u3c/i\u3e interaction

Fusarium graminearum (Fg) is an important fungal pathogen of small grain cereals that can also infect Arabidopsis thaliana. In Arabidopsis, jasmonic acid (JA) signalling involving JASMONATE RESISTANT 1 (JAR1), which synthesizes JA-isoleucine, a signalling form of JA, promotes susceptibility to Fg. Here we show that Arabidopsis MYZUS PERSICAE-INDUCED LIPASE 1 (MPL1), via its influence on limiting JA accumulation, restricts Fg infection. MPL1 expression was up-regulated in response to Fg infection, and MPL1-OE plants, which overexpress MPL1, exhibited enhanced resistance against Fg. In comparison, disease severity was higher on the mpl1 mutant than the wild type. JA content was lower in MPL1-OE and higher in mpl1 than in the wild type, indicating that MPL1 limits JA accumulation. Pharmacological experiments confirmed the importance of MPL1-determined restriction of JA accumulation on curtailment of Fg infection. Methyl-JA application attenuated the MPL1-OE- conferred resistance, while the JA biosynthesis inhibitor ibuprofen enhanced resistance in mpl1. Also, the JA biosynthesis-defective opr3 mutant was epistatic to mpl1, resulting in enhanced resistance in mpl1 opr3 plants. In comparison, JAR1 was not essential for the mpl1-conferred susceptibility to Fg. Considering that methyl-JA promotes Fg growth in culture, we suggest that in part MPL1 curtails disease by limiting the availability of a plant-derived Fg growth-promoting factor

Opposing effects of MYZUS PERSICAE-INDUCED LIPASE 1 and jasmonic acid influence the outcome of Arabidopsis thaliana–Fusarium graminearum interaction

Article presents research that shows Arabidopsis MYZUS PERSICAE-INDUCED LIPASE 1 (MPL1), via its influence on limiting jasmonic acid (JA) accumulation, restricts Fusarium graminearum (Fg) infection

CYP720A1 function in roots is required for flowering time and systemic acquired resistance in the foliage of Arabidopsis

Abstract Systemic acquired resistance (SAR) is an inducible defense mechanism that systemically enhances resistance against pathogens in foliar tissues. SAR, which engages salicylic acid (SA) signaling, shares molecular components with the autonomous pathway, which is involved in controlling flowering time in Arabidopsis thaliana. FLOWERING LOCUS D (FLD) is one such autonomous pathway component that is required for flowering time and the systemic accumulation of SA during SAR. Here, we show that CYP720A1, a putative cytochrome P450 monoxygenase, controls FLD expression and is required for the timing of flowering and the manifestation of SAR. The delayed flowering time in the cyp720a1 mutant correlated with the elevated transcript level of the floral repressor FLC, while the SAR deficiency phenotype of the cyp720a1 mutant correlated with the inability to systemically accumulate SA. CYP720A1 transcript abundance in shoots is poor compared with roots. Reciprocal root–shoot grafting confirmed that CYP720A1 function in the roots is critical for flowering time and SAR. We therefore suggest that root to shoot communication involving a CYP720A1-dependent factor contributes to the timing of reproductive development and defense in the foliage.</jats:p

<i>Arabidopsis thaliana FLOWERING LOCUS D</i> Is Required for Systemic Acquired Resistance

Localized infection in plants often induces systemic acquired resistance (SAR), which provides long-term protection against subsequent infections. A signal originating in the SAR-inducing organ is transported to the distal organs, where it stimulates salicylic acid (SA) accumulation and priming, a mechanism that results in more robust activation of defenses in response to subsequent pathogen infection. In recent years, several metabolites that promote long-distance SAR signaling have been identified. However, the mechanism or mechanisms by which plants perceive and respond to the SAR signals are largely obscure. Here, we show that, in Arabidopsis thaliana, the FLOWERING LOCUS D (FLD) is required for responding to the SAR signals leading to the systemic accumulation of SA and enhancement of disease resistance. Although the fld mutant was competent in accumulating the SAR-inducing signal, it was unable to respond to the SAR signal that accumulates in petiole exudates of wild-type leaves inoculated with a SAR-inducing pathogen. Supporting FLD's role in systemic SAR signaling, we observed that dehydroabietinal and azelaic acid, two metabolites that, in wild-type plants, promote SAR-associated systemic accumulation of SA and priming, respectively, were unable to promote SAR in the fld mutant. FLD also participates in flowering, where it functions to repress expression of the flowering repressor FLOWERING LOCUS C (FLC). However, epistasis analysis indicates that FLD's function in SAR is independent of FLC. </jats:p

Dehydroabietinal promotes flowering time and plant defense in Arabidopsis via the autonomous pathway genes FLOWERING LOCUS D, FVE, and RELATIVE OF EARLY FLOWERING 6

Abstract Abietane diterpenoids are tricyclic diterpenes whose biological functions in angiosperms are largely unknown. Here, we show that dehydroabietinal (DA) fosters transition from the vegetative phase to reproductive development in Arabidopsis thaliana by promoting flowering time. DA’s promotion of flowering time was mediated through up-regulation of the autonomous pathway genes FLOWERING LOCUS D (FLD), RELATIVE OF EARLY FLOWERING 6 (REF6), and FVE, which repress expression of FLOWERING LOCUS C (FLC), a negative regulator of the key floral integrator FLOWERING LOCUS T (FT). Our results further indicate that FLD, REF6, and FVE are also required for systemic acquired resistance (SAR), an inducible defense mechanism that is also activated by DA. However, unlike flowering time, FT was not required for DA-induced SAR. Conversely, salicylic acid, which is essential for the manifestation of SAR, was not required for the DA-promoted flowering time. Thus, although the autonomous pathway genes FLD, REF6, and FVE are involved in SAR and flowering time, these biological processes are not interdependent. We suggest that SAR and flowering time signaling pathways bifurcate at a step downstream of FLD, REF6, and FVE, with an FLC-dependent arm controlling flowering time, and an FLC-independent pathway controlling SAR.</jats:p

Interplay between <i>MYZUS PERSICAE-INDUCED LIPASE 1</i> and OPDA signaling in controlling green peach aphid infestation on <i>Arabidopsis thaliana</i>

AbstractMYZUS PERSICAE-INDUCED LIPASE1 (MPL1) encodes a lipase in Arabidopsis thaliana that is required for controlling infestation by the green peach aphid (GPA; Myzus persicae), an important phloem sap-consuming insect pest. Previously, we demonstrated that MPL1 expression was upregulated in response to GPA infestation, and GPA fecundity was higher on the mpl1 mutant, compared to the wild-type (WT), and lower on 35S:MPL1 plants that constitutively expressed MPL1 from the 35S promoter. Here, we show that the MPL1 promoter is active in the phloem and expression of the MPL1 coding sequence from the phloem-specific SUC2 promoter is sufficient to restore resistance to the GPA in the mpl1 mutant. The GPA infestation-associated upregulation of MPL1 requires CYCLOPHILIN 20-3 (CYP20-3), which encodes a 12-oxo- phytodienoic acid (OPDA)-binding protein that is involved in OPDA signaling and is required for controlling GPA infestation. OPDA promotes MPL1 expression to limit GPA fecundity, a process that requires CYP20-3 function. These results along with our observation that constitutive expression of MPL1 from the 35S promoter restores resistance to the GPA in the cyp20-3 mutant, and MPL1 feedbacks to limit OPDA levels in GPA-infested plants, suggest that an interplay between MPL1, OPDA, and CYP20-3 contributes to resistance to the GPA.HighlightInteraction between MYZUS PERSICAE-INDUCED LIPASE 1 function in the phloem, and 12-oxo-phytodienoic acid (OPDA) and CYCLOPHILIN 20-3, which encodes an OPDA-binding protein that is involved in OPDA signaling, is involved in controlling green peach aphid infestation on Arabidopsis thaliana.</jats:sec