Plant defense negates pathogen manipulation of vector behavior

1. Although many vector‐borne plant pathogens can alter vector behaviour to the pathogen\u27s benefit, how plants might counter such manipulation is unknown. 2. In the Tomato yellow leaf curl virus (‘TYLCV’)–Bemisia tabaci–tomato interaction, TYLCV‐mediated changes in Bemisia feeding improves viral uptake and transmission. We tested how jasmonic acid (‘JA’), a central regulator of plant antiherbivore defences, affected the ability of TYLCV to (A) manipulate Bemisia behaviour; and (B) infect plants. 3. Viruliferous Bemisia fed much more than virus‐free whiteflies on JA‐deficient plants, more than virus‐free whiteflies on controls, and similarly on high‐JA plants. 4. When TYLCV was transmitted via whiteflies, infection levels were lower in high‐JA plants relative to JA‐deficient and control plants. When TYLCV was transmitted via direct injection, JA‐overexpressed and JA‐deficient plants had similar infection levels. The JA‐mediated cessation of vector manipulation thus reduced infection and lessened pathogen impact. 5. The presence of the JA pathway in many plant species suggests that similar interactions may be widespread in nature

Variation in both host defense and prior herbivory can alter plant-vector-virus interactions

Background: While virus-vector-host interactions have been a major focus of both basic and applied ecological research, little is known about how different levels of plant defense interact with prior herbivory to affect these relationships. We used genetically-modified strains of tomato (Solanum lycopersicum) varying in the jasmonic acid (JA) plant defense pathways to explore how plant defense and prior herbivory affects a plant virus (tomato yellow leaf curl virus, ‘TYLCV’), its vector (the whitefly Bemisia tabaci MED), and the host. Results: Virus-free MED preferred low-JA over high-JA plants and had lower fitness on high-JA plants. Viruliferous MED preferred low-JA plants but their survival was unaffected by JA levels. While virus-free MED did not lower plant JA levels, viruliferous MED decreased both JA levels and the expression of JA-related genes. Infestation by viruliferous MED reduced plant JA levels. In preference tests, neither virus-free nor viruliferous MED discriminated among JA-varying plants previously exposed to virus-free MED. However, both virus-free and viruliferous MED preferred low-JA plant genotypes when choosing between plants that had both been previously exposed to viruliferous MED. The enhanced preference for low-JA genotypes appears linked to the volatile compound neophytadiene, which was found only in whitefly-infested plants and at concentrations inversely related to plant JA levels. Conclusions: Our findings illustrate how plant defense can interact with prior herbivory to affect both a plant virus and its whitefly vector, and confirm the induction of neophytadiene by MED. The apparent attraction of MED to neophytadiene may prove useful in pest detection and management

A Jasmonate Signaling Network Activates Root Stem Cells and Promotes Regeneration

Plants are sessile and have to cope with environmentally induced damage through modification of growth and defense pathways. How tissue regeneration is triggered in such responses and whether this involves stem cell activation is an open question. The stress hormone jasmonate (JA) plays well-established roles in wounding and defense responses. JA also affects growth, which is hitherto interpreted as a trade-off between growth and defense. Here, we describe a molecular network triggered by wound-induced JA that promotes stem cell activation and regeneration. JA regulates organizer cell activity in the root stem cell niche through the RBR-SCR network and stress response protein ERF115. Moreover, JA-induced ERF109 transcription stimulates CYCD6;1 expression, functions upstream of ERF115, and promotes regeneration. Soil penetration and response to nematode herbivory induce and require this JA-mediated regeneration response. Therefore, the JA tissue damage response pathway induces stem cell activation and regeneration and activates growth after environmental stress

Data from: Plant defense negates pathogen manipulation of vector behavior

1. Although many vector-borne plant pathogens can alter vector behavior to the pathogen's benefit, how plants might counter such manipulation is unknown. 2. In the Tomato yellow leaf curl virus (‘TYLCV’)-Bemisia tabaci-tomato interaction, TYLCV-mediated changes in Bemisia feeding improves viral uptake and transmission. We tested how jasmonic acid (‘JA’), a central regulator of plant anti-herbivore defenses, affected the ability of TYLCV to (A) manipulate Bemisia behavior; and (B) infect plants. 3. Viruliferous Bemisia fed much more than virus-free whiteflies on JA-deficient plants, more than virus-free whiteflies on controls, and similarly on high-JA plants. 4. When TYLCV was transmitted via whiteflies, infection levels were lower in high-JA plants relative to JA-deficient and control plants. When TYLCV was transmitted via direct injection, JA-overexpressed and JA-deficient plants had similar infection levels. The JA-mediated cessation of vector manipulation thus reduced infection and lessened pathogen impact. 5. The presence of the JA pathway in many plant species suggests that similar interactions may be widespread in nature

Role of β-Oxidation in Jasmonate Biosynthesis and Systemic Wound Signaling in Tomato

Jasmonic acid (JA) is a lipid-derived signal that regulates plant defense responses to biotic stress. Here, we report the characterization of a JA-deficient mutant of tomato (Lycopersicon esculentum) that lacks local and systemic expression of defensive proteinase inhibitors (PIs) in response to wounding. Map-based cloning studies demonstrated that this phenotype results from loss of function of an acyl-CoA oxidase (ACX1A) that catalyzes the first step in the peroxisomal β-oxidation stage of JA biosynthesis. Recombinant ACX1A exhibited a preference for C12 and C14 straight-chain acyl-CoAs and also was active in the metabolism of C18 cyclopentanoid-CoA precursors of JA. The overall growth, development, and reproduction of acx1 plants were similar to wild-type plants. However, the mutant was compromised in its defense against tobacco hornworm (Manduca sexta) attack. Grafting experiments showed that loss of ACX1A function disrupts the production of the transmissible signal for wound-induced PI expression but does not affect the recognition of this signal in undamaged responding leaves. We conclude that ACX1A is essential for the β-oxidation stage of JA biosynthesis and that JA or its derivatives is required both for antiherbivore resistance and the production of the systemic wound signal. These findings support a role for peroxisomes in the production of lipid-based signaling molecules that promote systemic defense responses