Jasmonate

thumb|[[Jasminum grandiflorum]]

Jasmonate (JA) and its derivatives are lipid-based plant hormones that regulate a wide range of processes in plants, ranging from growth and photosynthesis to reproductive development. In particular, JAs are critical for plant defense against herbivory and plant responses to poor environmental conditions and other kinds of abiotic and biotic challenges. Some JAs can also be released as volatile organic compounds (VOCs) to permit communication between plants in anticipation of mutual dangers.

History

The isolation of methyl jasmonate (MeJA) from jasmine oil derived from Jasminum grandiflorum led to the discovery of the molecular structure of jasmonates and their name in 1962 while jasmonic acid itself was isolated from Lasiodiplodia theobromae by Alderidge et al in 1971.

JA itself can be further metabolized into active or inactive derivatives. Methyl JA (MeJA) is a volatile compound that is potentially responsible for interplant communication. JA conjugated with amino acid isoleucine (Ile) results in JA-Ile ((+)-7-iso-jasmonoyl--isoleucine), which Fonseca et al 2009 finds is involved in most JA signaling - see also the review by Katsir et al 2008.

JA and its derivatives have also been implicated in plant development, symbiosis, and a host of other processes included in the list below.

• By studying mutants overexpressing JA, one of the earliest discoveries made was that JA inhibits root growth. The mechanism behind this event is still not understood, but mutants in the COI1-dependent signaling pathway tend to show reduced inhibition, demonstrating that the COI1 pathway is somehow necessary for inhibiting root growth.
• JA plays many roles in flower development. Mutants in JA synthesis or in JA signaling in Arabidopsis present with male sterility, typically due to delayed development. The same genes promoting male fertility in Arabidopsis promote female fertility in tomatoes. Overexpression of 12-OH-JA can also delay flowering.
• High levels of JA encourage the accumulation of storage proteins; genes encoding vegetative storage proteins are JA responsive. Specifically, tuberonic acid, a JA derivative, induces the formation of tubers.
• JAs also play a role in symbiosis between plants and microorganisms; however, its precise role is still unclear. JA currently appears to regulate signal exchange and nodulation regulation between legumes and rhizobium. On the other hand, elevated JA levels appear to regulate carbohydrate partitioning and stress tolerance in mycorrhizal plants.

thumb| Stages and timing of the [[Venus flytrap carnivory process, with JA signaling Knowable Magazine

Role in pathogenesis

Pseudomonas syringae causes bacterial speck disease in tomatoes by hijacking the plant's jasmonate (JA) signaling pathway. This bacteria utilizes a type III secretion system to inject a cocktail of viral effector proteins into host cells.

One of the molecules included in this mixture is the phytotoxin coronatine (COR). JA-insensitive plants are highly resistant to P. syringae and unresponsive to COR; additionally, applying MeJA was sufficient to rescue virulence in COR mutant bacteria. Infected plants also expressed downstream JA and wound response genes but repressed levels of pathogenesis-related (PR) genes. All these data suggest COR acts through the JA pathway to invade host plants. Activation of a wound response is hypothesized to come at the expense of pathogen defense. By activating the JA wound response pathway, P. syringae could divert resources from its host's immune system and infect more effectively.

Plants produce N-acylamides that confer resistance to necrotrophic pathogens by activating JA biosynthesis and signalling. Arachidonic acid (AA), the counterpart of the JA precursor α-LeA occurring in metazoan species but not in plants, is perceived by plants and acts through an increase in JA levels concomitantly with resistance to necrotrophic pathogens. AA is an evolutionarily conserved signalling molecule that acts in plants in response to stress similar to that in animal systems.

Cross talk with other defense pathways

While the jasmonate (JA) pathway is critical for wound response, it is not the only signaling pathway mediating defense in plants. To build an optimal yet efficient defense, the different defense pathways must be capable of cross talk to fine-tune and specify responses to abiotic and biotic challenges.

One of the best studied examples of JA cross talk occurs with salicylic acid (SA). SA, a hormone, mediates defense against pathogens by inducing both the expression of pathogenesis-related genes and systemic acquired resistance (SAR), in which the whole plant gains resistance to a pathogen after localized exposure to it.

Wound and pathogen response appear to be interact negatively. For example, silencing phenylalanine ammonia lyase (PAL), an enzyme synthesizing precursors to SA, reduces SAR but enhances herbivory resistance against insects. Similarly, overexpression of PAL enhances SAR but reduces wound response after insect herbivory. Generally, it has been found that pathogens living in live plant cells are more sensitive to SA-induced defenses, while herbivorous insects and pathogens that derive benefit from cell death are more susceptible to JA defenses. Thus, this trade-off in pathways optimizes defense and saves plant resources.

Cross talk also occurs between JA and other plant hormone pathways, such as those of abscisic acid (ABA) and ethylene (ET). These interactions similarly optimize defense against pathogens and herbivores of different lifestyles. For example, MYC2 activity can be stimulated by both JA and ABA pathways, allowing it to integrate signals from both pathways. Other transcription factors such as ERF1 arise as a result of JA and ET signaling. All these molecules can act in combination to activate specific wound response genes.

Because JAZ did not disappear in null coi1 mutant plant backgrounds, protein COI1 was shown to mediate JAZ degradation. COI1 belongs to the family of highly conserved F-box proteins, and it recruits substrates for the E3 ubiquitin ligase SCF^COI1. The complexes that ultimately form are known as SCF complexes. These complexes bind JAZ and target it for proteasomal degradation. However, given the large spectrum of JA molecules, not all JA derivatives activate this pathway for signaling, and the range of those participating in this pathway is unknown. co-purified and subsequently removed inositol pentakisphosphate (InsP₅) from COI1, demonstrating InsP₅ to be a necessary component of the co-receptor and playing a role in potentiating the co-receptor complex. Sheard's results may show varying binding specificity for various SCF-InsP-JAZ complexes.

Additionally, MYC2 will loop back and regulate JAZ expression levels, leading to a negative feedback loop.