A new paper in Proceedings of the National Academy of Sciences USA has uncovered a previously unknown activity of the phytopathogen Pseudomonas syringae: the ability to induce systemic-induced susceptibility (SIS) to subsequent infection, and has also identified the small molecule required to do so.

Generally, plants respond to an attack by microbial pathogens by inducing salicylic acid (SA)-dependent systemic resistance pathways — systemic acquired resistance (SAR) — whereas the resistance pathways induced in response to an attack by insect herbivores are jasmonic acid (JA)-dependent. It is known that the crosstalk between the two pathways, which can be additive or antagonistic, is complex and varies depending on the pathogens and plant hosts involved.

In previous work, a model system involving Arabidopsis, P. syringae and an insect herbivore, the cabbage looper (Trichoplusia ni), was established to investigate how infection by a bacterial pathogen affects the response of the plant to subsequent attack by other bacterial pathogens and insect herbivores. The results obtained suggested the presence of two signalling pathways, one of which was correlated with SAR and enhanced resistance to T. ni feeding and a second that enhanced susceptibility to T. ni feeding via an unknown signal.

In this latest work, infection of Arabidopsis lower leaves with virulent strains of P. syringae showed a small but reproducible SIS effect, with enhanced secondary growth of P. syringae in uninfected upper leaves. Further analysis pointed to the phytotoxin coronatine (COR), an important P. syringae virulence factor and a mimic of JA, as the molecule responsible for this effect. The authors hypothesized that the effects of COR could be mediated by antagonism of the SA-dependent SAR response. Experimental work showed that avirulent non-COR-producing strains elicited a stronger SAR response than did avirulent COR-producing strains, suggesting that COR could function by interfering with SA-dependent signalling.

The authors also analysed the effects of COR on insect herbivory, and interpret their observations as indicating that virulent P. syringae also induces systemic susceptibility to T. ni herbivory but not via COR. In fact, it was found that COR induces systemic resistance to T. ni, consistent with its role as a JA mimic.

So, this work has revealed a role for COR in P. syringae-mediated manipulation of plant systemic defences and has also confirmed that the interactions involved in these defences are extremely complex. Future work will provide further details on the role of COR and its interactions with the SA- and JA-mediated pathways, as well as continuing to analyse the molecular mechanisms responsible for P. syringae-mediated susceptibility to insect herbivores.