RESEARCH SUMMARY

We are interested in understanding how plants are able to perceive changes in their environment and integrate stress signals with their internal developmental programs, to induce adaptive responses and survive in nature. This integration depends on complex signalling networks that regulate the genetic reprogramming of the cell.

The main focus of my lab is to understand one of the pathways involved in this network, the jasmonate (JA) signalling pathway, in Arabidopsis thaliana.

JAs are fatty acid-derived signalling molecules essential for plant survival in nature, since they are important activators of stress responses and developmental programs. We aim to identify the components of this pathway and determine how they explain jasmonate pathway interactions with other pathways in the network.

We are also particularly interested in the molecular mechanisms underlying JA-mediated activation of plant responses to necrotrophic pathogens. This type of defence requires the concerted cooperation of at least two phytohormonal signalling pathways: JA and ethylene (ET). Since the plant uses these two hormones to signal many other developmental and stress responses, ET/JA crosstalk constitutes a unique (simple) system to study the regulation of signalling networks that allow the plant to discriminate between different stresses (e.g., pathogens and wounding) and select the correct set of responses to each.

To understand these biological questions, we are using genomic, genetic, biochemical and molecular tools, following two approaches:

1. Dissection of the JA signalling pathway in Arabidopsis

We have discovered several components of this pathway:

• The transcription factors (TF) ERF1 and AtMYC2/JIN1, which regulate expression of two subsets of JA/ET-related effector genes. The balance of activation of these two TF helps determine the type of response activated by the plant to a specific stress (pathogens or wounding).

• SGT1b/JAI4, a regulator of SCF (Skip-Cullin-Fbox) E3 ubiquitin ligase complexes, including the JA-signalling component SCFCOI1

• The JAZ family of nuclear repressors that regulate TF activity (i.e., AtMYC2) and are targeted by SCFCOI1 for degradation by the 26S proteasome. Discovery of the JAZ family of repressors linked the previous steps in the pathway (SCFCOI1 and the TF) and facilitated an integrated view of the core JA signalling module composed by SCFCOI1-JAZs-MYC2. It also evidenced the similarity between the JA and auxin pathways. Based on the crystal structure of the auxin receptor (F-box TIR1; closely related to COI1), we hypothesised that COI1 might also be the JA receptor. A combination of genetic and biochemical analyses supported this hypothesis. Using a screen for bioactive jasmonates, we found that the previously proposed hormone [(-)-JA-L-Ile] was inactive as a ligand of COI1, and discovered the real endogenous bioactive form of the hormone, (+)-7-iso-JA-L-Ile.

• NINJA, novel interactor of JAZ, is an adaptor protein that connects JAZ repressors to the general corepressor TOPLESS, providing a molecular mechanism of how JAZ proteins repress TF activity.

2. Dissection of the interaction between the oomycete Pythium irregulare and the plant Arabidopsis thaliana

We characterised the infection process and the hormone pathways involved in plant defence. We identified the genes responsible for plant resistance to this oomycete, and analysed the contribution of each of the “classical” defence hormones (JA, ET and SA) to the activation of this defence gene set. Finally, we found that abscissic acid (ABA) is essential for the activation of defences against P. irregulare and found that it precedes JA biosynthesis in response to the oomycete.