Chromatin targeting and remodelling by bacterial effectors in plant immunity

Projektinformationen

CHERI

ID Finanzhilfevereinbarung: 705631

DOI

10.3030/705631

Das Projekt endete am 31 Dezember 2017

EK-Unterschriftsdatum 24 Februar 2016

Startdatum 1 April 2016

Enddatum 31 März 2018

Finanziert unter

• EXCELLENT SCIENCE - Marie Skłodowska-Curie Actions

Gesamtkosten

€ 159 460,80

EU-Beitrag

€ 159 460,80

Koordiniert durch

MAX-PLANCK-GESELLSCHAFT ZUR FORDERUNG DER WISSENSCHAFTEN EV
Germany

Periodic Reporting for period 1 - CHERI (Chromatin targeting and remodelling by bacterial effectors in plant immunity)

Berichtszeitraum: 2016-04-01 bis 2018-03-31

Zusammenfassung vom Kontext und den Gesamtzielen des Projekts

In nature, plants are challenged by disease-causing pathogens such as viruses, bacteria and fungi. Understanding mechanisms of plant disease and disease resistance is of fundamental importance to sustainable agriculture and human health. Unlike mammals, plants lack a circulating immune system. Plants instead rely on the innate immune capacity of each cell and systemic signals that disseminate from infection sites. Successful pathogens use effectors to suppress plant immunity and cause disease. Plants have evolved disease resistance genes encoding immune receptors that perceive specific pathogen effectors to mount effector-triggered immunity. In Arabidopsis, a heteromeric pair of intracellular immune receptors forms a functional recognition complex which senses virulence activities of two structurally unrelated bacterial effectors at the nuclear chromatin. Results suggest that effector targeting of histone modifications and chromatin remodelling interferes with host basal immunity and that this is transduced by the receptor pair to activation of defence pathways. The underlying molecular mechanisms remain unclear. We have found that the two bacterial effectors interact with an overlapping set of chromatin-associated proteins and with certain immune receptor domains. We hypothesize that the effectors converge on the same chromatin machinery for promoting disease and that their actions are intercepted by the immune receptor system which is physically connected to basal immunity signalling components. By using the effectors as molecular probes, this proposal aims to elucidate how the chromatin environment is modulated during infection and how effector perturbations are converted to effective immunity.

Arbeit, die ab Beginn des Projekts bis zum Ende des durch den Bericht erfassten Berichtszeitraums geleistet wurde, und die wichtigsten bis dahin erzielten Ergebnisse

The project was initially divided in 3 objectives. Due to shifted schedules in the experimental plan, the objective 1 and 2 have not been fully completed. However, by initiating a fourth objective, the researcher has anticipated the potential non finalization of the project and generated new data related to the field.

By establishing, designing and using innovative experiment, the project has led to a better understanding of how an immuno-receptor complex can be targeted by a bacterial effector and might modify its conformation at the chromatin level. Exciting data generated by objective 4 have brought new insights about a bacterial effector molecular function and virulence activity never suspected before. This project opens new research guidelines that could be easily followed up within a PhD thesis or postdoc project and lead to high quality scientific outputs and publications.

Fortschritte, die über den aktuellen Stand der Technik hinausgehen und voraussichtliche potenzielle Auswirkungen (einschließlich der bis dato erzielten sozioökonomischen Auswirkungen und weiter gefassten gesellschaftlichen Auswirkungen des Projekts)

This pioneering project which uses the model plant A. thaliana opens a novel research area in the field of plant pathology and constitutes a new research axis in Parker group. Until now, the question of the involvement of chromatin remodeling processes (often referred as “epigenetic” mechanisms) in plant defense was addressed exclusively in the frame of the transcriptional induction of defense genes. Here, the work conducted went in a totally different direction and follow the idea that upon infection a pathogen might modulate host chromatin to circumvent plant defense.
In animals, pathogen-triggered chromatin remodeling is well documented and considered as a very promising area for future research on infectious diseases. However, to date plant pathogen-triggered chromatin remodeling has received very little attention. The CHERI project working model offers the opportunity to evaluate the importance of this process in the plant responses to different pathogens.

Upon infection a pathogen might modulate host chromatin to circumvent plant defense