Affiliation: | 1. Department of Life Sciences, Imperial College London, Imperial College Road, South Kensington Campus, London, London, SW7 2AZ UK;2. Department of Life Sciences, Imperial College London, Imperial College Road, South Kensington Campus, London, London, SW7 2AZ UK These authors contributed equally to this work.;3. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular ‘Dr Héctor N. Torres’ (INGEBI)–Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Vuelta de Obligado 2490, Ciudad Autónoma de Buenos Aires, C1428ADN Argentina;4. Facility for Imaging by Light Microscopy, Faculty of Medicine, National Heart & Lung Institute (NHLI), Imperial College London, South Kensington, SAF building, London, SW7 2AZ UK;5. Central Laser Facility, Science and Technology Facilities Council Harwell, Science and Technology Facilities Council, Rutherford Appleton Laboratory, Harwell, Didcot, OX11 0QX UK;6. Centre for Process Systems Engineering and Centre for Environmental Policy, Imperial College London, South Kensington Campus, London, London, SW7 2AZ UK The Alan Turing Institute, British Library, 96 Euston Road, London, London, NW1 2DB UK;7. Martin Luther Universität Halle-Wittenberg, Halle, 06108 Halle Germany;8. School of Biological Sciences, University of Bristol, University of Bristol, St Michael's Hill, Bristol, BS8 8DZ UK |
Abstract: | Upon immune activation, chloroplasts switch off photosynthesis, produce antimicrobial compounds and associate with the nucleus through tubular extensions called stromules. Although it is well established that chloroplasts alter their position in response to light, little is known about the dynamics of chloroplast movement in response to pathogen attack. Here, we report that during infection with the Irish potato famine pathogen Phytophthora infestans, chloroplasts accumulate at the pathogen interface, associating with the specialized membrane that engulfs the pathogen haustorium. The chemical inhibition of actin polymerization reduces the accumulation of chloroplasts at pathogen haustoria, suggesting that this process is partially dependent on the actin cytoskeleton. However, chloroplast accumulation at haustoria does not necessarily rely on movement of the nucleus to this interface and is not affected by light conditions. Stromules are typically induced during infection, embracing haustoria and facilitating chloroplast interactions, to form dynamic organelle clusters. We found that infection-triggered stromule formation relies on BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1)-mediated surface immune signaling, whereas chloroplast repositioning towards haustoria does not. Consistent with the defense-related induction of stromules, effector-mediated suppression of BAK1-mediated immune signaling reduced stromule formation during infection. On the other hand, immune recognition of the same effector stimulated stromules, presumably via a different pathway. These findings implicate chloroplasts in a polarized response upon pathogen attack and point to more complex functions of these organelles in plant–pathogen interactions. |