INTERACTION BETWEEN PLASTID AND MITOCHONDRIAL SIGNALLING PATHWAYS DURING CHANGES TO PLASTID REDOX STATUS

BLANCO N.E.; GUINEA-DIAZ M,; WHELAN, J.; STRAND, Å

Pultusk

Simposio; Biology of plastids ? towards a blueprint for synthethic organelles; 2014

ESF-EMBO

Interaction between plastid and mitochondrial retrograde signalling pathways during changes to cellular redox status . Mitochondria and chloroplasts are the main energy producers that satisfy the energy demand of the plant cell. These two membrane enclosed endosymbiotic derived organelles depend upon each other; photosynthesis provides substrates for mitochondrial respiration and mitochondrial metabolism is essential for sustaining photosynthetic carbon assimilation. Also, they must be able to balance the rates of energy production in response to environmental fluctuations, being necessary a tight regulation of dissipative mechanism to avoid oxidative damage. Therefore, plant mitochondrial respiration protects photosynthesis against photoinhibition by dissipating excess redox equivalents from the chloroplasts. Genetic defects in mitochondrial function result in an excessive reduction and energization of the chloroplast. Thus, it is clear that the activities of mitochondria and plastids need to be coordinated, but the manner by which the organelles communicate to coordinate their activities is unknown. The regulator of alternative oxidase (rao1) mutant was isolated as a mutant unable to induce AOX1a expression in response to the inhibitor of the mitochondrial cytochrome c reductase (complex III), antimycin A. RAO1 encodes the nuclear localized cyclin-dependent kinase E1 (CDKE;1). Interestingly, the rao1 mutant demonstrates a genome uncoupled phenotype also in response to redox changes in the photosynthetic electron transport chain. Thus,CDKE;1 was shown to regulate both LIGHT HARVESTING COMPLEX B (LHCB) and ALTERNATIVE OXIDASE 1 (AOX1a) expression in response to retrograde signals.Additionally, we evaluated the secondary components of these signalling pathways through the analysis of the localisation of one interactor of CDEK;1: SnRK1.1. The localisation of SnRK1.1 (also known as KIN10), the Arabidopsis (Arabidopsis thaliana) ortholog of the sucrose non-fermenting protein kinase from yeast (Saccharomyces cerevisiae) and a central mediator of energy and stress signalling in plants, was investigated with the aim of setting up the origin of the retrograde signal perceived by CDKE;1. Using its own promoter to drive expression, SnRK1.1-GFP was found to be co-localised with both mitochondria and nuclei. This dual localisation was sensitive to oxidative stress and treatments with H2O2 or 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and favoured a nuclear localisation upon these treatments. Re-localisation of SnRK1.1-GFP from mitochondria to the nucleus was coincident with changes in mitochondrial streaming and accumulation of plastids around the nuclei. Based on our results, we postulate CDKE1 is a central nuclear component integrating mitochondrial and plastid retrograde signals and plays a role in regulating energy metabolism during the response to stress. Moreover, the localisation of SnRK1.1 might be involved in the retrograde signal transduction.