Bidirectional regulation between TOR kinase and chloroplasts: emerging connections in photosynthetic organisms
Eukaryotic growth relies on intricate mechanisms that couple nutrient availability to the cell growth machinery. Central to this regulation is the evolutionarily conserved target of rapamycin (TOR), a large Ser/Thr kinase belonging to the atypical phosphatidylinositol kinase-related kinase family. TOR integrates diverse nutrient, energy, and hormonal signals to stimulate biosynthetic pathways and repress catabolism, thus promoting cell growth across eukaryotes-from yeast and algae to animals and plants. Despite extensive research on TOR signalling, the interplay between TOR activity and chloroplast function, particularly in regulating photosynthesis, has only recently begun to receive attention. Emerging evidence indicates a reciprocal relationship, where TOR influences chloroplast function through transcriptional and post-translational mechanisms, and where chloroplast-derived signals modulate TOR activity. This highlights crucial yet understudied links between nutrient signalling, chloroplast activity, and cellular growth. In this review, we discuss recent advances that emphasize the pivotal role of TOR as a mediator connecting stress and nutrient signals to chloroplast function in plants and algae.
Authors
- Benoît Menand (ORCID: https://orcid.org/0000-0001-9713-5275)
- Ben Field (ORCID: https://orcid.org/0000-0003-2142-4606)
- José L. Crespo (ORCID: https://orcid.org/0000-0003-3514-1025)
Institutions
- Aix-Marseille Université (FR)
- Commissariat à l'Énergie Atomique et aux Énergies Alternatives (FR)
- Instituto de Bioquímica Vegetal y Fotosíntesis (ES)
- CEA Cadarache (FR)
- Centro de Investigaciones Científicas Isla de la Cartuja (ES)
- Institut de Biosciences et Biotechnologies (FR)
Publication Details
- Journal
- Journal of Experimental Botany
- Published
- 2025-08-01
- DOI
- https://doi.org/10.1093/jxb/eraf338
- Primary Topic
- Photosynthetic Processes and Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00