The Arabidopsis thaliana RNA-binding protein FCA regulates thermotolerance by modulating the detoxification of reactive oxygen species.

Heat stress affects various aspects of plant growth and development by generating reactive oxygen species (ROS) which cause oxidative damage to cellular components. However, the mechanisms by which plants cope with ROS accumulation during their thermotolerance response remain largely unknown. Here, we demonstrate that the RNA-binding protein FCA, a key component of flowering pathways in Arabidopsis thaliana, is required for the acquisition of thermotolerance. Transgenic plants overexpressing the FCA gene (35S:FCA) were resistant to heat stress; the FCA-defective fca-9 mutant was sensitive to heat stress, consistent with induction of the FCA gene by heat. Furthermore, total antioxidant capacity was higher in the 35S:FCA transgenic plants but lower in the fca-9 mutant compared with wild-type controls. FCA interacts with the ABA-INSENSITIVE 5 (ABI5) transcription factor, which regulates the expression of genes encoding antioxidants, including 1-CYSTEINE PEROXIREDOXIN 1 (PER1). We found that FCA is needed for proper expression of the PER1 gene by ABI5. Our observations indicate that FCA plays a role in the induction of thermotolerance by triggering antioxidant accumulation under heat stress conditions, thus providing a novel role for FCA in heat stress responses in plants.