Figure 3. Light signaling pathways contributing to thermortolerance.
High temperature causes the induction of heat shock transcription factors (TFs) which results in thermotolerance. Under influence of light, a chloroplast-to-nucleus signal contributes to the induction of heat shock TFs. Independent of this chloroplast signal, the increase in HsfA1 upon heat stress causes a phyB-dependent increase in APX2expression resulting in ROS detoxification. The different photoreceptors are also involved in acquiring thermotolerance. Especially phyB, which is a thermosensor, and PIF4 play a central role. Thermal reversion and low R:FR ratios result in an inactivation of phyB, thereby resolving its inhibitory effect on PIF4. In turn, PIF4 stimulates the expression of auxin biosynthesis genes to regulate morphological adaptations like hyponasty or petiole elongation contributing to thermotolerance. PIF4 is inhibited by UVR8 and CRY1 as well. Also, other PIFs are regulated by phyB affecting FAD expression and fatty acid desaturation. phyB also influences ELF3 abundance which blocks PIF4 activity in an evening clock-independent and -dependent pathway involving also LUX and ELF4, other components of the EC. Blue light perceived by phototropins results in stomatal opening and increased leaf cooling. For more information concerning the different pathways, please refer to section 3.2. Abbreviations: R, red light; FR, far-red light; B, blue light; UV, ultraviolet light; ROS, reactive oxygen species; TFs, transcription factors; HsfA1, heat shock factor protein A1, PIFs, phytochrome interacting factors; EC, evening complex, FAD, fatty acid desaturase .