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 .