Prolongation of the light period causes photoperiod stress in plants. During the night following the prolonged light treatment, stress marker gene expression is induced, and stress hormones and ROS accumulate. The next day, the experienced strong photoperiod stress leads to the formation of water-soaked lesions in leaves and eventually programmed cell death ensues. In this study, the impact of light intensity and light quality on the photoperiod stress response has been investigated. A threshold light intensity of about 50 μmol m-2 s-1 was found to be necessary for the induction of photoperiod stress, hinting at the involvement of chloroplasts. Lower photoperiod stress symptoms in gun4, gun5, rcd1, and glk1 glk2 mutants revealed a possible role of retrograde signaling in photoperiod stress and corroborated the involvement of chloroplasts. Furthermore, starch and sugar content were higher in photoperiod stressed plants and starch biosynthesis mutants developed less photoperiod stress symptoms. This indicated that the starch and sugar metabolism might be affecting a plants’ response to photoperiod stress, strengthening the argument for the importance of chloroplast in photoperiod stress. Both monochromatic red and blue light caused a photoperiod stress response, but the response provoked by red light was stronger. Mutant analysis revealed the photoreceptors phyB and CRY2 as probable sensors of photoperiod stress. Among the downstream light signaling components, HY5 and PIF1 have demonstrated potential for involvement in sensing photoperiod stress. Although cry2 mutation did not rescue the strong photoperiod stress phenotype of cca1 lhy, some clock genes were differentially regulated in cry2. This indicates a possible involvement of CRY2 in photoperiod stress through its role in regulating the circadian rhythm. Overall, these results support that both plastid-dependent and photoreceptor-dependent signaling pathways are involved in sensing light conditions causing photoperiod stress and governing the response to it. Since co and ft tsf mutants demonstrated less photoperiod stress symptoms, participation of the photoperiodic flowering pathway in sensing and responding to photoperiod stress has been considered a possibility. Most ecotypes other than Columbia showed low sensitivity to photoperiod stress, suggesting that photoperiod stress sensitivity might be a rare trait in nature. The low photoperiod stress sensitivity of the F1 generation of crosses between Col-0 and some of the ecotypes that show low photoperiod stress sensitivity is evidence of the recessive nature of the photoperiod stress sensitivity trait.
