In the frame of this thesis, the effects of a suddenly occurring prolongation of the light period leading to photoperiod stress in Arabidopsis thaliana were investigated. In particular, the photoperiod stress response is characterised through three approaches. First, the response of plants to a prolonged light (PL) period of 0.5 h to 8 h is investigated in sensitivity experiments. Second, the effects of a photoperiod stress stimulus on plant responses to a subsequently occurring similar photoperiod stress are examined in cis-priming experiments. Third, the impact of photoperiod stress on plant responses to infections by pathogens are studied in trans-priming experiments. Transcriptome analysis by RNA-seq showed that a prolongation of the light period by one hour is sufficient to alter the expression level of 22 genes at the end of the following night in four-week-old short day-grown plants. The expression of the photoperiod stress marker genes ZINC FINGER OF ARABIDOPSIS THALIANA12 (ZAT12) and BON ASSOCIATION PROTEIN1 (BAP1) was not significantly affected by PL periods up to 2.5 h. An extension of the PL period by 2.5 h, 4 h or 8 h is associated with an increase in the number of genes regulated at the end of the night that follows a PL period. Three genes regulated independent of the duration of the PL period were identified: PHYTOCHROME INTERACTING FACTOR4, BES1-INTERACTING MYC-LIKE1, and COLD REGULATED 314 INNER MEMBRANE1. The cis-priming experiments revealed that photoperiod stress induced by a 4 h-prolonged light period (priming stimulus) causes in wild-type plants a different response to a second photoperiod stress (triggering stimulus). The first photoperiod stress induces the expression of ZAT12 and BAP1, an accumulation of peroxides, and a decrease in catalase activity. These responses are suppressed in response to a second photoperiod stress. The suppression to a second photoperiod stress lasts for several days over a stress-free lag phase indicating the existence of a memory. Transcriptome analysis by RNA-seq revealed different kinds of memory genes for photoperiod stress showing a sustained, altered, or sensitized expression when exposed to a 4 h-PL period after a first similar PL period. A prolongation of the light period up to 2 h results only in a weak photoperiod stress response in wild-type plants and is not sufficient to prime (induce) the plants’ resistance suggesting that the first stimulus needs to induce a substantial response to be memorized. The responsiveness of Arabidopsis wild-type plants to photoperiod stress and their ability to become primed by a photoperiod stress depends on their developmental phase. Analysis of plants of different age exposed to a 4 h-PL period showed that only three- to five-week-old plants responded to and were primed by the PL period indicated by induction of ZAT12 and BAP1 or by accumulation of peroxides and suppression of these responses, respectively. The memory of photoperiod stress-sensitive mutants arabidopsis histidine kinase2 (ahk2) ahk3 and circadian clock associated1 (cca1) long elongated hypocotyl (lhy) is shorter than the memory of wild- type plants indicating that a functional cytokinin signalling and circadian clock are required for maintaining memory. Trans-priming experiments revealed that photoperiod stress induced by an 8 h-PL period improves resistance of wild-type plants against infections with the bacterium Pseudomonas syringae pv. tomato DC3000 and the fungus Botrytis cinerea. Photoperiod stress-induced resistance against P. syringae and B. cinerea requires salicylic acid- and jasmonic acid-related responses as revealed by analysing mutants defective in salicylic acid or jasmonic acid biosynthesis/signalling. NONEXPRESSOR OF PATHOGENESIS RELATED GENES1 (NPR1) is crucial for the oxidative burst-like response of photoperiod stress, since npr1 mutants do not accumulate peroxides during photoperiod stress and several genes were differently regulated in these mutants. Further investigation is necessary to fully understand the molecular mechanisms involved in photoperiod stress-induced resistance against pathogens.
