Photoperiod stress is a novel type of abiotic stress in plants caused by a prolongation of the light period. It has been reported that plants require a functional circadian clock as well as a functional cytokinin synthesis, metabolism and signaling to cope with photoperiod stress. Within this thesis, additional factors influencing the sensitivity to photoperiod stress have been investigated. In the first chapter of this work, plants that are either unable to synthesize tZ-type cytokinins (cypDM) or transport them from the root to the shoot (abcg14) were exposed to photoperiod stress. As indicated by an increased lesion formation, a reduced photosynthetic capacity, an altered expression of marker genes and an accumulation of H2O2, these plants were more sensitive to a prolongation of the light period. Further experimental evidence for the importance of these type of cytokinins was provided by watering of cypDM plants with tZ-type cytokinins which rescued the photoperiod stress phenotype. Moreover, cytokinin levels were monitored throughout photoperiod stress treatment and development of stress symptoms in wild-type plants and indicated that the treatment leads to a general cytokinin accumulation. Apart from cytokinin synthesis and transport, mutant analysis led to the identification of AHP2, AHP3 and AHP5 as key components of cytokinin signaling during photoperiod stress. In addition, indications for a complex regulatory mechanism of ARR2, ARR10 and ARR12 transcription factors during photoperiod stress have been collected and based on these, a model in which ARRs either interact with each other or with unknown factors has been proposed. In the second chapter, the photoperiod stress sensitivity of young and mature plants and leaves and the contribution of different tissues to the photoperiod stress response has been investigated. The photoperiod stress sensitivity of wild-type and ahk2ahk3 plants and leaves of different age and the photoperiod stress response of leaves on a single rosette was determined. Results indicated that with an increasing leaf and plant age the ability to cope with prolongations of the light period decreased. Furthermore, analysis of MIR156B and MIM172 overexpressors demonstrated that there is no influence of the leaf identity (juvenile vs. adult leaves) on the photoperiod stress response. Moreover, the exposure of plants tissue-specifically expressing CKX1 to photoperiod stress indicated that the vasculature and epidermis are crucial to regulate the sensitivity to photoperiod stress. Lastly, the molecular response to photoperiod stress in leaves and roots of wild type and ahk2ahk3 was compared and indicates that roots differ substantially in their response from leaves. In the third chapter, the importance of the phytohormones auxin, ethylene and GA in coping with photoperiod stress was investigated. Auxin and GA measurements in wild-type leaves, transcriptome analysis of wild-type and ahk2ahk3 leaves as well as mutant analysis hints at a protective function of ethylene and a photoperiod stress inducing the role of auxin. Strikingly, a partial loss of auxin perception in ahk2ahk3 caused a partial rescue of the photoperiod stress phenotype and thus indicates that an imbalance in auxin homeostasis might be causative for the increased photoperiod stress sensitivity of plants with a lowered cytokinin status.