The phytohormone cytokinin was originally discovered as a regulator of cell division. Later, it was described to be involved in regulating numerous processes in plant growth and development including meristem activity, tissue patterning, and organ size. More recently, diverse functions for cytokinin in the response to abiotic and biotic stresses have been reported. Cytokinin is required for the defence against high light stress and to protect plants from a novel type of abiotic stress caused by an altered photoperiod. Additionally, cytokinin has a role in the response to temperature, drought, osmotic, salt, and nutrient stress. Similarly, the full response to certain plant pathogens and herbivores requires a functional cytokinin signalling pathway.Conversely, different types of stress impact cytokinin homeostasis. The diverse functions of cytokinin in responses to stress and crosstalk with other hormones are described. Its emerging roles as a priming agent and as a regulator of growthdefence trade-offs are discussed.

ORCID IDs: 0000-0002-9888-7003 (I.F.); 0000-0002-6299-347X (M.R.)The circadian clock helps plants measure daylength and adapt to changes in the day-night rhythm. We found that changes in the light-dark regime triggered stress responses, eventually leading to cell death, in leaves of Arabidopsis thaliana plants with reduced cytokinin levels or defective cytokinin signaling. Prolonged light treatment followed by a dark period induced stress and cell death marker genes while reducing photosynthetic efficiency. This response, called circadian stress, is also characterized by altered expression of clock and clock output genes. In particular, this treatment strongly reduced the expression of CIRCADIAN CLOCK ASSOCIATED1 (CCA1) and LATE ELONGATED HYPOCOTYL (LHY). Intriguingly, similar changes in gene expression and cell death were observed in clock mutants lacking proper CCA1 and LHY function. Circadian stress caused strong changes in reactive oxygen species-and jasmonic acid (JA)-related gene expression. The activation of the JA pathway, involving the accumulation of JA metabolites, was crucial for the induction of cell death, since the cell death phenotype was strongly reduced in the jasmonate resistant1 mutant background. We propose that adaptation to circadian stress regimes requires a normal cytokinin status which, acting primarily through the AHK3 receptor, supports circadian clock function to guard against the detrimental effects of circadian stress.

A role of the plant hormone cytokinin in regulating the development and activity of chloroplasts was described soon after its discovery as a plant growth regulator more than 50 years ago. Its promoting action on chloroplast ultrastructure and chlorophyll synthesis has been reported repeatedly, especially during etioplast-to-chloroplast transition. Recently, a protective role of the hormone for the photosynthetic apparatus during high light stress was shown. Details about the molecular mechanisms of cytokinin action on plastids are accumulating from genetic and transcriptomic studies. The cytokinin receptors AHK2 and AHK3 are mainly responsible for the transduction of the cytokinin signal to B-type response regulators, in particular ARR1, ARR10, and ARR12, which are transcription factors of the two-component system mediating cytokinin functions. Additional transcription factors linking cytokinin and chloroplast development include CGA1, GNC, HY5, GLK2, and CRF2. In this review, we summarize early and more recent findings of the long-known relationship between the hormone and the organelle and describe crosstalk between cytokinin, light, and other hormones during chloroplast development.

Light is important for plants as an energy source and a developmental signal, but it can also cause stress to plants and modulates responses to stress. Excess and fluctuating light result in photoinhibition and reactive oxygen species (ROS) accumulation around photosystems II and I, respectively. Ultraviolet light causes photodamage to DNA and a prolongation of the light period initiates the photoperiod stress syndrome. Changes in light quality and quantity, as well as in light duration are also key factors impacting the outcome of diverse abiotic and biotic stresses. Short day or shady environments enhance thermotolerance and increase cold acclimation. Similarly, shade conditions improve drought stress tolerance in plants. Additionally, the light environment affects the plants' responses to biotic intruders, such as pathogens or insect herbivores, often reducing growth‐defence trade‐offs. Understanding how plants use light information to modulate stress responses will support breeding strategies to enhance crop stress resilience. This review summarizes the effect of light as a stressor and the impact of the light environment on abiotic and biotic stress responses. There is a special focus on the role of the different light receptors and the crosstalk between light signalling and stress response pathways.

Cytokinins are plant hormones that regulate diverse processes in plant development and responses to biotic and abiotic stresses. In this study, we show that Arabidopsis (Arabidopsis thaliana) plants with a reduced cytokinin status (i.e. cytokinin receptor mutants and transgenic cytokinin-deficient plants) are more susceptible to light stress compared with wild-type plants. This was reflected by a stronger photoinhibition after 24 h of high light (approximately 1,000 mmol m 22 s 21), as shown by the decline in maximum quantum efficiency of photosystem II photochemistry. Photosystem II, especially the D1 protein, is highly sensitive to the detrimental impact of light. Therefore, photoinhibition is always observed when the rate of photodamage exceeds the rate of D1 repair. We demonstrate that in plants with a reduced cytokinin status, the D1 protein level was strongly decreased upon light stress. Inhibition of the D1 repair cycle by lincomycin treatment indicated that these plants experience stronger photodamage. The efficiency of photoprotective mechanisms, such as nonenzymatic and enzymatic scavenging systems, was decreased in plants with a reduced cytokinin status, which could be a cause for the increased photodamage and subsequent D1 degradation. Additionally, slow and incomplete recovery in these plants after light stress indicated insufficient D1 repair. Mutant analysis revealed that the protective function of cytokinin during light stress depends on the ARABIDOPSIS HISTIDINE KINASE2 (AHK2) and AHK3 receptors and the type B ARABIDOPSIS RESPONSE REGULATOR1 (ARR1) and ARR12. We conclude that proper cytokinin signaling and regulation of specific target genes are necessary to protect leaves efficiently from light stress.Light absorption, the subsequent conversion into biochemical energy, and the production of oxygen of plants play an essential role for life on earth. Although light is a prerequisite for this process, high light (HL) easily exceeds the plant's capacity to assimilate CO 2 , causing an overreduction of the electron transport chain that results in the inactivation of PSII (photoinhibition; Barber and Andersson, 1992; Aro et al., 1993;Yamamoto et al., 2008). One of the major targets of photoinhibition is the PSII core protein D1 (for review, see Adir et al., 2003;Edelman and Mattoo, 2008).Damaged D1 proteins are continuously replaced by de novo-synthesized D1 in a process called the D1 repair cycle (Aro et al., 1993(Aro et al., , 2005Baena-González and Aro, 2002). This cycle consists of (1) migration of damaged D1 protein from the grana to the stroma lamellae, (2) proteolytic degradation of damaged D1 protein by FILA-MENTATION TEMPERATURE SENSITIVE H (FTSH) protease and DEGRADATION OF PERIPLASMIC PRO-TEINS PROTEASE (DEGP), (3) de novo synthesis of precursor D1 protein (preD1) and cotranslational insertion into the thylakoid membrane, (4) C-terminal processing of preD1 catalyzed by the C-TERMINAL PEPTIDASE (CTP), and (5) migration to the grana thylakoids and formation of a fully functional PSII comple...