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...