AbstractsBiology & Animal Science

In the first part of this work plants with a reduced cytokinin (CK) status were analyzed regarding their response to high light (HL) stress. A stronger decline in the photosystem II maximum quantum efficiency (Fv/Fm) after HL treatment revealed stronger photoinhibition and hence a higher susceptibility to HL stress in these plants. CK receptor mutant analyses indicated that the CK receptor AHK3 is the key player in mediating this light stress response. In line with the stronger photoinhibtion, D1 protein levels were strongly decreased upon HL stress in CK-deficient plants. Experimentally induced inhibition of D1 repair indicated that this was a consequence of stronger photodamage in these plants. Slow and incomplete recovery in these plants after HL treatment indicated insufficient D1 repair. The total antioxidant capacity was decreased in plants with a reduced CK status. A more detailed analysis of different scavenging mechanisms revealed a pronounced deficiency in carotenoids after HL exposure. A lack of carotenoids could explain both a compromised D1 repair and a stronger photodamage. The second part of this work aimed to uncover a new phenomenon characterized by a pronounced cell death phenotype in plants with a reduced CK status after exposure to changed light-dark regimes. CK synthesis mutants, CKX-overexpressing transgenic plants and CK signaling mutants were affected upon these treatments, revealing the necessity of normal CK levels as well as functional CK signaling for this adaptive response. Also under this kind of stress the receptor AHK3 was found to be the key player. Cell death progression in CK-deficient plants was accompanied by necrotic and water-soaked lesions, loss of membrane integrity, and increased oxidative stress, correlating with a strong induction of stress- and cell death-related genes in the affected leaves. The exposure to different light-dark-temperature regimes clearly demonstrated that, although dependent on prolonged light periods, cell death initiation was not part of a light stress response since it required a dark period following the extended light treatment. Instead, the severity of cell death was determined by a specific interplay between entrainment, treatment, and post-treatment regime pointing to an involvement of the circadian clock. Transcript analyses showed that the induction of stress- and JA-related genes in CK-deficient plants coincided with a strongly diminished CCA1 and LHY expression. Misregulated clock output gene expression also indicated a perturbation of the circadian clock. Intriguingly, the cell death phenotype was also observed in clock mutants lacking proper CCA1 and LHY function. Additionally, these plants exhibited a highly similar molecular phenotype compared with CK-deficient plants regarding clock output, stress and cell death marker, and, interestingly, also A type ARR gene expression. These results confirmed the hypothesis that a malfunction of circadian timekeeping – “circadian stress” – was responsible for the cell death phenotype in…