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.

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.

Plants can acquire an improved resistance against pathogen attacks by exogenous application of natural or artificial compounds. In a process called chemical priming, application of these compounds causes earlier, faster and/or stronger responses to pathogen attacks. The primed defense may persist over a stress-free time (lag phase) and may be expressed also in plant organs that have not been directly treated with the compound. This review summarizes the current knowledge on the signaling pathways involved in chemical priming of plant defense responses to pathogen attacks. Chemical priming in induced systemic resistance (ISR) and systemic acquired resistance (SAR) is highlighted. The roles of the transcriptional coactivator NONEXPRESSOR OF PR1 (NPR1), a key regulator of plant immunity, induced resistance (IR) and salicylic acid signaling during chemical priming are underlined. Finally, we consider the potential usage of chemical priming to enhance plant resistance to pathogens in agriculture.

Cytokinin regulates chloroplast development during de-etiolation through the two-component signaling system by binding of B-type ARRs to the promotors of chloro

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 µmol m⁻² s⁻¹), 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.