The overall changes in the levels of chlorophyll a (chl a) and chlorophyll b (chl b) were similar. genes. Irrespective of light treatment a high UV-B dose led to clearly visible cell death a Rabbit polyclonal to AIM2 few days after irradiation. == Conclusions == High doses of UV-B have opposing effects on leaves depending on their light status after UV treatment. In darkened leaves short UV-B treatment delays the appearance of senescence symptoms. When followed by light treatment, the same doses of UV-B result in chlorophyll degradation. This restricts the potential usability of UV treatment in postharvest technology to crops which are stored in darkness. == Electronic supplementary material == The online version of this article (doi: 10. 1186/s12870-015-0667-2) contains supplementary material, which is accessible to authorized users. Keywords: Cell death, Chlorophyll degradation, Light, Photosynthesis, Senescence, UV-B == Background == Beside visible light the solar radiation which strikes the Earths atmosphere Harpagide also contains ultraviolet (UV) and infrared irradiation. Based on the biological effects it induces, UV is divided into UV-C (100280 nm), UV-B (280320 nm) and UV-A (320400 nm). UV-C, the most dangerous, is completely absorbed by the ozone layer in the atmosphere. As a consequence, UV-B is the shortest wavelength component of the sunlight which reaches the surface of the Earth. As an integral part of photo voltaic radiation, UV always accompanies visible light. This is of special importance for plants which are both sessile and photosynthetic organisms. The UV-B range is absorbed by many constituents from the cell with harmful consequences. UV-B is cytotoxic, harmful the cell at many levels, including nucleic acids, lipids, photosynthetic pigments and proteins [1]. Higher levels of UV-B cause the production of reactive oxygen species (ROS) and activate general stress signaling pathways [2]. Moreover, the UV-B-dependent formation of dimers between adjacent pyrimidines in DNA strands may be both mutagenic and genotoxic due to blocking the progress of DNA polymerase. As a result, the publicity of plants to high levels of UV can lead to cell death dependent on ROS signaling (for a review see: [3]). The depletion of the ozone layer offers resulted in an increase in the level of UV-B reaching the Earths Harpagide surface. That is why the impact of this wavelength range on living organisms started to be intensively investigated in the eighties. Most experiments have been performed in growth chambers with relatively low photosynthetically active radiation (PAR) supplemented with a high dose of UV-B [4]. They showed a very strong impact of UV-B on the content of photosynthesis dependent pigments, the activity of photosynthetic enzymes and photosynthetic efficiency (for a review see: [5]). UV-B Harpagide affects Photosystem II (PSII) to much greater extent than Photosystem I [1]. The degradation of integral components of PSII reaction centers, including D1 and D2 proteins, is an extensively studied aspect of the effect of UV-B on photosynthesis. Many compounds have been hypothesized as primary targets of UV-B action on photosynthesis, including the reaction centre itself, quinone acceptors and redox-active tyrosines [1]. UV-B is also assimilated by the oxygen-evolving Mn cluster and can cause its damage [6]. The reaction to UV depends both on its dose and the irradiation scheme. Acute treatment has a more severe effect than chronic publicity which activates acclimation responses [7, 8]. These responses are aimed at minimizing the impact of UV-B on plant cells. They include leaf thickening, alterations in cuticular wax layers and the biosynthesis of UV-B-absorbing phenolic compounds, such as flavonoids [5]. Leaf yellowing is one of the most visible symptoms of irradiation with high doses of UV-B. It results from chlorophyll degradation and the decreased expression of photosynthesis-related genes. There are similar symptoms Harpagide during many abiotic and biotic stresses, as well as during natural senescence [911]. Many of the stress conditions which cause leaf yellowing also induce the expression of senescence-associated genes (SAGs) [12]. Indeed, UV-B.