Abstract
Ultraviolet (UV)-B irradiation leads to DNA damage, cell cycle arrest, growth inhibition, and cell death. To evaluate the UV-B stress–induced changes in plant cells, we developed a model system based on tobacco Bright Yellow-2 (BY-2) cells. Both low-dose UV-B (low UV-B: 740 J m−2) and high-dose UV-B (high UV-B: 2960 J m−2) inhibited cell proliferation and induced cell death; these effects were more pronounced at high UV-B. Flow cytometry showed cell cycle arrest within 1 day after UV-B irradiation; neither low- nor high-UV-B–irradiated cells entered mitosis within 12 h. Cell cycle progression was gradually restored in low-UV-B–irradiated cells but not in high-UV-B–irradiated cells. UV-A irradiation, which activates cyclobutane pyrimidine dimer (CPD) photolyase, reduced inhibition of cell proliferation by low but not high UV-B and suppressed high-UV-B–induced cell death. UV-B induced CPD formation in a dose-dependent manner. The amounts of CPDs decreased gradually within 3 days in low-UV-B–irradiated cells, but remained elevated after 3 days in high-UV-B–irradiated cells. Low UV-B slightly increased the number of DNA single-strand breaks detected by the comet assay at 1 day after irradiation, and then decreased at 2 and 3 days after irradiation. High UV-B increased DNA fragmentation detected by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay 1 and 3 days after irradiation. Caffeine, an inhibitor of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) checkpoint kinases, reduced the rate of cell death in high-UV-B–irradiated cells. Our data suggest that low-UV-B–induced CPDs and/or DNA strand-breaks inhibit DNA replication and proliferation of BY-2 cells, whereas larger contents of high-UV-B–induced CPDs and/or DNA strand-breaks lead to cell death.
Highlights
Ultraviolet (UV)-B radiation (280–320 nm), a component of sunlight, is unavoidable for plants because of their sessile life
We found that ataxia telangiectasia mutated (ATM), ATR, or both kinases mediated UV-B stress–induced cell death
Cell proliferation was inhibited at 2 days after irradiation at all UV-B doses tested (Figure 1A)
Summary
Ultraviolet (UV)-B radiation (280–320 nm), a component of sunlight, is unavoidable for plants because of their sessile life. This radiation may lead to growth inhibition or even cell death. Higher plants have multiple DNA repair mechanisms (Mannuss et al, 2012). Under light, the UVB-induced photodimers are repaired by photolyases specific to each photodimer; mammals have no homologous genes (Ahmad et al, 1997; Nakajima et al, 1998; Hidema et al, 2000; Takeuchi et al, 2007). Endoreduplication in response to UV-B irradiation has been reported; whether it may play a protective role in UV-B tolerance is unknown (Radziejwoski et al, 2011)
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