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ABSTRACT: Daylight UV-B (UV-B) radiation (280-315 nm) is, because of its photochemical effects and potential destructive impact, an important environmental factor for plants. After decades of fruitless attempts, a receptor molecule, UVR8, for sensing of ambient UV-B radiation by plants has been characterized, and the initial steps in signal transduction have been identified. There are, however, other signaling pathways, and there are apparent contradictions in the literature. There is still much to find out about the complex signaling network in plants for processing of information about the daylight surrounding them.
Plant signaling & behavior 08/2012; 7(8):999-1003.
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ABSTRACT: UV-B (280-315 nm) is an integral part of solar radiation and can act either as a stress inducer or as a developmental signal. In recent years, increasing attention has been paid to the low-fluence UV-B-induced photomorphogenic response and several key players in this response have been identified, which include UVR8 (a UV-B-specific photoreceptor), COP1 (a WD40-repeat-containing RING finger protein), HY5 (a basic zipper transcription factor), and RUP1/2 (two UVR8-interacting proteins). Here we report that Arabidopsis SALT TOLERANCE (STO/BBX24), a known regulator for light signaling in plants, defines a new signaling component in UV-B-mediated photomorphogenesis. The bbx24 mutant is hypersensitive to UV-B radiation and becomes extremely dwarfed under UV-B treatment. By contrast, BBX24 overexpression transgenic lines respond much more weakly to UV-B than the bbx24 and wild-type plants. BBX24 expression is UV-B-inducible and its accumulation under UV-B requires COP1. Co-immunoprecipitation experiments indicate that BBX24 interacts with COP1 in planta upon UV-B illumination. Moreover, BBX24 interacts with HY5 and acts antagonistically with HY5 in UV-B-induced inhibition of hypocotyl elongation. Furthermore, BBX24 attenuates UV-B-induced HY5 accumulation and suppresses its transcription-activation activity. Taken together, our results reveal a previously uncharacterized function of the light-regulated BBX24 in UV-B responses and demonstrate that BBX24 functions as a negative regulator of photomorphogenic UV-B responses by interacting with both COP1 and HY5. The UV-B-inducible expression pattern and its suppression of HY5 activity suggest that BBX24 could be a new component of the feedback regulatory module of UV-B signaling in plants.
Cell Research 03/2012; 22(6):1046-57. · 8.19 Impact Factor
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ABSTRACT: UV-B radiation (280-315 nm) is an integral part of solar radiation and has many harmful effects on plant growth and development. However, the molecular mechanism for the inhibition of plant growth by UV-B remains largely unknown. UV-B radiation induces various responses such as growth inhibition, DNA damage and changes of gene expression. Recently, by using synchronous root tip culture, we found that UV-B modulates the expression of cell cycle regulatory genes through DNA damage. Western blotting analysis revealed that UV-B induced G1-to-S arrest did not correlate with the protein abundance of CDKB1;1 and CYCD3;1 gene regulating proteins, but may with the posttranslational control. We extended the expression analysis of cell cycle related genes based on the published microarray data and the results strengthen our assumption that cell cycle arrest could occur in plant under solar UV-B radiation. Further study is needed to elucidate the relationship between cell cycle regulation and protective pathway induced by low dose of UV-B radiation fundamental molecular mechanism for how plants respond to solar UV-B radiation.
Plant signaling & behavior 06/2011; 6(6):892-4.
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ABSTRACT: Even though a number of studies have shown that UV-B radiation inhibits plant growth and regulates the cell cycle progress, little is known about the molecular and cellular mechanisms. Here, we developed a synchronous root-tip cell system to investigate expression changes of cell cycle marker genes and DNA damage under UV-B radiation. Expression analysis of cell cycle marker genes revealed that G1-to-S transition in root-tip cells was accomplished within 6 h. In the in vivo synchronous root-tip cells, high level of UV-B radiation (0.45 W m(-2)) induced expression changes of the cell cycle regulatory genes. Genes involved in G1-to-S transition, Histone H4 and E2Fa, were down-regulated by UV-B radiation during 2-6 h; whereas transcripts for KRP2, a negative regulator of G1-to-S transition, were up-regulated by UV-B at 2 h. The peak time for transcript level of CYCD3;1, a positive factor in G1-to-S transition, was delayed by UV-B radiation. Interestingly, a medium level of UV-B radiation (0.25 W m(-2)) did not change the expression of these genes in root tip cells from wild type. However, cell cycle regulatory genes were greatly affected in uvh1 mutant, which exhibited higher content of cyclobutane pyrimidine dimers (CPDs). Ascorbic acid treatment did not change the expression pattern of cell cycle regulatory genes that were affected by high-level UV-B. Our results implied that UV-B-induced DNA damage results in the delay of G1-to-S transition of plant cell cycle. UV-B-induced G1-to-S arrest may be a protective mechanism that prevents cells with damaged DNA from dividing and may explain the plant growth inhibition under increased solar UV-B radiation.
Planta 01/2011; 233(4):831-41. · 3.00 Impact Factor
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ABSTRACT: The Arabidopsis radical-induced cell death1 (rcd1) mutant is sensitive to ozone fumigation and apoplastic superoxide, but tolerant to methyl viologen. In the present article, we report that the rcd1 mutant is also tolerant to supplementary UV-B radiation. The rcd1-1 mutant exhibits less accumulation of TT dimers, increased hypocotyl growth inhibition and higher accumulation of flavonoids under supplemental UV-B radiation. Moreover, the expression of HY5 (elongated hypocotyl5) is increased in the mutant after UV-B treatment. Gene expression downstream of UV-B signaling reveals that COP1 (constitutively photomorphogenic1)-regulated genes have an elevated expression in rcd1-1 mutant under UV-B radiation, while expression of UVR8 (UV resistance locus 8)-regulated and HY5-independent genes are not changed. Interestingly, the expression of RCD1 genes is not significantly changed by UV-B radiation. Previous study has shown that STO protein is interacting with RCD1 in vitro. Here, we found the mRNA level of STO (salt tolerance) is greatly increased in rcd1-1 mutant after UV-B radiation. However, UV-B-induced HY5 and CHS expression is partially inhibited in sto mutant. Based on the above results, it is deduced that the RCD1, working together with STO, is involved in Arabidopsis UV-B signaling.
Photochemical and Photobiological Sciences 07/2009; 8(6):838-46. · 2.58 Impact Factor
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ABSTRACT: The single-cell gel electrophoresis or comet assay is now widely used to detect DNA damage in animal cells induced by radiation or chemicals. Here, we apply the comet assay to measure ultraviolet (UV)-B-induced DNA damage in plant cells. The accepted animal cell protocol for the comet assay was modified to adapt it to plant cells. The major modifications were conversion of the plant cells to protoplasts and the use of T4 endonuclease V. As a positive control hydrogen peroxide was applied. Significant DNA damage was detected at 100 μM H2O2. This type of DNA damage was not affected by T4 endonuclease V treatment, which implies that the mechanism of H2O2-induced DNA damage was different from UV-B-induced DNA damage. Our results also indicate that both UV-A and UV-B radiation can induce DNA single-strand breaks in plant cells, while UV-B was more effective than UV-A for inducing pyrimidine dimer formation.
Physiologia Plantarum 12/2006; 129(3):652 - 657. · 3.11 Impact Factor
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ABSTRACT: DNA damage in the form of cyclobutane pyrimidine dimers(CPDs) and (6-4) photoproducts(6-4PPs) induced by UV-B radiation in Arabidopsis thaliana at different temperatures was investigated using ELISA with specific monoclonal antibodies. CPDs and 6-4PPs increased during 3 h UV-B exposure, but further exposure led to decreases. Contrary to the commonly accepted view that DNA damage induced by UV-B radiation is temperature-independent because of its photochemical nature, we found UV-B-induction of CPDs and 6-4PPs in Arabidopsis to be slower at a low than at a high temperature. Photorepair of CPDs at 24 degrees C was much faster than that at 0 degrees C and 12 degrees C, with 50% CPDs removal during 1 h exposure to white light. Photorepair of 6-4PPs at 12 degrees C was very slow as compared with that at 24 degrees C, and almost no removal of 6-4PPs was detected after 4 h exposure to white light at 0 degrees C. There was evidence to suggest that temperature-dependent DNA damage and photorepair could have important ecological implications.
Journal of Environmental Sciences 02/2004; 16(1):173-6. · 1.66 Impact Factor
