UV-B-induced DNA damage mediates expression changes of cell cycle regulatory genes in Arabidopsis root tips
UV-B-induced DNA damage mediates expression changes of cell cycle regulatory genes in Arabidopsis root tips
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UV-B诱导的DNA损伤介导拟南芥根尖细胞周期调控基因的表达变化
DOI:
10.1007/s00425-010-1340-5
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发表时间:
2011-04-01
期刊:
影响因子:
4.3
通讯作者:
Li, Shaoshan
中科院分区:
文献类型:
--
作者:
Jiang, Lei;Wang, Yan;Li, Shaoshan
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.