UV-B-induced photomorphogenesis in Arabidopsis thaliana

UV-B-induced photomorphogenesis in Arabidopsis thaliana
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DOI:
10.1046/j.1365-313x.1998.00246.x
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发表时间:
1998-09-01
期刊:
影响因子:
7.2
通讯作者:
Last, RL
Last, RL
中科院分区:
生物学1区
文献类型:
--
作者:
Kim, BC;Tennessen, DJ;Last, RL

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植物对紫外线B(UV-B,290-320 nm)辐射的光形态发生反应类型和信号转导途径知之甚少。在野生型拟南芥幼苗中,下胚轴生长抑制和子叶扩展都可重复地促进连续UV-B。下胚轴伸长的注量率反应进行了检查,并表现出双相反应。虽然在低剂量下观察到光形态发生反应,但较高的能量密度导致损伤症状。在支持我们的理论,光形态建成,但没有损害,发生在低剂量的UV-B,UV-B敏感突变体的光形态建成反应是难以区分的野生型植物在低剂量。这使我们能够研究UV-B诱导的光形态发生在感光细胞缺陷的植物和组成型光形态发生突变体。cry 1隐花色素结构基因突变体和光敏色素缺陷hy 1、phyA和phyB突变体幼苗与野生型幼苗相似,而phyA/phyB双突变体对UV-B光形态建成效应不太敏感。这些结果表明,无论是phyA或phyB是必需的UV-B诱导的光形态建成。组成型光形态发生突变体cop 1和def 2没有表现出显着的抑制下胚轴的生长响应UV-B,而det 2受到强烈的UV-B辐射。这表明COP 1和DET 1在UV-B信号通路的下游起作用。
Relatively little is known about the types of photomorphogenic responses and signal transduction pathways that plants employ in response to ultraviolet-B (UV-B, 290-320 nm) radiation. In wild-type Arabidopsis seedlings, hypocotyl growth inhibition and cotyledon expansion were both reproducibly promoted by continuous UV-B. The fluence rate response of hypocotyl elongation was examined and showed a biphasic response. Whereas photomorphogenic responses were observed at low doses, higher fluences resulted in damage symptoms. In support of our theory that photomorphogenesis, but not damage, occurs at low doses of UV-B, photomorphogenic responses of UV-B sensitive mutants were indistinguishable from wild type plants at the low dose. This allowed us to examine UV-B-induced photomorphogenesis in photoreceptor deficient plants and constitutive photomorphogenic mutants. The cry1 cryptochrome structural gene mutant, and phytochrome deficient hy1, phyA and phyB mutant seedlings resembled wild-type seedlings, while phyA/phyB double mutants were less sensitive to the photomorphogenic effects of UV-B. These results suggest that either phyA or phyB is required for UV-B-induced photomorphogenesis. The constitutive photomorphogenic mutants cop1 and def2 did not show significant inhibition of hypocotyl growth in response to UV-B, while det2 was strongly affected by UV-B irradiation. This suggests that COP1 and DET1 work downstream of the UV-B signaling pathway.