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由G蛋白介导的充足苯丙氨酸合成对于保护黄化的拟南芥幼苗免受紫外线辐射损伤至关重要。

Adequate phenylalanine synthesis mediated by G protein is critical for protection from UV radiation damage in young etiolated Arabidopsis thaliana seedlings.

作者信息

Warpeha Katherine M, Gibbons Jack, Carol Andrew, Slusser James, Tree Roger, Durham William, Kaufman Lon S

机构信息

Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, Chicago, IL 60607, USA.

出版信息

Plant Cell Environ. 2008 Dec;31(12):1756-70. doi: 10.1111/j.1365-3040.2008.01878.x. Epub 2008 Aug 26.

DOI:10.1111/j.1365-3040.2008.01878.x
PMID:18761702
Abstract

Etiolated Arabidopsis thaliana seedlings, lacking a functional prephenate dehydratase1 gene (PD1), also lack the ability to synthesize phenylalanine (Phe) and, as a consequence, phenylpropanoid pigments. We find that low doses of ultraviolet (UV)-C (254 nm) are lethal and low doses of UV-B cause severe damage to etiolated pd1 mutants, but not to wild-type (wt) seedlings. Furthermore, exposure to UV-C is lethal to etiolated gcr1 (encoding a putative G protein-coupled receptor in Arabidopsis) mutants and gpa1 (encoding the sole G protein alpha subunit in Arabidopsis) mutants. Addition of Phe to growth media restores wt levels of UV resistance to pd1 mutants. The data indicate that the Arabidopsis G protein-signalling pathway is critical to providing protection from UV, and does so via the activation of PD1, resulting in the synthesis of Phe. Cotyledons of etiolated pd1 mutants have proplastids (compared with etioplasts in wt), less cuticular wax and fewer long-chain fatty acids. Phe-derived pigments do not collect in the epidermal cells of pd1 mutants when seedlings are treated with UV, particularly at the cotyledon tip. Addition of Phe to the growth media restores a wt phenotype to pd1 mutants.

摘要

缺乏功能性预苯酸脱水酶1基因(PD1)的黄化拟南芥幼苗也缺乏合成苯丙氨酸(Phe)的能力,因此也无法合成苯丙烷类色素。我们发现低剂量的紫外线-C(254nm)具有致死性,低剂量的紫外线-B会对黄化的pd1突变体造成严重损害,但对野生型(wt)幼苗则无影响。此外,紫外线-C照射对黄化的gcr1(编码拟南芥中一种假定的G蛋白偶联受体)突变体和gpa1(编码拟南芥中唯一的G蛋白α亚基)突变体具有致死性。在生长培养基中添加苯丙氨酸可使pd1突变体的紫外线抗性恢复到野生型水平。数据表明,拟南芥G蛋白信号通路对于提供紫外线防护至关重要,并且通过激活PD1来实现,从而导致苯丙氨酸的合成。黄化的pd1突变体的子叶含有原质体(与野生型中的黄化质体相比),角质层蜡较少且长链脂肪酸较少。当用紫外线处理幼苗时,尤其是在子叶尖端,苯丙氨酸衍生的色素不会在pd1突变体的表皮细胞中积累。在生长培养基中添加苯丙氨酸可使pd1突变体恢复野生型表型。

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