Genetic and Developmental Control of Nuclear Accumulation of COP1, a Repressor of Photomorphogenesis in Arabidopsis
Genetic and Developmental Control of Nuclear Accumulation of COP1, a Repressor of Photomorphogenesis in Arabidopsis
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DOI：
10.1104/pp.114.3.779
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发表时间：
1997-07
期刊：
影响因子：
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通讯作者：
A. Arnim;M. Osterlund;S. Kwok;X. Deng
中科院分区：
文献类型：
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作者：
A. Arnim;M. Osterlund;S. Kwok;X. Deng
利用[β]-葡萄糖醛酸酶(GUS)报告基因-COP1融合转基因，先前已证明拟南芥COP1在细胞核内作为幼苗光形态发生发育的抑制因子，并且COP1的光灭活伴随着COP1核丰度的降低(A.G.von Arnim，X.-W.邓[1994]Cell 79：1035-1045)。在此，我们报道了GUS-COP1融合转基因可以完全修复Cop1突变的缺陷，从而在幼苗发育过程中发挥完全的功能。在光/暗转换过程中，GUS-COP1在Cop1缺失突变背景中的重新定位动力学表明，功能核COP1水平的调节在稳定维持承诺幼苗的发育命运方面发挥了作用，而不是导致这种承诺。GUS-COP1在所有其他多效性CoP/Det/fus基因座突变的下胚轴中的细胞定位分析表明，在所有被测试的突变体中，GUS-COP1在黑暗和光照条件下的核定位都减少了，而在不太多效性的Cop4突变体中核定位没有受到影响。利用油菜素内酯缺失突变体DET2和油菜素内酯对野生型幼苗的处理，我们证明油菜素内酯不是通过调节COP1的核定位来控制下胚轴细胞的伸长。生长调节剂细胞分裂素在没有光的情况下也显著地降低了下胚轴细胞的伸长，但并没有阻止GUS-COP1在黑暗生长的幼苗中的核定位。我们的结果表明，所有先前描述的多效性COP/DET/FUS基因座都是在黑暗中正确定位COP1蛋白所必需的，而被测试的不那么多效性的COP/DET基因座或植物调节剂可能作用于COP1下游或通过独立的途径。
Using a [beta]-glucuronidase (GUS) reporter-COP1 fusion transgene, it was shown previously that Arabidopsis COP1 acts within the nucleus as a repressor of seedling photomorphogenic development and that light inactivation of COP1 was accompanied by a reduction of COP1 nuclear abundance (A.G. von Arnim, X.-W. Deng [1994] Cell 79: 1035–1045). Here we report that the GUS-COP1 fusion transgene can completely rescue the defect of cop1 mutations and thus is fully functional during seedling development. The kinetics of GUS-COP1 relocalization in a cop1 null mutant background during dark/light transitions imply that the regulation of the functional nuclear COP1 level plays a role in stably maintaining a committed seedling's developmental fate rather than in causing such a commitment. Analysis of GUS-COP1 cellular localization in mutant hypocotyls of all other pleiotropic COP/DET/FUS loci revealed that nuclear localization of GUS-COP1 was diminished under both dark and light conditions in all mutants tested, whereas nuclear localization was not affected in the less pleiotropic cop4 mutant. Using both the brassinosteroid-deficient mutant det2 and brassinosteroid treatment of wild-type seedlings, we have demonstrated that brassinosteroid does not control the hypocotyl cell elongation through regulating nuclear localization of COP1. The growth regulator cytokinin, which also dramatically reduced hypocotyl cell elongation in the absence of light, did not prevent GUS-COP1 nuclear localization in dark-grown seedlings. Our results suggest that all of the previously characterized pleiotropic COP/DET/FUS loci are required for the proper nuclear localization of the COP1 protein in the dark, whereas the less pleiotropic COP/DET loci or plant regulators tested are likely to act either downstream of COP1 or by independent pathways.