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COP1b是通过可变剪接产生的COP1的一种同工型,在调节拟南芥光依赖型幼苗发育过程中,对COP1的功能具有负面影响。

COP1b, an isoform of COP1 generated by alternative splicing, has a negative effect on COP1 function in regulating light-dependent seedling development in Arabidopsis.

作者信息

Zhou D X, Kim Y J, Li Y F, Carol P, Mache R

机构信息

Laboratoire de Génétique Moléculaire des Plantes, Université Joseph Fourier, Grenoble, France.

出版信息

Mol Gen Genet. 1998 Feb;257(4):387-91. doi: 10.1007/s004380050662.

DOI:10.1007/s004380050662
PMID:9529519
Abstract

COP1 is a negative regulator of Arabidopsis light-dependent development. Mutation of the COP1 locus causes constitutive photomorphogenesis in the dark. Here, we report the identification of an isoform of the COP1 protein, named COP1b, which is generated by alternative splicing. COP1b has a 60-amino acid deletion in the WD-40 repeat domain relative to the full-length COP1. This splicing step is light-independent and takes place mostly in mature seeds and in germinating seedlings. Transgenic Arabidopsis plants that overexpress COP1b show a de-etiolated phenotype in the dark, with a short hypocotyl, open and developed cotyledons. The transgenic seedlings are adult-lethal. These phenotypes closely resemble that of severe cop-1 mutants, indicating that COP1b has a dominant negative effect on COP1 function.

摘要

COP1是拟南芥光依赖型发育的负调控因子。COP1基因座的突变会导致在黑暗中组成型光形态建成。在此,我们报告了一种COP1蛋白异构体的鉴定,名为COP1b,它是通过可变剪接产生的。相对于全长COP1,COP1b在WD-40重复结构域中有一个60个氨基酸的缺失。这一剪接步骤不依赖光照,主要发生在成熟种子和萌发的幼苗中。过表达COP1b的转基因拟南芥植株在黑暗中表现出去黄化表型,下胚轴短,子叶开放且发育。转基因幼苗是成年致死的。这些表型与严重的cop-1突变体非常相似,表明COP1b对COP1功能具有显性负效应。

相似文献

1
COP1b, an isoform of COP1 generated by alternative splicing, has a negative effect on COP1 function in regulating light-dependent seedling development in Arabidopsis.COP1b是通过可变剪接产生的COP1的一种同工型,在调节拟南芥光依赖型幼苗发育过程中,对COP1的功能具有负面影响。
Mol Gen Genet. 1998 Feb;257(4):387-91. doi: 10.1007/s004380050662.
2
Expression of an N-terminal fragment of COP1 confers a dominant-negative effect on light-regulated seedling development in Arabidopsis.COP1的N端片段的表达对拟南芥中光调节的幼苗发育具有显性负效应。
Plant Cell. 1996 Sep;8(9):1491-503. doi: 10.1105/tpc.8.9.1491.
3
Overexpression of Arabidopsis COP1 results in partial suppression of light-mediated development: evidence for a light-inactivable repressor of photomorphogenesis.拟南芥COP1的过表达导致光介导发育的部分抑制:光形态建成的光灭活阻遏物的证据。
Plant Cell. 1994 Oct;6(10):1391-400. doi: 10.1105/tpc.6.10.1391.
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Genetic and developmental control of nuclear accumulation of COP1, a repressor of photomorphogenesis in Arabidopsis.拟南芥中光形态建成抑制因子COP1核积累的遗传与发育调控
Plant Physiol. 1997 Jul;114(3):779-88. doi: 10.1104/pp.114.3.779.
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AtMYB21, a gene encoding a flower-specific transcription factor, is regulated by COP1.AtMYB21是一个编码花特异性转录因子的基因,受COP1调控。
Plant J. 2002 Apr;30(1):23-32. doi: 10.1046/j.1365-313x.2002.01264.x.
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Functional analysis of COP1 and SPA orthologs from Physcomitrella and rice during photomorphogenesis of transgenic Arabidopsis reveals distinct evolutionary conservation.来自小立碗藓和水稻的COP1及SPA直系同源基因在转基因拟南芥光形态建成过程中的功能分析揭示了明显的进化保守性。
BMC Plant Biol. 2014 Jul 1;14:178. doi: 10.1186/1471-2229-14-178.
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FAR-RED INSENSITIVE219 modulates CONSTITUTIVE PHOTOMORPHOGENIC1 activity via physical interaction to regulate hypocotyl elongation in Arabidopsis.远红光不敏感 219 通过物理相互作用调节 CONSTITUTIVE PHOTOMORPHOGENIC1 的活性,从而调控拟南芥下胚轴伸长。
Plant Physiol. 2011 Jun;156(2):631-46. doi: 10.1104/pp.111.177667. Epub 2011 Apr 27.
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Short communication: the N-terminal fragment of Arabidopsis photomorphogenic repressor COP1 maintains partial function and acts in a concentration-dependent manner.短讯:拟南芥光形态建成抑制因子COP1的N端片段保持部分功能并以浓度依赖方式发挥作用。
Plant J. 1999 Dec;20(6):713-7. doi: 10.1046/j.1365-313x.1999.00639.x.
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Functional dissection of Arabidopsis COP1 reveals specific roles of its three structural modules in light control of seedling development.拟南芥COP1的功能剖析揭示了其三个结构模块在光调控幼苗发育中的特定作用。
EMBO J. 1998 Oct 1;17(19):5577-87. doi: 10.1093/emboj/17.19.5577.
10
Two interacting bZIP proteins are direct targets of COP1-mediated control of light-dependent gene expression in Arabidopsis.两个相互作用的bZIP蛋白是拟南芥中COP1介导的光依赖性基因表达调控的直接靶点。
Genes Dev. 2002 May 15;16(10):1247-59. doi: 10.1101/gad.969702.

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