A novel myb oncogene homologue in Arabidopsis thaliana related to hypersensitive cell death

A novel myb oncogene homologue in Arabidopsis thaliana related to hypersensitive cell death
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DOI:
10.1046/j.1365-313x.1999.00578.x
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发表时间:
1999-10-01
期刊:
影响因子:
7.2
通讯作者:
Roby, D
Roby, D
中科院分区:
生物学1区
文献类型:
--
作者:
Daniel, X;Lacomme, C;Roby, D

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通过对野油菜黄单胞菌(Xanthomonas Campestris PV)cDNA文库的差异筛选,获得了一个新的MYB癌基因同源物(AtMYB30)。Campestris(X.campestris)-接种在环己亚胺存在下培养的拟南芥细胞。AtMYB30是一个单拷贝基因,编码的蛋白含有一个与其他动植物MYB蛋白高度同源的MYB结构域。用野油菜和紫丁香假单胞菌的强毒或无毒菌株感染刺参植株或培养的刺参细胞进行转录水平分析。结果表明,该基因的最高转录水平发生在过敏反应过程中。此外,在控制细胞死亡起始的突变体(Isd3、Isd4和Isd5)中,在病斑阳性植株中观察到结构性表达或表达,而在突变Isd5和Isd4的抑制子中,AtMYB30转录本没有积累。然而,在Isd1突变体中不能检测到AtMYB30的表达,该突变体对细胞死亡启动子高度反应,无论环境条件如何,都不能限制细胞死亡的程度。研究结果表明,AtMYB30与基因控制的细胞死亡有很强的相关性,在细胞死亡的启动中起作用,而不是在其程度上受到限制。我们的结果进一步表明,ISD突变体构成了一个合适的遗传模型,用于研究该基因在细胞过敏性死亡中的作用,以及它们与导致细胞死亡的不同步骤(S)的关系。
A novel myb oncogene homologue (AtMYB30) has been isolated by differential screening of a cDNA library prepared from Xanthomonas campestris pv. campestris (X. campestris)-inoculated Arabidopsis thaliana cells cultured in the presence of cycloheximide. AtMYB30 is a single-copy gene, and the encoded protein contains a MYB domain highly homologous to other plant and animal MYB proteins. Analyses of transcript levels in A. thaliana plants, or in cultured A. thaliana cells infected with either virulent or avirulent strains of the pathogens X. campestris and Pseudomonas syringae pv. tomato, showed that maximal levels of transcription of this gene occurred during the hypersensitive response. Furthermore, in A. thaliana mutants affected in the control of cell death initiation (Isd3, Isd4 and Isd5), constitutive expression or expression in lesion-positive plants was observed, while in suppressors of the mutations Isd5 and Isd4, AtMYB30 transcripts did not accumulate. However, AtMYB30 expression could not be detected in the Isd1 mutant, which was hyperresponsive to cell death initiators and unable to limit the extent of cell death, whatever the environmental conditions. The results presented here suggest a strong correlation between AtMYB30 and genetically controlled cell death, with a role in the initiation of cell death rather than in the limitation of its extent. Our results further indicate that the Isd mutants constitute an appropriate genetic model for studying the role of this gene in hypersensitive cell death, and their relation to different steps of the pathway(s) leading to cell death.