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首页> 美国卫生研究院文献>Springer Open Choice >Arabidopsis suppressor mutant of abh1 shows a new face of the already known players: ABH1 (CBP80) and ABI4—in response to ABA and abiotic stresses during seed germination
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Arabidopsis suppressor mutant of abh1 shows a new face of the already known players: ABH1 (CBP80) and ABI4—in response to ABA and abiotic stresses during seed germination

机译：abh1的拟南芥抑制突变体显示出已知参与者的新面孔：ABH1（CBP80）和ABI4-响应种子发芽期间的ABA和非生物胁迫

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Although the importance of abscisic acid (ABA) in plant development and response to abiotic and biotic stresses is well recognized, the molecular basis of the signaling pathway has not been fully elucidated. Mutants in genes related to ABA are widely used as a tool for gaining insight into the mechanisms of ABA signal transduction and ABA-dependent stress response. We used a genetic approach of a suppressor screening in order to decipher the interaction between ABH1 (CBP80) and other components of ABA signaling. ABH1 (CBP80) encodes a large subunit of CBC (CAP BINDING COMPLEX) and the abh1 mutant is drought-tolerant and hypersensitive to ABA during seed germination. The suppressor mutants of abh1 were generated after chemical mutagenesis. The mutant named soa1 (suppressor of abh1 hypersensitivity to ABA 1) displayed an ABA-insensitive phenotype during seed germination. The genetic analysis showed that the soa1 phenotype is dominant in relation to abh1 and segregates as a single locus. Based on soa1’s response to a wide spectrum of physiological assays during different stages of development, we used the candidate-genes approach in order to identify a suppressor gene. The molecular analysis revealed that mutation causing the phenotype of soa1 occurred in the ABI4 (ABA insensitive 4) gene. Analysis of pre-miR159 expression, whose processing depends on CBC, as well as targets of miR159: MYB33 and MYB101, which are positive regulators of ABA signaling, revealed a possible link between CBP80 (ABH1) and ABI4 presented here.Electronic supplementary materialThe online version of this article (doi:10.1007/s11103-012-9991-1) contains supplementary material, which is available to authorized users.
机译：尽管脱落酸（ABA）在植物发育以及对非生物和生物胁迫的响应中的重要性已得到公认，但信号传导途径的分子基础尚未得到充分阐明。与ABA相关的基因突变被广泛用作了解ABA信号转导和ABA依赖性应激反应机制的工具。我们使用了一种抑制子筛选的遗传方法，以破译ABH1（CBP80）与ABA信号传导的其他组件之间的相互作用。 ABH1（CBP80）编码CBC的一个大亚基（CAP BINDING COMPLEX），而abh1突变体在种子萌发过程中耐干旱并且对ABA敏感。化学诱变后产生了abh1的抑制突变体。名为soa1的突变体（对ABA 1的abh1超敏性的抑制剂）在种子萌发过程中表现出ABA不敏感的表型。遗传分析表明，相对于abh1，soa1表型占主导地位，并作为单个位点分离。基于soa1在开发的不同阶段对各种生理测定的反应，我们使用了候选基因方法来鉴定抑制基因。分子分析表明，引起soa1表型的突变发生在ABI4（ABA不敏感4）基因中。对前miR159表达的分析（其处理取决于CBC）以及作为ABA信号正调控子的miR159：MYB33和MYB101的靶标，揭示了此处介绍的CBP80（ABH1）和ABI4之间的可能联系。本文的版本（doi：10.1007 / s11103-012-9991-1）包含补充材料，可供授权用户使用。

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