Antagonistic regulation of Arabidopsis growth by brassinosteroids and abiotic stresses.

Antagonistic regulation of Arabidopsis growth by brassinosteroids and abiotic stresses.
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DOI:
10.14348/molcells.2014.0127
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发表时间:
2014-11
影响因子:
3.8
通讯作者:
Choe S
Choe S
中科院分区:
生物学3区
文献类型:
--
作者:
Chung Y;Kwon SI;Choe S

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为了抵御不断变化的环境胁迫,植物配备了植物激素介导的胁迫抗性机制。盐胁迫触发脱落酸(阿坝)信号传导,其以生长为代价增强胁迫耐受性。阿坝被认为抑制生长促进激素的作用,包括油菜素类固醇(BR)。然而,协调阿坝和BR活性的调节机制仍有待发现。我们注意到ABA处理的幼苗表现出小而圆的叶子和短根,这是BR信号转导突变体油菜素类固醇不敏感1 -9(bri 1 -9)的特征表型。为了确定阿坝和BR拮抗调节的基因,我们研究了已发表的拟南芥微阵列数据集。在鉴定的基因列表中,那些被阿坝上调但被BR下调的基因在其启动子序列中富含BRRE基序。在使用定量RT-PCR验证微阵列数据后,我们将重点放在盐胁迫诱导的RD 26上。表达RD 26 pro:GUS的转基因拟南芥植株的组织化学分析表明,在NaCl处理后GUS表达的诱导被BR的共处理抑制,但被BR生物合成抑制剂丙环唑的共处理增强。类似地,用BIKININ(BIN 2激酶的抑制剂)处理不仅抑制RD 26的表达,而且降低了暴露于盐胁迫后植物的存活率。我们的研究结果表明,阿坝和BR拮抗作用于其靶基因在BR信号通路中的BIN 2步骤或之后,并提出了一种机制,植物微调其生长,特别是当压力反应和生长竞争资源。
To withstand ever-changing environmental stresses, plants are equipped with phytohormone-mediated stress resistance mechanisms. Salt stress triggers abscisic acid (ABA) signaling, which enhances stress tolerance at the expense of growth. ABA is thought to inhibit the action of growth-promoting hormones, including brassinosteroids (BRs). However, the regulatory mechanisms that coordinate ABA and BR activity remain to be discovered. We noticed that ABA-treated seedlings exhibited small, round leaves and short roots, a phenotype that is characteristic of the BR signaling mutant, brassinosteroid insensitive1-9 (bri1-9). To identify genes that are antagonistically regulated by ABA and BRs, we examined published Arabidopsis microarray data sets. Of the list of genes identified, those upregulated by ABA but downregulated by BRs were enriched with a BRRE motif in their promoter sequences. After validating the microarray data using quantitative RT-PCR, we focused on RD26, which is induced by salt stress. Histochemical analysis of transgenic Arabidopsis plants expressing RD26pro:GUS revealed that the induction of GUS expression after NaCl treatment was suppressed by co-treatment with BRs, but enhanced by co-treatment with propiconazole, a BR biosynthetic inhibitor. Similarly, treatment with bikinin, an inhibitor of BIN2 kinase, not only inhibited RD26 expression, but also reduced the survival rate of the plant following exposure to salt stress. Our results suggest that ABA and BRs act antagonistically on their target genes at or after the BIN2 step in BR signaling pathways, and suggest a mechanism by which plants fine-tune their growth, particularly when stress responses and growth compete for resources.