The primary signaling outputs of brassinosteroids are regulated by abscisic acid signaling
The primary signaling outputs of brassinosteroids are regulated by abscisic acid signaling
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油菜素类固醇的主要信号输出受脱落酸信号调节
DOI：
10.1073/pnas.0900349106
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发表时间：
2009-03
期刊：
影响因子：
--
通讯作者：
王学路
中科院分区：
文献类型：
--
作者：
王学路
植物激素在协调调节大量发育过程中起着重要作用。研究表明，油菜素类固醇（BR）和脱落酸（阿坝）相互作用调节数百个基因的表达，控制许多生物学过程。然而，它们的相互作用是通过它们的主要信号级联的修饰或交叉，还是通过独立或平行的途径仍然是一个很大的谜。使用BR信号和阿坝生物合成突变体的生化和分子标记，我们证明了外源阿坝迅速抑制BR信号输出所示的磷酸化状态的BES 1和BR响应基因的表达。使用bri 1无效等位基因bri 1 -116的实验和对BKI 1-YFP的亚细胞定位的分析进一步揭示了BR受体复合物不是阿坝作用于BR信号输出所必需的。然而，当BR下游信号组分BIN 2被LiCl抑制时，阿坝不能抑制BR信号输出。此外，使用一组阿坝不敏感的突变体，我们发现，调节阿坝对BR的主要信号通路依赖于阿坝早期信号组件，ABI 1和ABI 2。我们建议，信号级联的阿坝和BR主要是在BR感知后的串扰，但在其转录激活。该模型为为什么大部分BR反应基因也受阿坝调控提供了合理的解释，并为BR与阿坝相互作用的分子机制提供了深入了解。
Phytohormones have essential roles in coordinately regulating a large array of developmental processes. Studies have revealed that brassinosteroids (BRs) and abscisic acid (ABA) interact to regulate hundreds of expression in genes, governing many biological processes. However, whether their interaction is through modification or intersection of their primary signaling cascades, or by independent or parallel pathways remains a big mystery. Using biochemical and molecular markers of BR signaling and ABA biosynthetic mutants, we demonstrated that exogenous ABA rapidly inhibits BR signaling outputs as indicated by the phosphorylation status of BES1 and BR-responsive gene expression. Experiments using a bri1 null-allele, bri1-116, and analysis of subcellular localization of BKI1-YFP further revealed that the BR receptor complex is not required for ABA to act on BR signaling outputs. However, when the BR downstream signaling component BIN2 is inhibited by LiCl, ABA failed to inhibit BR signaling outputs. Also, using a set of ABA insensitive mutants, we found that regulation of ABA on the BR primary signaling pathway depends on the ABA early signaling components, ABI1 and ABI2. We propose that the signaling cascades of ABA and BR primarily cross-talk after BR perception, but before their transcriptional activation. This model provides a reasonable explanation for why a large proportion of BR-responsive genes are also regulated by ABA, and provides an insight into the molecular mechanisms by which BRs could interact with ABA.
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