An ABA-increased interaction of the PYL6 ABA receptor with MYC2 Transcription Factor: A putative link of ABA and JA signaling.

An ABA-increased interaction of the PYL6 ABA receptor with MYC2 Transcription Factor: A putative link of ABA and JA signaling.
复制标题

DOI:
10.1038/srep28941
复制
发表时间:
2016-06-30
期刊:
影响因子:
4.6
通讯作者:
Schroeder JI
Schroeder JI
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Aleman F;Yazaki J;Lee M;Takahashi Y;Kim AY;Li Z;Kinoshita T;Ecker JR;Schroeder JI

文献摘要

被引文献

相似文献

脱落酸(阿坝)是一种植物激素,具有调节植物生长和发育的作用。阿坝与PYL/RCAR阿坝受体家族的成员结合,所述PYL/RCAR ABA受体家族启动抑制2C型蛋白磷酸酶的信号转导。虽然阿坝和茉莉酸(JA)激素之间的串扰已被证明,介导这种相互作用的分子实体尚未完全阐明。我们报告了阿坝和JA信号之间的联系,通过阿坝受体PYL 6(RCAR 9)与碱性螺旋-环-螺旋转录因子MYC 2的直接相互作用。PYL 6和MYC 2在酵母双杂交测定中相互作用,并且在阿坝存在下相互作用增强。PYL 6和MYC 2基于蛋白质的双分子荧光互补和免疫共沉淀在植物中相互作用。此外,PYL 6能够在酵母单杂交测定中使用JAZ 6和JAZ 8 DNA启动子元件修饰由MYC 2驱动的转录。最后,pyl 6 T-DNA突变体植物在子叶扩展实验中显示出对添加JA沿着阿坝的增加的敏感性。总体而言,本研究确定了一个直接的机制,转录调节介导的阿坝受体不同的核心阿坝信号通路,和一个假定的机械连接阿坝和JA信号通路。
Abscisic acid (ABA) is a plant hormone that mediates abiotic stress tolerance and regulates growth and development. ABA binds to members of the PYL/RCAR ABA receptor family that initiate signal transduction inhibiting type 2C protein phosphatases. Although crosstalk between ABA and the hormone Jasmonic Acid (JA) has been shown, the molecular entities that mediate this interaction have yet to be fully elucidated. We report a link between ABA and JA signaling through a direct interaction of the ABA receptor PYL6 (RCAR9) with the basic helix-loop-helix transcription factor MYC2. PYL6 and MYC2 interact in yeast two hybrid assays and the interaction is enhanced in the presence of ABA. PYL6 and MYC2 interact in planta based on bimolecular fluorescence complementation and co-immunoprecipitation of the proteins. Furthermore, PYL6 was able to modify transcription driven by MYC2 using JAZ6 and JAZ8 DNA promoter elements in yeast one hybrid assays. Finally, pyl6 T-DNA mutant plants show an increased sensitivity to the addition of JA along with ABA in cotyledon expansion experiments. Overall, the present study identifies a direct mechanism for transcriptional modulation mediated by an ABA receptor different from the core ABA signaling pathway, and a putative mechanistic link connecting ABA and JA signaling pathways.