赤霉素（Gibberellins,，GAs）調(diào)控茉莉酸甲酯（JA）的信號(hào)轉(zhuǎn)導(dǎo)途徑，而JA信號(hào)途徑在植物發(fā)育和脅迫誘導(dǎo)中起著非常重要的作用,。JA作為植物發(fā)育中重要的信號(hào)途徑,，一直是研究熱點(diǎn)。然而,，植物各種信號(hào)途徑之間的調(diào)控網(wǎng)絡(luò)復(fù)雜,，大部分植物激素之間的相互作用仍然不清楚。
DELLAs通過(guò)與JAZs的競(jìng)爭(zhēng)性結(jié)合調(diào)控JA信號(hào)途徑的“抑制釋放模型”圖
中科院華南植物園植物種質(zhì)創(chuàng)新與基因發(fā)掘領(lǐng)域夏快飛博士與新加坡國(guó)立大學(xué)植物發(fā)育學(xué)實(shí)驗(yàn)室的侯興亮博士后,，一起致力于JA調(diào)控途徑中JAZ1(茉莉酸受體ZIM結(jié)構(gòu)域蛋白),、DELLA(DELLA家族蛋白)、MYC2(MYC轉(zhuǎn)錄因子)及GA（赤霉素）之間的相互作用研究,，發(fā)現(xiàn)DELLAs在JA信號(hào)途徑中起著重要作用,，同時(shí)也揭示JA信號(hào)途徑可能通過(guò)DELLAs與別的信號(hào)途徑起著重要的聯(lián)系作用。沒(méi)有JA,，JAZs能穩(wěn)定的與MYC2結(jié)合,，因此抑制了MYC2作為轉(zhuǎn)錄激活子的活性。而加入JA,，JA則與JAZs結(jié)合,，釋放出MYC2，從而激活了JA途徑中的反應(yīng)基因的表達(dá),。在JA信號(hào)途徑中沒(méi)有GA,，DELLAs能穩(wěn)定的與JAZs結(jié)合，釋放出MYC2激活JA途徑,。加入GA,，則GA促進(jìn)了DELLAs的降解，導(dǎo)致JAZ-MYC2復(fù)合子的形成,，從而抑制了JA信號(hào)途徑,。
該研究結(jié)果已發(fā)表在國(guó)際重要刊物Developmental Cell（DOI 10.1016/j.devcel. 2010.10.024）上。（生物谷Bioon.com）
生物谷推薦原文出處：
Developmental Cell DOI 10.1016/j.devcel. 2010.10.024
DELLAs Modulate Jasmonate Signaling via Competitive Binding to JAZs
Authors
Xingliang Hou, Li Yen Candy Lee, Kuaifei Xia, Yuanyuan Yan, Hao Yu
Highlights
Gibberellins (GAs) inhibit DELLA-mediated upregulation of jasmonate (JA) target genes
DELLAs compete the JA signaling repressor JAZ1 away from the JA effector MYC2
DELLA/JAZ binding derepresses MYC2's ability to regulate JA-responsive genes
DELLAs promote cellular competence to respond to JA
Summary
Gibberellins (GAs) modulate jasmonate (JA) signaling, which is essential for stress response and development in plants. However, the molecular details of such phytohormone interaction remain largely unknown. Here, we show that the JA ZIM-domain 1 (JAZ1) protein, a key repressor of JA signaling, interacts in vivo with DELLA proteins, repressors of the GA pathway. DELLAs prevent inhibitory JAZ1 interaction with a key transcriptional activator of JA responses, MYC2, and, thus, enhance the ability of MYC2 to regulate its target genes. Conversely, GA triggers degradation of DELLAs, which allows JAZ1 to bind MYC2 and suppress MYC2-dependent JA-signaling outputs. Therefore, our results reveal one means by which GAs suppress cellular competence to respond to JA. Because DELLAs serve as central regulators that mediate the crosstalk of various phytohormones, our model also suggests a candidate mechanism by which JA signaling may be fine-tuned by other signaling pathways through DELLAs.
