Tissue-specific expression of stabilized SOLITARY-ROOT/IAA14 alters lateral root development in Arabidopsis

Tissue-specific expression of stabilized SOLITARY-ROOT/IAA14 alters lateral root development in Arabidopsis
复制标题

DOI:
10.1111/j.1365-313x.2005.02537.x
复制
发表时间:
2005-11-01
期刊:
影响因子:
7.2
通讯作者:
Tasaka, M
Tasaka, M
中科院分区:
生物学1区
文献类型:
--
作者:
Fukaki, H;Nakao, Y;Tasaka, M

文献摘要

被引文献

相似文献

生长素对侧根的发生和侧根原基的发育具有重要作用。然而,组织特异性生长素信号在这些过程中的作用知之甚少。我们分析了在组织特异性启动子控制下表达稳定突变体吲哚-3乙酸14(IAA 14)/孤根(mIAA 14)蛋白作为生长素反应因子(ARF)的阻遏物的转基因拟南芥植物。我们发现,在天然IAA 14启动子控制下表达mIAA 14-糖皮质激素受体(GR)融合蛋白的植物具有孤根/iaa 14突变体表型,包括在地塞米松(Dex)处理下缺乏LR形成,表明mIAA 14-GR在Dex存在下具有功能。然后,我们证明了中柱特异性SHORT-ROOT启动子控制下的mIAA 14-GR的表达抑制LR的形成,并表明mIAA 14-GR在原木质部附近的周皮层中的表达也阻断LR的形成,表明在原木质部周皮层中由生长素/吲哚-3-乙酸(Aux/IAA)信号传导介导的正常生长素反应是LR形成所必需的。此外,我们证明了在ARF 7或ARF 19启动子下mIAA 14-GR的表达也抑制了LR的形成,如在arf 7和arf 19双突变体中,并且IAA 14与酵母中的ARF 7和ARF 19相互作用。这些结果强烈表明,mIAA 14-GR直接灭活ARF 7/ARF 19功能,从而阻断LR形成。在LR原基形成期间在特定细胞谱系中表达的SCARECROW启动子下的mIAA 14-GR的胚后表达导致LR发育紊乱。这表明,正常的生长素信号在LR原基,其中涉及未知的ARF和Aux/IAAs,是必要的LR原基组织的建立。因此,我们的数据表明,组织特异性表达的一个稳定的Aux/IAA蛋白允许分析组织特异性生长素反应LR发展通过灭活ARF功能。
Auxin is important for lateral root (LR) initiation and subsequent LR primordium development. However, the roles of tissue-specific auxin signaling in these processes are poorly understood. We analyzed transgenic Arabidopsis plants expressing the stabilized mutant INDOLE-3 ACETIC ACID 14 (IAA14)/SOLITARY-ROOT (mIAA14) protein as a repressor of the auxin response factors (ARFs), under the control of tissue-specific promoters. We showed that plants expressing the mIAA14-glucocorticoid receptor (GR) fusion protein under the control of the native IAA14 promoter had the solitary-root/ iaa14 mutant phenotypes, including the lack of LR formation under dexamethasone (Dex) treatment, indicating that mIAA14-GR is functional in the presence of Dex. We then demonstrated that expression of mIAA14-GR under the control of the stele-specific SHORT-ROOT promoter suppressed LR formation, and showed that mIAA14-GR expression in the protoxylem-adjacent pericycle also blocked LR formation, indicating that the normal auxin response mediated by auxin/ indole-3 acetic acid (Aux/IAA) signaling in the protoxylem pericycle is necessary for LR formation. In addition, we demonstrated that expression of mIAA14-GR under either the ARF7 or the ARF19 promoter also suppressed LR formation as in the arf7 arf19 double mutants, and that IAA14 interacted with ARF7 and ARF19 in yeasts. These results strongly suggest that mIAA14-GR directly inactivates ARF7/ARF19 functions, thereby blocking LR formation. Post-embryonic expression of mIAA14-GR under the SCARECROW promoter, which is expressed in the specific cell lineage during LR primordium formation, caused disorganized LR development. This indicates that normal auxin signaling in LR primordia, which involves the unknown ARFs and Aux/IAAs, is necessary for the establishment of LR primordium organization. Thus, our data show that tissue-specific expression of a stabilized Aux/IAA protein allows analysis of tissue-specific auxin responses in LR development by inactivating ARF functions.