Dominant and Pleiotropic Effects of a GAI Gene in Wheat Results from a Lack of Interaction between DELLA and GID1

Dominant and Pleiotropic Effects of a GAI Gene in Wheat Results from a Lack of Interaction between DELLA and GID1
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小麦中 GAI 基因的显性和多效性作用是由于 DELLA 和 GID1 之间缺乏相互作用造成的

DOI:
10.1104/pp.111.185272
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发表时间:
2011-12-01
期刊:
影响因子:
7.4
通讯作者:
Jia, Jizeng
Jia, Jizeng
中科院分区:
生物学1区
文献类型:
--
作者:
Wu, Jing;Kong, Xiuying;Jia, Jizeng

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显性、半显性和隐性是孟德尔遗传的重要模式。赤霉素(giberellin, GA)是一种调节植物生长发育过程的激素。此前在小麦(Triticum aestivum)中克隆到的半显性ga不敏感基因(GAI) Rht1和Rht2是绿色革命的基础。然而,目前还没有克隆出完全显性的GAI基因。在这里,我们报告了Rht-B1c的分子特征,Rht-B1c是小麦GAI的显性等位基因,比其不完全显性等位基因具有更极端的特征。Rht-B1c是由末端重复反转录转座子微型插入到DELLA结构域引起的。酵母双杂交实验表明,Rht-B1c蛋白不能与GA不敏感的DWARF1 (GID1)相互作用,从而阻断GA反应,导致极端的侏儒症和多效性效应。相比之下,Rht-B1b蛋白仅减少与GID1的相互作用。此外,我们利用近等基因系分析了其功能,并对其在转基因水稻中的分子机制进行了研究。这些结果表明,GID1和DELLA蛋白之间的亲和力是调控DELLA蛋白稳定性的关键,而差异相互作用决定了显性和半显性基因对GA的反应。
Dominance, semidominance, and recessiveness are important modes of Mendelian inheritance. The phytohormone gibberellin (GA) regulates many plant growth and developmental processes. The previously cloned semidominant GA-insensitive (GAI) genes Reduced height1 (Rht1) and Rht2 in wheat (Triticum aestivum) were the basis of the Green Revolution. However, no completely dominant GAI gene has been cloned. Here, we report the molecular characterization of Rht-B1c, a dominant GAI allele in wheat that confers more extreme characteristics than its incompletely dominant alleles. Rht-B1c is caused by a terminal repeat retrotransposons in miniature insertion in the DELLA domain. Yeast two-hybrid assays showed that Rht-B1c protein fails to interact with GA-INSENSITIVE DWARF1 (GID1), thereby blocking GA responses and resulting in extreme dwarfism and pleiotropic effects. By contrast, Rht-B1b protein only reduces interaction with GID1. Furthermore, we analyzed its functions using near-isogenic lines and examined its molecular mechanisms in transgenic rice. These results indicated that the affinity between GID1 and DELLA proteins is key to regulation of the stability of DELLA proteins, and differential interactions determine dominant and semidominant gene responses to GA.