Rothamsted Research, Harpenden, Hertfordshire AL5 2JQ, UK.
Plant Physiol. 2011 Dec;157(4):1820-31. doi: 10.1104/pp.111.183657. Epub 2011 Oct 19.
The introduction of the Reduced height (Rht)-B1b and Rht-D1b semidwarfing genes led to impressive increases in wheat (Triticum aestivum) yields during the Green Revolution. The reduction in stem elongation in varieties containing these alleles is caused by a limited response to the phytohormone gibberellin (GA), resulting in improved resistance to stem lodging and yield benefits through an increase in grain number. Rht-B1 and Rht-D1 encode DELLA proteins, which act to repress GA-responsive growth, and their mutant alleles Rht-B1b and Rht-D1b are thought to confer dwarfism by producing more active forms of these growth repressors. While no semidwarfing alleles of Rht-A1 have been identified, we show that this gene is expressed at comparable levels to the other homeologs and represents a potential target for producing novel dwarfing alleles. In this study, we have characterized additional dwarfing mutations in Rht-B1 and Rht-D1. We show that the severe dwarfism conferred by Rht-B1c is caused by an intragenic insertion, which results in an in-frame 90-bp insertion in the transcript and a predicted 30-amino acid insertion within the highly conserved amino-terminal DELLA domain. In contrast, the extreme dwarfism of Rht-D1c is due to overexpression of the semidwarfing Rht-D1b allele, caused by an increase in gene copy number. We show also that the semidwarfing alleles Rht-B1d and Rht-B1e introduce premature stop codons within the amino-terminal coding region. Yeast two-hybrid assays indicate that these newly characterized mutations in Rht-B1 and Rht-D1 confer "GA-insensitive" dwarfism by producing DELLA proteins that do not bind the GA receptor GA INSENSITIVE DWARF1, potentially compromising their targeted degradation.
矮秆基因 Rht-B1b 和 Rht-D1b 的引入促成了“绿色革命”期间小麦产量的显著提高。含有这些等位基因的品种茎伸长减少是由于对植物激素赤霉素（GA）的反应有限，导致茎倒伏抗性提高，并通过增加粒数提高产量。Rht-B1 和 Rht-D1 编码 DELLA 蛋白，其作用是抑制 GA 响应性生长，其突变等位基因 Rht-B1b 和 Rht-D1b 被认为通过产生更多这些生长抑制剂的活性形式而导致矮化。虽然尚未鉴定出 Rht-A1 的半矮化等位基因，但我们表明该基因的表达水平与其他同源基因相当，代表了产生新型矮化等位基因的潜在靶标。在这项研究中，我们对 Rht-B1 和 Rht-D1 中的其他矮化突变进行了特征描述。我们表明，Rht-B1c 赋予的严重矮化是由内含子插入引起的，该插入导致转录本中 90bp 的框内插入和高度保守的氨基末端 DELLA 结构域内预测的 30 个氨基酸插入。相比之下，Rht-D1c 的极端矮化是由于半矮化等位基因 Rht-D1b 的过表达引起的，这是由于基因拷贝数增加所致。我们还表明，半矮化等位基因 Rht-B1d 和 Rht-B1e 在氨基末端编码区引入了过早的终止密码子。酵母双杂交测定表明，Rht-B1 和 Rht-D1 中的这些新鉴定的突变通过产生不与 GA 受体 GA INSENSITIVE DWARF1 结合的 DELLA 蛋白赋予“GA 不敏感”矮化，可能使其靶向降解受到损害。
