Silverstone A L, Mak P Y, Martínez E C, Sun T P
Department of Botany, Duke University, Durham, North Carolina 27708-1000, USA.
Genetics. 1997 Jul;146(3):1087-99. doi: 10.1093/genetics/146.3.1087.
We have identified a new locus involved in gibberellin (GA) signal transduction by screening for suppressors of the Arabidopsis thaliana GA biosynthetic mutant gal-3. The locus is named RGA for repressor of gal-3. Based on the recessive phenotype of the digenic rga/gal-3 mutant, the wild-type gene product of RGA is probably a negative regulator of GA responses. Our screen for suppressors of gal-3 identified 17 mutant alleles of RGA as well as 10 new mutant alleles at the previously identified SPY locus. The digenic (double homozygous) rga/gal-3 mutants are able to partially repress several defects of gal-3 including stem growth, leaf abaxial trichome initiation, flowering time, and apical dominance. The phenotype of the trigenic mutant (triple homozygous) rga/spy/gal-3 shows that rga and spy have additive effects regulating flowering time, abaxial leaf trichome initiation and apical dominance. This trigenic mutant is similar to wild type with respect to each of these developmental events. Because rga/spy/gal-3 is almost insensitive to GA for hypocotyl growth and its bolting stem is taller than the wild-type plant, the combined effects of the rga and spy mutations appear to allow GA-independent stem growth. Our studies indicate that RGA lies on a separate branch of the GA signal transduction pathway from SPY, which leads us to propose a modified model of the GA response pathway.
通过筛选拟南芥赤霉素(GA)生物合成突变体gal-3的抑制子,我们鉴定出了一个参与GA信号转导的新位点。该位点被命名为RGA,即gal-3的抑制子。基于双基因rga/gal-3突变体的隐性表型,RGA的野生型基因产物可能是GA反应的负调控因子。我们对gal-3抑制子的筛选鉴定出了17个RGA突变等位基因以及先前鉴定的SPY位点的10个新突变等位基因。双基因(双纯合)rga/gal-3突变体能够部分抑制gal-3的几种缺陷,包括茎生长、叶背毛状体起始、开花时间和顶端优势。三基因突变体(三纯合)rga/spy/gal-3的表型表明,rga和spy在调节开花时间、叶背毛状体起始和顶端优势方面具有累加效应。在这些发育事件的每一个方面,这个三基因突变体都与野生型相似。由于rga/spy/gal-3对GA诱导的下胚轴生长几乎不敏感,并且其抽薹茎比野生型植株高,rga和spy突变的联合效应似乎允许不依赖GA的茎生长。我们的研究表明,RGA位于与SPY不同的GA信号转导途径分支上,这使我们提出了一个GA反应途径的修正模型。