目的:大麦(大麦)双突变体Hv-Hd/tw2,通过杂交形成,以遗传表型不稳定性和几个新特征为特征,如苞片/叶状结构,长钉上的裸露缝隙,以及基本和异位花的广泛变化,在单个突变体中不存在。这些特征中的一些类似于生长素分布中的突变,因此,这项研究的目的是确定生长素失衡是否与表型变异和不稳定性有关。因此检查了生长素抑制剂和2,4-D(2,4-二氯苯氧基乙酸)对基本和异位花变异的影响,以及2,4-D对穗部结构的影响。
方法:在愈伤组织培养物和单个同源Hv-tw2和Hv-Hooded/Kap(在BKn3基因中)突变体和替代双突变体系的完整植物中,比较了表型不稳定性的特征以及生长素抑制剂和2,4-D的作用:来自远端杂种世代(F9-F10)中单个植物的后代,这些后代都具有相同的B对于完整的植物,两种生长素抑制剂,9-羟基芴-9-羧酸(HFCA)和对氯苯氧基异丁酸(PCIB),被使用。
结果:Hv-tw2突变体的愈伤组织生长和花/穗结构对HFCA和PCIB的反应不同。观察到暴露于生长素抑制剂后正常基础花的增加和由2,4-D引起的频率降低,异位花的光谱也发生了变化,尤其是那些有性器官的人,但效果取决于基因型。暴露于2,4-D降低了Hv-tw2中短间隙和浆片转化的频率,以及双突变体中长裸露间隙的频率。
结论:生长素抑制剂和2,4-D的作用表明,在花序/花原基的各个区域出现了异位生长素最大值或缺陷。根据观察到的表型不稳定性,可以检测到异位花结构发育的明确趋势,从芒上微不足道的生长到器官不育的花。表型不稳定的大麦双突变体为研究基因表达模块和趋势顺序提供了非常有前途的遗传系统。
OBJECTIVE: Barley (Hordeum vulgare) double mutants Hv-Hd/tw2, formed by hybridization, are characterized by inherited phenotypic instability and by several new features, such as bract/leaf-like structures, long naked gaps in the spike, and a wide spectrum of variations in the basic and ectopic flowers, which are absent in single mutants. Several of these features resemble those of mutations in auxin distribution, and thus the aim of this study was to determine whether auxin imbalances are related to phenotypic variations and instability. The effects of auxin inhibitors and 2,4-D (2,4-dichlorophenoxyacetic acid) on variation in basic and ectopic flowers were therefore examined, together with the effects of 2,4-D on spike structure.
METHODS: The character of phenotypic instability and the effects of auxin inhibitors and 2,4-D were compared in callus cultures and intact plants of single homeotic Hv-tw2 and Hv-Hooded/Kap (in the BKn3 gene) mutants and alternative double mutant lines: offspring from individual plants in distal hybrid generations (F9-F10) that all had the same BKn3 allele as determined by DNA sequencing. For intact plants, two auxin inhibitors, 9-hydroxyfluorene-9-carboxylic acid (HFCA) and p-chlorophenoxyisobutyric acid (PCIB), were used.
RESULTS: Callus growth and flower/spike structures of the Hv-tw2 mutant differed in their responses to HFCA and PCIB. An increase in normal basic flowers after exposure to auxin inhibitors and a decrease in their frequencies caused by 2,4-D were observed, and there were also modifications in the spectra of ectopic flowers, especially those with sexual organs, but the effects depended on the genotype. Exposure to 2,4-D decreased the frequency of short gaps and lodicule transformations in Hv-tw2 and of long naked gaps in double mutants.
CONCLUSIONS: The effects of auxin inhibitors and 2,4-D suggest that ectopic auxin maxima or deficiencies arise in various regions of the inflorescence/flower primordia. Based on the phenotypic instability observed, definite trends in the development of ectopic flower structures may be detected, from insignificant outgrowths on awns to flowers with sterile organs. Phenotypically unstable barley double mutants provide a highly promising genetic system for the investigation of gene expression modules and trend orders.