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作 者:李爱宏[1] 武茹[1] 张亚芳[1] 汤雯[1] 吴昌银[2] 潘学彪[1]
机构地区:[1]扬州大学植物功能基因组学江苏省重点实验室 [2]华中农业大学作物遗传改良国家重点实验室,湖北武汉430070
出 处:《中国水稻科学》2006年第4期348-354,共7页Chinese Journal of Rice Science
基 金:国家重大专项"功能基因组和生物芯片"资助项目
摘 要:从T-DNA插入突变体库中筛选获得1份多重颖壳突变体。解剖镜下观察发现其内外稃伸长,同时伴有类颖壳状结构而普遍呈现多重颖壳。在所观察的215朵颖花中,14.27%的颖花没有雌、雄蕊,23.72%的颖花包含有额外小花,62.01%的颖花其雌、雄蕊数耳变化分别为1~3枚和1~9枚,部分颖花的花丝基部可看到泡状透明瘤状物;突变体浆片稃片化而使其颖花在自然条件下不能开放;完全雄性和雌性不育。扫描电镜观察揭示其颖花原基分化正常,但进人雌、雄蕊原基的分化较迟,会继续进行类似多重颖壳状器官的分化;同时,颖花原基进行不均衡分裂,产生数目不等的雌、雄蕊。遗传分析显示该突变是一个单基因控制的隐性性状,并与T-DNA插入表现共分离。推断它是E类基因引起的功能突变。A multi-glume (mg) mutant was obtained by screening the T-DNA inserted mutant pool. Anatomical observation revealed that the florets of the mutant showed elongated leafy paleas/lemmas and palea/lemma-like structures, just llke multi-glumes. In the 215 observed florets of the mutant, 14.27 % failed in forming pistils and stamens; 23.72 % showed extra floret generated on the same rachilla; 62.01% of single floret consisted of one to nine stamens and one to three pistils. And that the transparent bulged vesile-like tissue could be observed at the base of filament in some cases. The mutant showed glumaceous lodicules which prevented the florets from opening in natural conditions, and absolute male and female sterility was another obvious characteristics of this mutant. The process of floral organ morphogenesis was investigated using scanning electron microscopy (SEM), and the results showed that no difference in phenotype of floret primordial was found between the wild type and the mutant, but for the mutant, the beginning of stamen and pistil primordial differentiation was later compared with the wide type and the palea/lemma-like structure continually differentiated after the normal palea and lemma bad formed. Furthermore, un-equipotent division of floral primordial in the mutant caused the variation in numbers of stamens and pistils. Genetic analyses supported this mutation phenotype was a recessive trait controlled by a single gene and co-segregated with the T-DNA. According to its phenotype, it was deduced the mutant was the result of homeotic conversion from the E loss-of-function.
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