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水稻脆杆突变体bcm581-1茎杆形态结构观察、理化测定和遗传分析
引用本文:沈革志,王新其,王江,宛新杉,李琳,张景六.水稻脆杆突变体bcm581-1茎杆形态结构观察、理化测定和遗传分析[J].实验生物学报,2002,35(4):307-312.
作者姓名:沈革志  王新其  王江  宛新杉  李琳  张景六
作者单位:[1]上海市农业科学院作物所,上海201106 [2]中国科学院上海植物生理研究所,上海200032
摘    要:在根癌农杆菌介导的Ds转座因子转化的水稻株系中,发现了脆杆突变体bcm581-1。经Basta除草剂抗性检测和PCR检测,这个脆杆突变不是由Ds转座因子插入引起;通过光学显微镜观察发现突变体的小维管束数目多于对照,小维管束之间的凹陷比对照深,而皮层纤维细胞层数少于对照;扫描电镜观察发现突变体表皮细胞外侧的硅质没有对照丰富。虽然,单位面积内的细胞数与对照相近。但是,突变体的细胞壁薄,维管束内纤维细胞壁的加厚程度也低于对照。因此,细胞腔明显比对照大。茎杆的力学测定结果表明:突变体的载荷低于对照9.6倍;延伸低5.4倍;延伸率低6.9倍;应力低6倍。茎杆的相对含水量和粗纤维含量测定表明:突变体的含水量高于对照3.5%,粗纤维含量则低于对照8.12%。bcm581-1与中花11号杂交试验显示,F1植株全部正常,F2群体中,正常杆和脆杆以3:1分离,以中花11号为回交亲本的F181植株,表现正常;而以脆杆为回交亲本的F181植株,正常茎杆和脆杆则以1:1分离,结果表明:bcm581-1的茎杆变脆是受隐性单基因控制的突变。

关 键 词:茎杆  突变体  植株  维管束  回交  粗纤维含量  水稻  对照  正常  观察

The morphology observation, mechanics intensity test and genetic analysis of brittle culm mutant bcm581-1 in rice]
Ge Zhi Shen,Xin Qi Wang,Jiang Wang,Xin Shan Wan,Lin Li,Jing Liu Zhang.The morphology observation, mechanics intensity test and genetic analysis of brittle culm mutant bcm581-1 in rice][J].Acta Biologiae Experimentalis Sinica,2002,35(4):307-312.
Authors:Ge Zhi Shen  Xin Qi Wang  Jiang Wang  Xin Shan Wan  Lin Li  Jing Liu Zhang
Institution:Crop Institute, Shanghai Academy of Agricultural Sciences, Shanghai 201106.
Abstract:A rice brittle culm mutant bcm581-1 which derived from the Ds transposone transformation population was found, but the mutant was identified that it was not to be induced by Ds transposone insertion through PCR. The examination of the vascular bundle and cortical fibre cells in culm under the light and electron microscope showed that, the number of cortical vascular bundle of mutant was much more, the hollow among the cortical vascular bundle was deeper, and the cell walls of cortical fibre cells were thinner than the normal. The test of culm mechanics intensity showed that the load, elongation, strain, and stress of bcm581-1 were 5-9 times lower than normal. The moisture content and the wide fibre content of culm were test, the former was 3.5% higher, but the latter was 8.12% lower than normal. The analysis of genetic segregation in F2 and F1B1 population indicated that the brittle culm mutant was controlled by one recessive gene.
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