水稻类病变突变体cdb的遗传分析与基因定位

Genetic Analysis and Gene Mapping of Lesion Mimic Mutant cdb in Rice(Oryza sativa L.)

水稻类病变突变体是解析植物细胞死亡和相关抗性机制的重要材料。本研究通过EMS诱变粳稻品种‘黎榆B’,获得了一个遗传稳定的类病变突变体cdb(Cell death like blast)。突变体从分蘖期开始在叶片上出现中间部位呈褐色、边缘为橙黄色的不规则坏死斑,出斑2~3周之内扩散至整个叶片和叶鞘,成熟期坏死斑蔓延至整株,叶片早枯,植株失去再生能力。与野生型相比较,突变体cdb粒型发生显著变化,粒宽增加,粒厚减小,花粉育性有一定丧失,结实率显著下降。遮光实验结果表明,cdb病斑表型的发生受自然光照的激发。光合色素含量测定和光合速率指标测量结果发现,突变体cdb的光合色素含量与野生型相比明显降低,净光合速率呈极显著下降。遗传分析结果表明,突变体cdb的病斑性状受单隐性核基因控制。基因定位发现该基因位于12号染色体上,在标记RM12CD05和RM1047之间约5.0 cM区域内,该区域内未存在明确定位克隆的水稻类病变突变基因,说明cdb是一种新的水稻类病变突变体。本研究为下一步该类病变基因的克隆、功能分析、类病变形成机制探究以及突变基因应用提供理论依据。

Lesion mimic mutant in rice(Oryza sativa L.)are important materials for analyzing plant cell death and related resistance mechanisms.In this study,cdb(cell death like blast)is a genetic stability lesion mimic mutant from the japonica rice’LiyuB’induced by ethyl methylsulfonate(EMS).From the tillering stage,the mutant showed brown irregular necrotic spots in the middle and orange-yellow edges on the leaves,spread to the entire leaf and leaf sheath within 2~3 weeks.At mature stage,the necrosis spread almost all of leaves and finally resulted in the senescence of leaves,and plants lost ability to regenerate.Compared with the wild type(WT),grain width was increased,grain thickness,pollen fertility,seed setting rate were significantly reduced.The initiation of the lesions phenotype was stimulated by nature light.The results showed that the photosynthetic pigment content and the net photosynthetic rate of the mutant cdb was significantly reduced.Genetic analysis indicated that the mutant spot phenotype was controlled by a single recessive nuclear gene.Gene mapping showed that the gene was mapping in the 5.0 cM region between markers RM12CD05 and RM1047 in chromosome 12,and there are no lesion mimic mutant clearly located and cloned in this region,indicating that cdb was a new lesion mimic mutant in rice.This study provides a theoretical basis for the further cloning,functional analysis,the formation mechanism of similar lesions and the application of mutant genes.