大豆黄绿叶突变体NJ9903-5性状表现与基因定位研究

叶色突变体既可用于作物叶绿素合成、降解和光合作用等研究,也可作为标记基因为作物育种利用。本文对一个新发现的大豆黄绿叶自发突变体NJ9903-5进行遗传鉴定。结果表明:从对生真叶开始,该突变体幼嫩叶呈黄色,随着生长叶片逐渐转变为绿色。黄化叶片叶绿体数目下降,基质片层减少且排列疏松,叶绿素a、b、类胡萝卜素含量都极显著下降;其对株高、主茎节数、单株粒数、单株荚数有负效应,但对百粒重、蛋白质含量、油脂含量影响小,杂交后代中上述性状变异大。3个杂交群体遗传分析表明该性状受一对隐性核基因控制,利用F2隐性个体将目标基因ygl定位在SSR标记BARCSOYSSR_02_1445和BARCSOYSSR_02_1477之间约366 kb区段,包含36个候选基因。测序分析发现在突变体中,叶绿体膜转运蛋白相关基因Glyma.02G233700第1个外显子第38个碱基G缺失,移码突变导致蛋白翻译提前终止,结合前人研究结果,推测其为黄绿叶的目的基因ygl。

Gene Mapping and Character Performance of A Yellow-green Leaf Mutant NJ9903-5 in Soybean

Leaf color mutants are specific experimental materials in the study of chlorophyll synthesis,degradation and photosynthesis and can also be used as a marker trait in crop breeding.The results of the study on a spontaneous yellow-green seedling mutant NJ9903-5 showed that the young leaves from the opposite unifoliolate at VC growth stage to each trifoliolate ones exhibited yellow and gradually turn to green till mature.The number of chloroplast in yellow leaves decreased with less and loosely arranged stroma lamellae.Moreover,the contents of chlorophyll a,b and carotenoid significandy decreased.A large number of variations of seven agronomic and quality traits were found in two F2 populations from the crosses between NJ9903-5 and normal parents.The mutant F2 plants had significantly low values of plant height,number of nodes on main stem,pods and seeds number per plant in comparison with normal plants,while no significant differences were detected for 100-seed weight,protein and oil content.Genetic analysis revealed that the mutant trait was controlled by a recessive nuclear gene designated as ygl.The gene was mapped in a physical interval of 366 kb region between SSR markers BARCSOYSSR 02 1445 and BARCSOYSSR 02 1477 on chromosome 2.Among the 36 annotation genes in the region,Glyma.02G233700,a predicted chloroplast membrane transport protein,was identified.Sequencing analysis showed that a deletion of G nucleotide at the 38 base of exon 1 was detected in the NJ9903-5,and the frame shift mutation of Glyma.02G233700 can lead to a premature termination of the protein translation.