花生油酸和亚油酸含量的遗传模式分析

【目的】利用F2遗传群体分析油酸和亚油酸含量的遗传模式，为高油酸种质的利用奠定基础。【方法】利用高油酸亲本wt08-0932和wt08-0934与普通（低）油酸含量品种配制杂交组合，建立不同杂交组合的遗传模型，并进行遗传参数估计，明确控制油酸性状的主基因个数、加性或显性效应值、遗传力等。【结果】获得控制油酸和亚油酸性状遗传的2对主基因加性-显性-上位性遗传模型，油酸和亚油酸性状的2对主基因遗传力分别为66%-89%和70%-85%，并存在多基因效应。控制油酸含量的2个主基因显性效应值均为负值，控制亚油酸含量的2个主基因的显性效应值均为正值。【结论】花生的油酸和亚油酸性状分别由2对主基因控制，同时存在基因互作及多基因效应。第一对主基因的加性和显性效应均大于第二对主基因。2对主基因同时变异形成高油酸性状；2对主基因之间的加性和显性效应的差异导致在1对主基因变异时形成中低油酸含量和中高油酸含量的性状表现。

Inheritance Analysis of Oleic Acid and Linoleic Acid Content of Arachis hypogaea L.

【Objective】In order to understand the genetic basis of oleic acid content in peanut,the genetic models of oleic acid and linoleic acid was proposed by using F2 populations derived from crosses between normal-oleic and high-oleic genotypes.【Method】Four cross combinations were made between 4 genotypes with normal oleic acid content and 2 high-oleic genotypes,wt08-0932 and wt08-0934,respectively.The number of major genes controlling oleic acid and linoleic acid contents,their additive and/or dominant effects and heritabilities were estimated using genetic parameters based on genetic models.【Result】The results indicated that oleic acid and linoleic acid contents were controlled by two major genes with additive-dominant-epistatic effects.The heritabilities of the two major genes were 66%-89% for oleic acid and 70%-85% for linoleic acid,respectively,implying the existence of polygenic effects.Negative dominant effects were observed for both major genes controlling oleic acid content,while positive dominant effects were detected for linoleic acid content.【Conclusion】The oleic and linoleic acid contents in peanut were controlled by two major genes together with gene interactions and polygene effects.Both of the additive and dominant effects of the first major gene were much higher than that of the second one.The high oleic acid content resulted from the mutation effects of the two major genes and the medium-low and medium-high oleic acid content was the result of the single gene mutation depending on the additive and dominant effects of the individual gene.