Campa Ana, Rodríguez-Suárez Cristina, Giraldez Ramón, Ferreira Juan José
Área de Cultivos Hortofrutícolas y Forestales, SERIDA, Apdo, 13, 33300 Villaviciosa, Asturias, Spain.
BMC Plant Biol. 2014 Apr 30;14:115. doi: 10.1186/1471-2229-14-115.
Bean anthracnose is caused by the fungus Colletotrichum lindemuthianum (Sacc. & Magnus) Lams.- Scrib. Resistance to C. lindemuthianum in common bean (Phaseolus vulgaris L.) generally follows a qualitative mode of inheritance. The pathogen shows extensive pathogenic variation and up to 20 anthracnose resistance loci (named Co-), conferring resistance to specific races, have been described. Anthracnose resistance has generally been investigated by analyzing a limited number of isolates or races in segregating populations. In this work, we analyzed the response against eleven C. lindemuthianum races in a recombinant inbred line (RIL) common bean population derived from the cross Xana × Cornell 49242 in which a saturated linkage map was previously developed.
A systematic genetic analysis was carried out to dissect the complex resistance segregations observed, which included contingency analyses, subpopulations and genetic mapping. Twenty two resistance genes were identified, some with a complementary mode of action. The Cornell 49242 genotype carries a complex cluster of resistance genes at the end of linkage group (LG) Pv11 corresponding to the previously described anthracnose resistance cluster Co-2. In this position, specific resistance genes to races 3, 6, 7, 19, 38, 39, 65, 357, 449 and 453 were identified, with one of them showing a complementary mode of action. In addition, Cornell 49242 had an independent gene on LG Pv09 showing a complementary mode of action for resistance to race 453. Resistance genes in genotype Xana were located on three regions involving LGs Pv01, Pv02 and Pv04. All resistance genes identified in Xana showed a complementary mode of action, except for two controlling resistance to races 65 and 73 located on LG Pv01, in the position of the previously described anthracnose resistance cluster Co-1.
Results shown herein reveal a complex and specific interaction between bean and fungus genotypes leading to anthracnose resistance. Organization of specific resistance genes in clusters including resistance genes with different modes of action (dominant and complementary genes) was also confirmed. Finally, new locations for anthracnose resistance genes were identified in LG Pv09.
菜豆炭疽病由真菌菜豆炭疽菌(Colletotrichum lindemuthianum (Sacc. & Magnus) Lams.- Scrib.)引起。普通菜豆(Phaseolus vulgaris L.)对菜豆炭疽菌的抗性通常遵循质量遗传模式。该病原菌表现出广泛的致病性变异,已描述了多达20个炭疽病抗性位点(命名为Co-),这些位点赋予对特定小种的抗性。炭疽病抗性通常通过分析分离群体中有限数量的分离株或小种来进行研究。在本研究中,我们分析了一个重组自交系(RIL)普通菜豆群体对11个菜豆炭疽菌小种的反应,该群体源自Xana×Cornell 49242的杂交,此前已构建了一个饱和连锁图谱。
进行了系统的遗传分析以剖析观察到的复杂抗性分离情况,包括列联分析、亚群分析和基因定位。鉴定出22个抗性基因,其中一些具有互补作用模式。Cornell 49242基因型在连锁群(LG)Pv11末端携带一个复杂的抗性基因簇,对应于先前描述的炭疽病抗性簇Co-2。在这个位置,鉴定出了对小种3、6、7、19、38、39、65、357、449和453的特异性抗性基因,其中一个表现出互补作用模式。此外,Cornell 49242在LG Pv09上有一个独立基因,对小种453的抗性表现出互补作用模式。Xana基因型中的抗性基因位于涉及LG Pv01、Pv02和Pv04的三个区域。Xana中鉴定出的所有抗性基因均表现出互补作用模式,但位于LG Pv01上、先前描述的炭疽病抗性簇Co-1位置的两个控制对小种65和73抗性的基因除外。
本文所示结果揭示了菜豆和真菌基因型之间导致炭疽病抗性的复杂且特异性的相互作用。还证实了包括具有不同作用模式的抗性基因(显性基因和互补基因)在内的抗性基因在簇中的组织方式。最后,在LG Pv09中鉴定出了炭疽病抗性基因的新位置。