INTERVAL MAPPING OF GENES FOR QUANTITATIVE RESISTANCE OF MAIZE TO SETOSPHAERIA-TURCICA, CAUSE OF NORTHERN LEAF-BLIGHT, IN A TROPICAL ENVIRONMENT

Citation
Al. Dingerdissen et al., INTERVAL MAPPING OF GENES FOR QUANTITATIVE RESISTANCE OF MAIZE TO SETOSPHAERIA-TURCICA, CAUSE OF NORTHERN LEAF-BLIGHT, IN A TROPICAL ENVIRONMENT, Molecular breeding, 2(2), 1996, pp. 143-156
Citations number
57
Categorie Soggetti
Biology,"Plant Sciences","Biothechnology & Applied Migrobiology
Journal title
ISSN journal
13803743
Volume
2
Issue
2
Year of publication
1996
Pages
143 - 156
Database
ISI
SICI code
1380-3743(1996)2:2<143:IMOGFQ>2.0.ZU;2-J
Abstract
Quantitative trait loci (QTL) involved in the resistance of maize to S etosphaeria turcica, the causal agent of northern leaf blight, were lo cated by interval mapping analysis of 121 F-2:3 lines derived from a c ross between Mo17 (moderately resistant) and B52 (susceptible). A link age map spanning 112 RFLP loci with 15 cM mean interval length was con structed, based on marker data recorded in a previous study. Field tes ts with artificial inoculation were conducted at three sites in tropic al mid- to high-altitude regions of Kenya, East Africa. Host-plant res ponse was measured in terms of incubation period, disease severity (fi ve scoring dates), and the area under the disease progress curve (AUDP C). Heritability of all traits was high (around 0.75). QTL associated with the incubation period were located on chromosomes 2S and 8L. For disease severity and AUDPC, significant QTL were detected in the putat ive centromeric region of chromosome 1 and on 2S, 3L, 5S, 6L, 7L, 8L a nd 9S. On 2S the same marker interval which carried a gene enhancing l atent period was also associated with reduced disease severity of juve nile plants. QTL on chromosomes 3L, 5S, 7L and 8L were significant acr oss environments but all other QTL were affected by a large genotype x environment interaction. Partially dominant gene action for resistanc e as well as for susceptibility was prevailing. Single QTL explained 1 0 to 38 % of the phenotypic variation of the traits. All but the QTL o n chromosomes 1, 6 and 9 were contributed by the resistant parent Mo17 . On chromosome 8L a QTL mapped to the same region as the major race-s pecific gene Ht2, supporting the hypothesis that some qualitative and quantitative resistance genes may be allelic.