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Quantitative and qualitative trait loci affecting host-plant response toExserohilum turcicumin maize (Zea maysL.)

โœ Scribed by P. J. Freymark; M. Lee; W. L. Woodman; C. A. Martinson


Publisher
Springer
Year
1993
Tongue
English
Weight
877 KB
Volume
87
Category
Article
ISSN
0040-5752

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โœฆ Synopsis


Molecular markers at 103 loci were used to identify the location of quantitative sources of resistance to Exserohilum turcicum in 150 F2โˆถ3 lines of a B52/Mo17 maize population. Host-plant response was measured in terms of the average number of lesions per leaf, the average percent leaf tissue diseased (severity), and the average size of lesions. The location of quantitative trait loci were compared with three loci having known qualitative effects, namely Ht1, Ht2 and bx1. Chromosomal regions containing the Ht1 and Ht2 loci showed a small contribution in determining lesion size, even though alleles with dominant, qualitative effects at these loci have never been reported in either inbred parent. Similar effects were not observed for the number of lesions or for disease severity. Likewise, some contribution was observed for chromosomal regions encompassing the bx1 locus in determining lesion size but not the number of lesions or disease severity. Overall the contribution of loci in the vicinity of Ht1, Ht2 and bx1 was small relative to variation attributable to loci with quantitative effects identified in this study. Molecular-marker-facilitated mapping concurred with previous reciprocal translocation mapping studies on the importance of chromosomes 3, 5 and 7, despite the fact that these studies utilized diverse sources of resistant germplasm.


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Molecular-marker-facilitated investigati
โœ P. J. Freymark; M. Lee; C. A. Martinson; W. L. Woodman ๐Ÿ“‚ Article ๐Ÿ“… 1994 ๐Ÿ› Springer ๐ŸŒ English โš– 862 KB

RFLPs were used to investigate components of host-plant response to Exserohilum turcicum in 150 unselected F2โˆถ3 lines of a B52/Mo17 maize population. Following inoculation with spore suspensions of the pathogen (race 0), components of disease development were measured and then quantitative trait map