Inheritance of kernel resistance to Fusarium graminearum in maize

Inheritance of maize (Zea mays L.) kernel resistance to ear rot caused by Fusarium graminearum Schwabe was investigated in generations derived from a cross between resistant (CO325) and susceptible (CO265) maize inbred parents. Parents, F1, F2, and backcross generations were evaluated in two locatio...

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Bibliographic Details
Published in:The Journal of heredity 1996-09, Vol.87 (5), p.382-385
Main Authors: Chungu, C. (McGill University, Quebec, Canada.), Mather, D.E, Reid, L.M, Hamilton, R.I
Format: Article
Language:English
Subjects:
AMANDE DE LA GRAINE
Botany
Corn
DISTRIBUCION GEOGRAFICA
DISTRIBUTION GEOGRAPHIQUE
ENFERMEDADES FUNGOSAS
Fungi
Fusarium graminearum
GENETICA
Genetics
GENETIQUE
GERMEN
GIBBERELLA ZEAE
HEREDITE
Heredity
HERENCIA GENETICA
MALADIE FONGIQUE
ONTARIO
QUEBEC
RESISTANCE AUX MALADIES
RESISTENCIA A LA ENFERMEDAD
VARIACION GENETICA
VARIATION GENETIQUE
ZEA MAYS
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Summary:Inheritance of maize (Zea mays L.) kernel resistance to ear rot caused by Fusarium graminearum Schwabe was investigated in generations derived from a cross between resistant (CO325) and susceptible (CO265) maize inbred parents. Parents, F1, F2, and backcross generations were evaluated in two locations in eastern Canada in 1993 and 1994. Plants were inoculated with a macroconidial suspension using a kernel-stab method 15 days after silk emergence. Disease severity was assessed at harvest using a seven-class rating scale. Significant differences were observed among the generation means in all environments. In general, the F1 did not differ significantly from the resistant parent except at one location in 1993. The frequency distribution of the F2 and backcross generations showed continuous variation. Generation means analysis indicated that resistance to F. graminearum was under genetic control with both simple (additive and dominance) and digenic (dominance X dominance) effects contributing to the total genetic variation among the generation means. Weighted least square regression indicated that more than 68% of the genetic variation could be explained by additive effects. Estimates of the number of effective factors affecting kernel resistance ranged from 4.6 to 13.7
ISSN:0022-1503
1465-7333
1471-8505
DOI:10.1093/oxfordjournals.jhered.a023019