CHLOROTIC LESION RESPONSE OF MAIZE TO CERCOSPORA-ZEAE-MAYDIS AND ITS EFFECT ON GRAY LEAF-SPOT DISEASE

Citation
Jt. Freppon et al., CHLOROTIC LESION RESPONSE OF MAIZE TO CERCOSPORA-ZEAE-MAYDIS AND ITS EFFECT ON GRAY LEAF-SPOT DISEASE, Phytopathology, 86(7), 1996, pp. 733-738
Citations number
28
Categorie Soggetti
Plant Sciences
Journal title
ISSN journal
0031949X
Volume
86
Issue
7
Year of publication
1996
Pages
733 - 738
Database
ISI
SICI code
0031-949X(1996)86:7<733:CLROMT>2.0.ZU;2-I
Abstract
Chlorotic lesions (CL) developed on certain F-2:3 and F-3:4 families d erived from a cross between a previously described CL-resistant maize inbred (NC250A) and a susceptible (S) lesion maize inbred (B73) in res ponse to infection by Cercospora zeae-maydis. CL trait expression was consistent (displayed phenotype across locations at midepidemic assess ment) on 12 of the 60 F-2:3 families studied. Heterogeneous (CL/S) les ion phenotypes were displayed by 36 families at midepidemic. Consisten t, characteristic S lesions were exhibited by 12 F-2:3 families. Selec ted F-2:3 families representing each lesion type class produced F-3:4 progenies that predominantly displayed lesion phenotypes consistent wi th the parental class. Families exhibiting the CL trait at midepidemic assessment had significantly lower apparent infection rates, percent leaf area affected (PLAA), and area under disease progress curves base d on PLAA and lesion area. Heterogeneous families tended to have inter mediate mean gray leaf spot severity, whereas disease severity and pro gress were highest on homozygous S lesion-type families. Because the C L trait was associated with decreased gray leaf spot severity and prog ress, selection for this trait in a population derived from NC250A x B 73 would decrease the impact of epidemics caused by C. zeae-maydis. Se gregation analyses of midepidemic CL responses of F-2:3 and F-3:4 fami lies during 1992 and 1993 suggested the presence of a major factor in inheritance of the CL response. Segregation ratios observed at a later assessment date during 1992 did not support monogenic inheritance.