Genetic mapping of maize streak virus resistance from the Mascarene source. II. Resistance in line CIRAD390 and stability across germplasm

Citation
A. Pernet et al., Genetic mapping of maize streak virus resistance from the Mascarene source. II. Resistance in line CIRAD390 and stability across germplasm, THEOR A GEN, 99(3-4), 1999, pp. 540-553
Citations number
33
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
THEORETICAL AND APPLIED GENETICS
ISSN journal
00405752 → ACNP
Volume
99
Issue
3-4
Year of publication
1999
Pages
540 - 553
Database
ISI
SICI code
0040-5752(199908)99:3-4<540:GMOMSV>2.0.ZU;2-S
Abstract
The streak disease has a major effect on maize in sub-Saharan Africa. Vario us genetic factors for resistance to the virus have been identified and map ped in several populations; these factors derive from different sources of resistance. We have focused on the Reunion island source and have recently identified several factors in the D211 line. A second very resistant line, CI-RAD390, was crossed to;the same susceptible;parent, B73. The linkage map comprised 124 RFLP markers, of which 79 were common with the D211xB73 map. A row-column design was used to evaluate the resistance to maize streak vi rus (MSV) of 191 F-2:3 families under artificial infestation at two locatio ns: Harare (Zimbabwe) and in Reunion island. Weekly ratings of resistance w ere taken and disease incidence and severity calculated. QTL analyses were conducted for each scoring date and for the integration over time of the di sease scores, of incidence, and of severity. Heritability estimates (71-98% ) were as high as for the D211xB73 population. Eight QTLs were detected on chromosomes 1, 2, 3, 5 (two QTLs), 6, 8, and 10. The chr1-QTL explained the highest proportion of phenotypic variation, about 45%. The QTLs on chromos omes 1, 2, and la were located in the same chromosomal bin as QTLs for MSV resistance in the D211xB73 population. In a simultaneous fit, QTLs explaine d together 43-67% of the phenotypic variation. The QTLs on chromosomes 3, 5 , and 6 appeared to be specific for one or the other component of the resis tance. For the chr3-QTL, resistance was contributed by the susceptible pare nt. There were significant QTL x environment interactions for some of the v ariables studied, but QTLs were stable in the two environments. They also a ppeared to be stable over time. Global gene action ranged from partial domi nance to overdominance, except for disease severity. Some additional putati ve QTLs were also detected. The major QTL on chromosome 1 seemed to be comm on to the other sources of resistance, namely Tzi4, a tolerant line from II TA, and CML202 from CI-MMYT. However, the distribution of the other QTLs wi thin the genome revealed differences in Reunion germplasm and across these other resistance sources. This diversity is of great importance when consid ering the durability of the resistance.