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
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.