Genetic analysis of maize streak virus disease resistance on tropical maize.
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Maize streak virus (MSV) disease, transmitted by leafhoppers (Cicadulina mbila) is a major contributing factor to low maize yields in Africa. The disease threatens maize production in Zimbabwe, thus the importance of breeding Zimbabwe maize varieties that carry resistance to this disease. Cimmyt has developed inbred lines, good for other traits, for example, high general combining ability (GCA) effects for grain yield performance, but susceptible to MSV hence efforts are being made in CIMMYT to introduce MSV resistance genes from MSV resistant donor lines known to be good for important traits, especially yield, but bad for MSV resistance. This study was designed to assess newly developed tropical maize inbred lines with complete resistance to MSV and to compare disease progression between the MSV susceptible and resistant inbred lines artificially infect plants with virulent leafhoppers. Breeders usually cross two resistant parents to exploit the potential contribution of beneficial resistance alleles originating from them to generate transgressive segregation that can lead the development of new maize inbred lines with much higher levels of resistance to MSVD and desirable agronomic traits. Twelve inbred lines from CIMMYT were evaluated to determine their level of resistance. Genotype effects on MSV scores were significant from week 1-6 as well as for the average (p < 0.05). Significant effects on MSV scores were also observed on each week interval, except for week 4. Broad-sense heritability (H2) estimates for MSV scores was high (<50%) on each week interval as well as for the average MSV score. Genotypic effects showed to be more important than the environmental variances on each week MSV recordings were taken. This study showed that inbred line CML536 was highly resistant confirming previous observations made with artificial infection in Zimbabwe. Candidate lines CL1210634 and CL1210635 showed complete resistance to MSV meaning they may share the same major gene Msv1 with CML539 and CML536 check inbred. The data we obtained provide quantification of conclusions of visual observations: (a) some varieties bred for resistance are less affected by MSD than others, even when infected at the same stage; (b) early infection is more damaging than late infection, but resistant varieties differ in their response, and; (c) varieties carrying no resistance can be little damaged if infected late. In order to avoid the over-dependence on Msv1, further studies should be carried out to identify a second gene for MSD resistance to compliment Msv1 gene in conferring enhanced and durable resistance to MSD. Enhanced resistance through additional phenotypic selection will also help prevent possible breakdown of Msv1.