Mode of Gene Action for Resistance in Maize to Maize Streak Virus

Abstract

Maize streak virus (MSV) transmitted by Cicadulina leafhoppers causes severe yield loss of maize (Zea mays L.) in Africa. This paper summarizes our studies on gene action for resistance to MSV using generation mean analysis. Crosses were made between a resistant inbred (IB32) and four susceptible inbreds (BI4, B68, B73, and Moi7). A total of II 255 plants from the four sets of biparentul crosses, their F2, backcross, and F3 progenies were grown in four experiments under severe artifically induced MSV epiphytotics at the International Institute of Tropical Agriculture (IITA), Ibadan, Nigeria. Severity of streak symptoms on test plants was classified on a five‐point scale based on the amount of streaking of leaves. Under severe artificial infestation inside a screenhouse, average ratings of resistant and susceptible parents were 1.3 and 5.0, respectively. The average F1 rating was 3.13, which was close to the mean midparent value (3.15). The average F2 rating was 2.83, which was 0.3 units more resistant than the F1 value. The average rating of four F1 crosses in the field was 2.22, 0.81 units more resistant than the mean midparental value (3.03). Average rating of the F2 populations was 2.22, which was similar to that of the F1 (2.27). Backcross ratings were close to mean of the F1 and recurrent parent. Individual F3 plants derived from same rating of F2 plants showed considerable variation in ratings. Resistance to MSV from IB32 appeared to be inherited quantitatively with relatively small numbers of genes involved. The symptoms of MSV varied with the genetic background of the susceptible parent. Simple recurrent selection or modified backcross breeding methods could be used to breed for MSV resistance in Africa.

Breeding maize lines for complete and partial resistance to maize streak virus (MSV)

“…The disease can cause serious damage to maize crops and complete yield losses have been reported (Guthrie, 1978). Widespread epidemics occurred in many African countries in 1982-83-84-86 and 87 (Malithano et al, 1987;Kim et al, 1989).…”

Tolerance Expression of Maize Genotypes to Exserohilum turcicum in North and South Korea

“…Numerous examples of the breakdown of a single gene for high resistance have been reported with other biotic stresses including Puccinia sorghi Brewbaker 1976, 1977), P. polysora (Brewbaker et al, 2011;Kim 1993;Kim et al, 1988), B. maydis (Kim et al, 1988), maize streak virus (Kim et al, 1989), and Striga hermonthica (Kim 1994a;Kim 1994b;Kim 1996). The importance of quantitatively inherited genes for tolerance against diseases, parasitic weeds, and insects has been studied by many groups in details (Brewbaker 1974;Brewbaker et al, 1990Brewbaker et al, , 2011Carson and Van Dyke, 1994;Kim 1993Kim , 2002Nelson 1973;Pataky 1994;Robinson 1996;Van der Plank 1968;Zadocks 1993).…”

Use of IPM in the control of multiple diseases in maize: Strategies for selection of host resistance

“…On-going efforts to breed for resistance in sub-Saharan Africa primarily have been undertaken by national programs, private sector, and international agricultural research centers. Maize breeding programs at the International Institute for Tropical Agriculture (IITA) and the Centro Internacional de Mehoriamento de Mais y Trigo (CIMMYT, the International Center for the Improvement of Maize and Wheat) have resulted in the improvement of numerous populations and inbred lines (Kim et al, 1989;Ceballos et al, 1991). Much progress has been made in the development of genetic resistance for many maize diseases: however, large areas are still planted with farmers' varieties that lack resistance to economic pathogens (Paliwal, 2000;Renfro, 1985).…”

“…The MSV resistance in inbred TZ-Y was considered to be simply inherited (Soto et al, 1982), but Kim et al (1989) reported that resistance in inbred IB32 (Ibadan 32 -developed from TZ-Y) was quantitatively inherited through additive action of up to several genes. More recent studies of genetic control of MSV resistance in population CVR3-C3 have shown that multiple genetic systems for resistance to MSV may indeed exist (Rodier et al, 1995).…”