Cochliobolus heterostrophus (southern leaf spot)

Destroying or burying crop residues can be a beneficial practice. Lower levels of disease developed in ploughed plots than in tillage systems in which more crop residues were left on the surface (Sumner and Littrell, 1974). The germination of spores exposed on the soil surface was significantly greater than the germination of buried spores (Kingsland, 1972). Continuous maize culture increased the severity of the disease (Bekele and Sumner, 1983).

Race T, the cause of the 1970 epidemic of southern corn leaf blight, only attacks maize with Texas male-sterile cytoplasm (T-cms). The pathogenicity of race T is expressed by the action of T-toxin produced by the fungus. The toxin has been associated with disruption of the mitochondrial function in susceptible plants (Holden and Sze, 1989). The mitochondrial gene, T-urf13, from T-cms maize, is responsible for sensitivity to T toxin produced by the pathogen (Braun et al., 1989). The molecular basis of disease susceptibility in the T-cms maize is currently under investigation (Levings and Siedow, 1992). Race O attacks a broad range of genotypes. The recessive gene, rhm, confers chlorotic-lesion resistance to C. heterostrophus race O, in otherwise susceptible maize plants (Zaitlin et al., 1993). Ultrastructural observations on 1-4-day-old seedlings of an inbred line of male-fertile maize inoculated with race O conidia revealed that, although mesophyll cells degenerated at an early stage, bundle sheath and phloem cells remained intact even in 4-day-old lesions (Smith and Toth, 1982).Molecular studies of resistance indicate that the rhm gene is tightly linked to two RFLP marker loci (UMC85 and p144) that map to the short arm of chromosome 6. Polymerase chain reaction assays confirmed the linkage between rhm and the p144 RFLP marker locus in a second unrelated F2 population (Zaitlin et al., 1993). Tagging the rhm gene with transposable elements suggested that there are two linked recessive genes controlling resistance (Chang and Peterson, 1995).Field and laboratory experiments in China showed that the subgroup CI (CMS-C) of group C maize was particularly susceptible to C. heterostrophus race C, but subgroups CII (CMS-RB) and CIII (CMS-ES) were not seriously infected (Liu et al., 1991).Various screening methods for resistance have been investigated, including detached leaf techniques (Lakshmi and Sharma, 1987), tissue culture (Kuehnle and Earle, 1988) and seedling assays (Tajimi et al., 1985). Conventional pedigree or recurrent selection methods continue to be effective in breeding for improved resistance to southern leaf blight (Shieh and Lu, 1993).

Foliar applied fungicides that effectively control C. heterostrophus include dinocap and carbendazim (Saxena et al., 1985), mancozeb (Schenck and Stelter, 1974), maneb, dithane, propiconazole and chlorothalonil (Burnette and White, 1985; Comstock et al., 1974).

No biological control methods or products exist for C. heterostrophus; however, potential biological control agents have been identified. Antifungal agents include the substance Ac-1 produced by a Streptomyces sp. (Matsuyama, 1991); the bacterium Pseudomonas cepacia (Upadhyay and Jayaswal, 1992); and the fungus Trichosporon sp. (Wang and Wu, 1987). Some saprophytic fungi occurring on the phylloplane of maize show antagonistic activity in vitro against C. heterotrophus (Mangiarotti, 1987). Microorganisms which were antagonistic to C. heterostrophus in culture were isolated from conidia and lesions on maize leaves (Sleesman and Leben, 1976). Natural products that show some fungicidal activity against the fungus include an extract of Portulaca oleracea (Noriel and Robles, 1990) and 1,3,7-trimethylxanthine, isolated from coffee (Rizvi et al., 1980).