This fungus more commonly known as Bipolaris zeicola is usually an insignificant corn pathogen that is a good example of the complexity of dynamics between corn and potential diseases. Both the host and fungus genetics interact within their environments. The fungus is saprophytic digesting and growing on dead plant tissue, especially in grasses. Some genetic variants of the fungus produce a toxin that kills a small area of a living leaf, forming a lesion, allowing the fungus to receive nutrition. The plant tissue responds by limiting the fungus from further growth. The fungus responds by producing spores, to spread to more potential host areas. This interaction is common throughout nature. Corn interaction is probably clearer because of the extreme genetic variability of the host across years and environments.
Race 0 of B. zeicolacauses very small flecks on most corn varieties. It apparently can be found on dead corn tissue, perhaps on dead tissue on living plants that were killed by other causes. Race 1 of this pathogen shows up periodically as a susceptible inbred is grown. It produces a toxin that kills leaf tissue in area of about 1 cm in length and 0.5 cm wide before the plant successfully stops the pathogen but spore production spreads it to more leaves. It also can invade the kernels on ears. Susceptibility must be genetically simple, as it appears occasionally in breeding programs. It can be significant to seed production. Race 2 became notable especially on a different set of inbreds, such as W64A especially in the northern USA corn belt. Those inbreds susceptible to Race 1 were not susceptible to Race 2 and vice-versa.
Race 3 became apparent after invasion of the US corn belt by Race t of a related species Helminthosporium maydis(Bipolaris maydis) in 1969-1970. The two species have been shown to cross in culture and it is hypothesized that the mix of the two species with the northern exposure to the other species allowed for new genetic combinations. Race 3 of causes longer more narrow lesions on susceptible inbreds. Race 4 of B. zeicola became apparent in 1980 in seed production fields with B73 derived inbreds. These lesions differed from Race 3 with wider lesions and significant losses in seed production fields that spraying is needed. There is evidence that this race, and probably others, successfully invades the production field by producing initial spores on nearby grasses.
Genetic variability in potential pathogens, multiple hosts and genetic variability in the corn species and among ‘new’ varieties can result in unexpected corn diseases. We usually don’t become aware of the new interactions until the incidences are large enough to get attention.
About Corn Journal
The purpose of this blog is to share perspectives of the biology of corn, its seed and diseases in a mix of technical and not so technical terms with all who are interested in this major crop. With more technical references to any of the topics easily available on the web with a search of key words, the blog will rarely cite references but will attempt to be accurate. Comments are welcome but will be screened before publishing. Comments and questions directed to the author by emails are encouraged.