Most leaf pathogens have a means of destroying leaf tissue, creating a nutrition source before the host defense system limits their progress. The invading fungus quickly dominates the dead tissue before saprophytic competitors arrive. From this base, they produce spores to invade new leaf areas. Often the death to the tissue is related to production of a plant toxin affecting cell membranes. Bipolaris zeicola (Cochliobolus carbonum) and Bipolaris maydis (Cochliobolus maydis) share this mechanism. These related species generally had limited success in destroying leaf tissue except when attacking a corn genotype that was particularly slow in stopping the infection. Race 1 of B. zeicola is very damaging to inbreds with the homozygous recessive hm gene. Race 2 of this pathogen can be notable on a few inbreds.
B. maydis was known a problem on some inbreds and hybrids in the more southern USA and subtropical corn growing areas but generally adequate resistance was found. This changed in 1969, when it was discovered that a variant of this pathogen produced a toxin attacking the unique membrane of mitochondria in T cytoplasm corn. The unique mitochondria responsible for producing defective pollen grains, allowing cost saving in seed production, also resulted in extreme susceptibility to Race T of B. maydis. Resistance to this pathogen race inherited via chromosomes had little effect on restricting this disease spread in 1970. Use of T cytoplasm in corn throughout the USA, favorable weather and extreme pathogenicity of the new race allowed the spread of B. maydis into areas overlapping the normal distribution of B. zeicola.
Virtually all t cytoplasm corn had been removed from the market by the summer of 1972. But lesions started were showing up on inbreds that were not as severe as race t on t cytoplasm but more vigorous than those caused traditional B. zeicola. The fungal spores associated with these lesions varied in pigment and curvature from traditional B. zeicola or B. maydis. It was known, experimentally, that the two species could cross. It was thus easy to hypothesize that the widespread distribution and intensity of race T allowed many opportunities for the two species to cross and we were witnessing new segregating populations of the population. No longer having the T cytoplasm to attack the new mix of pathogenic genes created new race possibilities. One caused lone very narrow lesions on some inbreds that became known as Race 3 of Bipolaris zeicola. Another pathotype (or race) was identified as causing more oval shaped lesions on some inbreds, especially with B73 background in 1990. It was named B. zeicola pathotype 4.
Two related species apparently crossed in a strange coincidence of circumstances, new opportunities for new pathogen variants were created. Biologies of corn and fungi often mix in the real world of agriculture.
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.