Cochliobolus carbonum on maize in the field, circa 1981, Cornell University. Image provided by Jonathan Walton, Michigan State University.

The filamentous ascomycete genus Cochliobolus (anamorph Bipolaris/Curvularia) is comprised of more than forty closely related species, some of which are highly aggressive, superpathogens with particular specificity to their host plants. All members of the genus known to cause serious crop diseases fall in a tight phylogenetic group suggesting that a progenitor within the genus gave rise, over a relatively short period of time to the series of distinct biotypes (1), each distinguished by unique pathogenic capability to individual types of cereal.  Aggressive members include the necrotrophic corn pathogens Cochliobolus heterostrophus and Cochliobolus carbonum, the oat pathogen, Cochliobolus victoriae, the rice pathogen, Cochliobolus miyabeanus, the sorghum pathogen, Bipolaris sorghicola, the sugarcane pathogen, Bipolaris sacchari and the hemibiotrophic generalized cereal and grass pathogen, Cochliobolus sativus.  
Many necrotrophic Cochliobolus spp. and related taxa (e.g., Pyrenophora tritici repentis, Stagonospora nodorum, Alternaria alternata) are notorious for their ability to evolve novel, highly virulent, races producing Host Selective Toxins (HSTs), and their concomitant capacity to cause diseases on cereal crops that were bred, inadvertently, for susceptibility to the HST-producing pathogen (2).  In contrast to the plant host requirements for susceptibility to C. heterostrophus and C. victoriae, which require dominant host genes, maize susceptibility to Northern Corn Leaf Spot caused by C. carbonum (Bipolaris zeicola) is conferred by a homozygous recessive gene(s). Resistance is determined by two genes, Hm1 and Hm2 and full susceptibility is achieved only when plants are homozygous recessive at both loci (3,4).  C. carbonum race 1 produces the cyclic-tetrapeptide HST, HC-toxin, which is specifically active against corn with the genotype hmhm, as is the fungus itself (5,6,7).  Hm1 encodes a carbonyl reductase which inactivates the toxin (16); hmhm lines, thus, cannot inactivate the toxin, and are therefore sensitive. The site of action of HC-toxin in susceptible corn is histone deacetylase; it is hypothesized that HC-toxin acts to promote infection of maize of genotype hm1hm1 by inhibiting this enzyme, resulting in accumulation of hyperacetylated core (nucleosomal) histones.  This then alters expression of genes encoding regulatory proteins involved in plant defense (8,9).  C. carbonum races 2 and 3 do not produce the toxin.

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3. Johal GS, Briggs SP (1992) Reductase activity encoded by the HM1 disease resistance gene in maize. Science 258: 985-987.
4. Multani DS, Meeley RB, Paterson AH, Gray J, Briggs SP, et al. (1998) Plant-pathogen microevolution: Molecular basis for the origin of a fungal disease in maize. Proc Natl Acad Sci USA 95: 1686-1691.
5. Yoder OC (1980) Toxins in pathogenesis. Ann Rev Phytopathol 18: 103-129.
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7. Walton JD (1996) Host-selective toxins: agents of compatibility. Plant Cell 8: 1723-1733.
8. Ransom RF, Walton JD (1997) Histone hyperacetylation in maize in response to treatment with HC-toxin or infection by the filamentous fungus Cochliobolus carbonum. Plant Physiol 115: 1021-1027.
9. Walton JD (2006) HC-toxin. Phytochemistry 67: 1406-1413.