Cochliobolus heterostrophus C4 v1.0
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Photo of Cochliobolus heterostrophus C4 v1.0
Cochliobolus heterostrophus race T strain C4 produces T-toxin, in contrast to race O strain C5. (Picture courtesy of Gillian Turgeon)

Cochliobolus heterostrophus race T strain C4

In 1970, race T, a previously unseen strain of the filamentous ascomycete, Cochliobolus heterostrophus caused the worst epidemic [Southern Corn Leaf Blight (SCLB)] in US agricultural history, destroying more than 15% of the maize crop. Subsequent research over the ensuing four decades has demonstrated that the epidemic was triggered by the unfortunate confluence of complex DNA recombination events in both the fungal pathogen and the plant host.  Before 1970, C. heterostrophus was known as an endemic pathogen of minor economic importance, first described in 1925; after the appearance of race T, this race was named “race O”.

Race O strain C5, which is near isogenic to race T strain C4, has been sequenced previously by JGI.  Race T is genetically distinct from race O; it possesses an extra 1.2 Mb of DNA, inseparably linked to the both breakpoints of a pair of race T chromosomes that are reciprocally translocated with respect to the corresponding pair of race O chromosomes.  This extra DNA carries genes for biosynthesis of a polyketide secondary metabolite, T-toxin, a host selective toxin (HST), essential for high virulence.  These genes are missing in race O.  On the plant side, the presence of a hybrid mitochondrial gene composed of segments of two mitochondrial genes and one chloroplast gene, called T-urf13, in Texas male sterile cytoplasm (Tcms) maize, is essential for susceptibility.  This type of corn was widely planted at the time of the SCLB epidemic because it is male sterile, a trait important to breeders concerned with hybrid vigor issues but disastrous from the perspective of pathogen attack as it served as a monoculture of susceptible germplasm. Note both fungal races are pathogenic to corn, but race T is highly and specifically virulent on Tcms corn.

The SCLB epidemic of 1970 generated enormous concern about the genetic vulnerability of our essential crops and its effects on growers’ incomes and corn market prices (as reflected in the two accompanying excerpts from the New York Times, August, 1970).  Segments from an article by J. Doyle (Altered harvest: Agriculture, genetics, and the fate of the world's food supply. Viking Penguin, N.Y., 1985)  serve also to illustrate the SCLB impact:
… “ In the summer of 1968, …  the first signs of trouble went almost unnoticed. Out in the heartland, …
…“The new fungus moved like wildfire through one corn field after another. In some cases it would wipe out an entire stand of corn in ten days. “…
…“… with the opening of business that Monday, panic gripped the commodity and futures markets. Estimates that the blight might wipe out half the nation's corn crop fueled frantic trading and speculation. At the Chicago Board of Trade, the nation's largest commodities market, 193 million bushels of corn changed hands in one day, smashing a trading record that had stood for 122 years. The Dow Jones index for commodity futures hit 145.27, and had its highest one-day advance in nineteen years….

An appreciation of genetic differences and evolutionary mechanisms associated with appearance of highly aggressive superpathogens, such as race T, contributes to the body of knowledge on genetic agility of fungal (and other) genomes, evolution of novel genome structures, acquisition of virulence/pathogenicity factors, strain/species diversification, secondary metabolite-associated gene amplification and divergence, and also has broad relevance for disease prevention strategies, whether for plants or humans/animals.  This is especially true considering that T-toxin is a secondary metabolite and metabolites of this type have positively revolutionized human health practices (e.g. the antibiotic penicillin, the immunosuppressant cyclosporin, the cholesterol-lowering lovastatin) while, on the downside, caused devastation of crops (e.g., phytotoxins such as T-toxin) or compromised food safety (e.g., aflatoxins/mycotoxins), both with calamitous economic consequences.

C. heterostrophus  race T and related taxa (Alternaria, Pyrenophora) are notorious for their ability to produce HSTs.  These usually are secondary metabolites (although protein HSTs are known), necessary for high virulence or pathogenicity towards particular host plants. T-toxin, for example, a linear polyketide, is required by C. heterostrophus for high virulence to corn, while HC-toxin and victorin are small, but different, cyclic peptide toxins required by Cochliobolus carbonum and Cochliobolus victoriae, respectively, for specific pathogenicity to corn and to oats, respectively.  Alternaria alternata subspecies each produce unique HSTs that confer host specificity.  All members of the genus Cochliobolus that are known to cause serious crop diseases, e.g., C. heterostrophus (host = corn), C. carbonum (corn), C. victoriae (oats), C. sativus (cereals), C. miyabeanus (rice), Bipolaris sorghicola (sorghum) and Bipolaris sacchari (sugarcane) are found in a relatively tight phylogenetic group. Phylogenetic data suggest that a progenitor within the genus gave rise, over a relatively short period of time, to this series of distinct biotypes, each distinguished by having unique pathogenic capability to a particular type of plant, and often associated with HST production.

The stories of the SCLB and Victoria blight epidemics are dramatic examples of interactions between crops, whose ‘evolution’ is driven by human intervention (breeders) and their pathogens, which evolve naturally to exploit new genetic susceptibilities.  Both the Tcms and Pc-2 (essential for susceptibility to C. victoriae) genes were introduced into maize and oats, respectively, by breeders fewer than 30 years before the epidemic outbreaks. Specifically, Tcms was discovered in the 1940’s, then incorporated into elite corn inbred lines increasingly throughout the 1960’s, and was present in almost all of the hybrid corn in the U.S. by 1970. It is currently unclear whether C. heterostrophus race T evolved around the time of the epidemic or had been ‘lurking’ in the field for a long time.  Regardless of the answer, the vast monoculture of Tcms maize was the perfect host for this previously unknown race.

Genome Reference(s)