Maize leaves inoculated with Didymella zeae-maydis. Arrows point to chlorotic regions caused by PM-toxin which accompany necrotic lesions.
Image Credit: B. Gillian Turgeon

The dothideomycete Didymella zeae-maydis, the causal agent of Yellow Leaf Blight of maize, was first observed in Ohio in 1965 [1] then soon after in most corn growing states of the US and Canada.  The fungus was initially described as Phyllosticta zeae [2, 3], then Phyllosticta maydis [4]. When the teleomorph was discovered in 1973, it was renamed Mycosphaerella zeae-maydis [5], then Didymella zeae-maydis [6].  The name Peyronellaea zeae-maydis is suggested by authors of a recent publication [7] reporting multilocus sequence typing.
From the beginning, it was clear that only Texas male sterile cytoplasm (Tcms) was highly susceptible to attack by D. zeae-maydis.  Moreover in 1973, a polyketide secondary metabolite, PM-toxin [8], with toxicity only to Tcms was identified.  Tcms carries the Urf13 protein target of the toxin in the inner mitochondrial membrane.  PM-toxin has exactly the same biological specificity as the polyketide secondary metabolite, T-toxin, produced by Cochliobolus heterostrophus race T causal agent of the 1970 Southern Corn Leaf Blight epidemic.  Race T was unknown until the time of the epidemic, although race O, which does not produce T-toxin was discovered decades earlier.   Both T-toxin and PM-toxin are families of linear polyketides, however PM-toxin, as a family, consists of shorter carbon chain backbones (C33 to C35) than the T-toxin family (C35 to C41). In contrast to C. heterostrophus with two known races, no toxin-minus isolate of D. zeae-maydis is known.  The history of evolution of genes conferring toxin-producing activity is under investigation.
D. zeae-maydis is genetically tractable and there are established protocols for transformation, gene disruption and targeted gene manipulation [9].  The fungus is homothallic [10].
D. zeae-maydis strain 3018 was sequenced using an Illumina HiSeq 2000-based whole-genome shotgun strategy (S-H Yun, Dept. of Medical Biotechnology, Soonchunhyang University, Asan, South Korea).

Acknowledgement
This research was supported by a grant from the Next-Generation Bio Green21 Program (no. PJ0111802015), the Rural Development Administration, Republic of Korea.

References

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