Communication

Characterization of the host-specific pathotoxin produced by Helminthosporium maydis, race T, affecting corn with Texas male sterile cytoplasm☆

Fungal pathogenesis to plants is an intricate developmental process requiring biological components found in most fungi, as well as factors that are unique to fungal taxa that participate in particular fungus–plant interactions. The host‐selective polyketide toxin known as T‐toxin produced by Cochliobolus heterostrophus race T, a highly virulent pathogen of maize, is an intriguing example of the latter type of virulence determinant. The Tox1 locus, which controls biosynthesis of T‐toxin, originally defined as a single genetic locus, it is, in fact, two exceedingly complex loci on two chromosomes that are reciprocally translocated with respect to their counterparts in weakly pathogenic race O. Race O lacks the Tox1 locus and does not produce T‐toxin. Highly virulent race T was first recognized when it caused an epidemic of Southern Corn Leaf Blight, which devastated the US corn crop in 1970. The evolutionary origin of the Tox1 locus remains unknown.

This chapter reviews the genetics, pathology, and molecular biology of T-cytoplasm male sterility in maize. The chapter discusses the role of cytoplasmic male sterility systems in facilitating the production of hybrid seeds. The effects of widespread planting of T-cytoplasm maize on the severe 1970 epidemic and effect of a mitochondria1 gene on disease susceptibility and male sterility are discussed. It also discusses the involvement of nuclear cytoplasmic interactions in restoration of cms-T, the perspectives of cms-T researchers, and future directions. In cms-T plants, male sterility is associated with premature breakdown of the mitochondria-rich, tapetal cell layer of the anther; this layer is crucial to pollen production because it supplies nutrients to the developing microspores. In many species, cms is associated with the expression of novel open-reading frames in the mitochondrial genome. The studies provided a foundation for further research that resulted in the cloning of the T-urf13 and Rf2 genes from maize and the ChPKSl gene from C. heterostrophus, and the generation of models for the topology of urf13 in the inner mitochondrial membrane, Rfl-mediated processing of T-urfl3 transcripts, and the evolution of toxin biosynthesis in C. heterostrophus and M. zeae-maydis.

Two phytotoxins are isolated from culture filtrates of an Alternaria alternata pathogenic to sunflower. One was identified by chemical and physicochemical techniques as the tetrapeptide Ser-Val-Gly-Glu. This peptide, for which we suggested the name AS-I toxin, was further characterised by synthesis and by its phytotoxic effect on sunflower and other plants.

Syringomycin E, syringopeptin 22-A and syringopeptin 25-A, the main phytotoxins isolated from cultures of several strains ofPseudomonas syringaepv.syringae, were separately tested for their activity on some mitochondrial functions. It was shown that syringopeptins were several-fold more active uncouplers of oxidative phosphorylation than syringomycin E. They were also more active in increasing the respiration of succinate and NADH and the hydrolysis of ATP in isolated maize and pea mitochondria, and in decreasing the membrane potential of those mitochondria. These results explain the apparent contrast between the findings obtained some years ago with toxin preparations which had been considered homogeneous, but in fact contained multiple forms of syringomycins and syringopeptins, and those obtained using pure syringomycin E.

Several times in this century, new and sometimes devastating diseases of cereal crops, caused by fungi in the genus Cochliobolus, have suddenly appeared. In many fungal diseases of plants the factors required for pathogenicity are unknown; in contrast, the key elements in each of several Cochliobolus diseases are known to be host-selective toxins. Recent research on these systems has given surprising insights into the genetic basis of fungal pathogenicity and plant susceptibility to disease.