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Sorghum ergot, initially restricted to Asia and Africa, was recently found in the Americas and Australia. Three species causing the disease have been reported: Claviceps sorghi in India, C. sorghicola in Japan, and C. africana in all ergot-positive countries. The objective of our study was to study the intraspecific variation in C. africana isolates in the Americas, Africa, India, and Australia. We confirmed C. africana, C. sorghi, and C. sorghicola as different species using differences in nucleotide sequences of internal transcribed spacer 1 and 5.8S rDNA regions. Sequences of this region obtained from the representative American, Indian, and Australian isolates of C. africana were identical. In addition, random amplified polymorphic DNA (RAPD) banding patterns of sorghum ergot pathogen isolates from the United States, Mexico, Puerto Rico, Bolivia, Australia, and India were evaluated with nearly 100 primers. A total of 65 primers gave identical patterns for all isolates, which confirmed that all were C. africana. The identity of RAPD pattern and rDNA sequence of Indian isolates with those of C. africana confirmed that the species is now present in India. Only 20 primers gave small pattern differences and 7 of them were used for routine testing. All of the American isolates were identical and three isolates of the same type were also found in South Africa, suggesting Africa as the origin of the invasion clone in the Americas. Australian and Indian isolates were distinguishable by a single band difference; therefore, migration from the Asian region to Australia is suspected. Another distinct group was found in Africa. Cluster analysis of the informative bands revealed that the American and African group are on the same moderately (69%) supported clade. Isolates from Australia and India belonged to another clade.

Ergot disease spread rapidly in Zimbabwe amongst replicated plots of male‐sterile sorghum A‐lines, from a group of centrally situated and precociously inoculated plants. Prominent secondary conidiation by the pathogen, Claviceps africana, on the surface of exuded honeydew provided airborne spores which were trapped in a Burkard continuous spore trap and showed diurnal peaks of concentration in air close to the primary source of inoculum. The rate of disease spread (r=0·2; range 0·14–0·58) closely matched that recorded for other plant pathogens such as Phytophthora infestans and Puccinia graminis tritici, and it is concluded that the characteristic secondary conidia of C. africana were the principal epidemiological agents within the experimental area. Ergot spread by windborne secondary conidia has significant epidemiological and economic implications for sorghum hybrid breeding in southern Africa.

Secondary conidiation of Sphacelia sorghi on sorghum, a novel factor in the epidemiology of ergot disease. bAycological Research 93 (4): 497-502 (1989). Sphacelia sorghi, the ergot pathogen of sorghum in Zimbabwe, causes copious exudation of honeydew containing macroconidia. Within a few days the exudate develops a white crust consisting of a layer of secondary conidia borne above the honeydew surface on a palisade of sterigma-like projecting hyphae which arise from the macroconidia immediately below the honeydew surface Secondary conidia are windbome, initiate infection and are recognized for the first time to have an important role in the epidemiology of ergot disease of sorghum in Southern Africa.

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Nitric oxide (NO) regulates the deployment of a phalanx of immune responses, chief among which is the activation of a constellation of defence-related genes. However, the underlying molecular mechanisms remain largely unknown. The Arabidopsis thaliana zinc finger transcription factor (ZF-TF), S-nitrosothiol (SNO) Regulated 1 (SRG1), is a central target of NO bioactivity during plant immunity. Here we characterize the remaining members of the SRG gene family. Both SRG2 and, especially, SRG3 were positive regulators of salicylic acid-dependent plant immunity. Analysis of SRG single, double and triple mutants implied that SRG family members have additive functions in plant immunity and, surprisingly, are under reciprocal regulation. SRG2 and SRG3 localized to the nucleus and functioned as ethylene-responsive element binding factor-associated amphiphilic repression (EAR) domain-dependent transcriptional repressors: NO abolished this activity for SRG3 but not for SRG2. Consistently, loss of GSNOR function, resulting in increased (S)NO concentrations, fully suppressed the disease resistance phenotype established from SRG3 but not SRG2 overexpression. Remarkably, SRG3 but not SRG2 was S-nitrosylated in vitro and in vivo. Our findings suggest that the SRG family has separable functions in plant immunity, and, surprisingly, these ZF-TFs exhibit reciprocal regulation. It is remarkable that, through neofunctionalization, the SRG family has evolved to become differentially regulated by the key immune-related redox cue, NO.

Forty‐four local Ethiopian and Rwandan sorghums (Sorghum bicolor) were observed to remain free of ergot, or had only low incidence, in their natural equatorial latitudes and were potentially of interest, in the design of male‐sterile lines for F1 hybrid breeding, if they possessed a physiologically based resistance mechanism. These sorghums were therefore also investigated under natural and artificial disease pressures in Zimbabwe where unadapted development and inappropriate long daylength prevented flowering in 18 accessions. Of the remaining 16 Ethiopian and 10 Rwandan accessions which flowered, only one from each country remained free of ergot. The susceptibility expressed was ascribed to observed asynchrony of stigma exsertion with anthesis. In the Rwandan accession that persistently remained free of ergot in Zimbabwe, histology of ovules showed pollination before floret gaping, so that a general principle of disease escape due to efficient pollination is proposed for the Ethiopian and Rwandan sorghums in their native climates. The findings emphasize that cleistogamy is a desirable character for avoiding ergot infection in self‐fertile sorghums and suggest that the Ethiopian and Rwandan sorghums may not generally be useful for breeding ergot‐resistant male‐sterile female lines. However, a few accessions deserve more detailed study as a potential genetic resource, before a firm conclusion that all apparent resistance is disease escape owing to efficient pollination.