The importance of food security and nourishment is recognized in Southern African region and in many communities, globally. However, the attainment of food security in Southern African countries is affected by many factors, including adverse environmental conditions, pests and diseases. Scientists have been insistently looking for innovative strategies to optimize crop production and combat challenges militating against attainment of food security. In agriculture, strategies of increasing crop production include but not limited to improved crop varieties, farming practices, extension services, irrigation services, mechanization, information technology, use of fertilizers and agrochemicals. Equally important is genetic modification (GM) technology, which brings new prospects in addressing food security problems. Nonetheless, since the introduction of genetically modified crops (GMOs) three decades ago, it has been a topic of public discourse across the globe, conspicuously so in Southern African region. This is regardless of the evidence that planting GMOs positively influenced farmer’s incomes, economic access to food and increased tolerance of crops to various biotic and abiotic stresses. This paper looks at the issues surrounding GMOs adoption in Southern Africa and lack thereof, the discourse, and its potential in contributing to the attainment of food security for the present as well as future generations.

A survey of anastomosis groups (AG) of Rhizoctonia spp. associated with potato diseases was conducted in South Africa. In total, 112 Rhizoctonia solani and 19 binucleate Rhizoctonia (BNR) isolates were recovered from diseased potato plants, characterized for AG and pathogenicity. The AG identity of the isolates was confirmed using phylogenetic analysis of the internal transcribed spacer region of ribosomal DNA. R. solani isolates recovered belonged to AG 3-PT, AG 2-2IIIB, AG 4HG-I, AG 4HG-III, and AG 5, while BNR isolates belonged to AG A and AG R, with frequencies of 74, 6.1, 2.3, 2.3, 0.8, 12.2, and 2.3%, respectively. R. solani AG 3-PT was the most predominant AG and occurred in all the potato-growing regions sampled, whereas the other AG occurred in distinct locations. Different AG grouped into distinct clades, with high maximum parsimony and maximum-likelihood bootstrap support for both R. solani and BNR. An experiment under greenhouse conditions with representative isolates from different AG showed differences in aggressiveness between and within AG. Isolates of AG 2-2IIIB, AG 4HG-III, and AG R were the most aggressive in causing stem canker while AG 3-PT, AG 5, and AG R caused black scurf. This is the first comprehensive survey of R. solani and BNR on potato in South Africa using a molecular-based approach. This is the first report of R. solani AG 2-2IIIB and AG 4 HG-I causing stem and stolon canker and BNR AG A and AG R causing stem canker and black scurf on potato in South Africa.

Rhizoctonia is a major pathogen of potato causing substantial yield losses worldwide. Control of Rhizoctonia diseases is based predominantly on the application of fungicides. However, little is known about the fungicide response variability of different Rhizoctonia anastomosis groups associated with potato diseases in South Africa. A total of 131 Rhizoctonia isolates were obtained from potato growing regions of South Africa from 2012 to 2014 and evaluated for sensitivity to fungicides in vitro and in vivo. The fungicides comprised six chemical formulations and one bio-fungicide representing seven Fungicide Resistance Action Committee groups. All Rhizoctonia anastomosis groups were sensitive to tolclofos-methyl (EC₅₀: 0.001 to 0.098 μg a.i. ml⁻¹) and fludioxonil (EC₅₀: 0.06 to 0.09 μg a.i. ml⁻¹) and showed variation in sensitivity to pencycuron, iprodione, benomyl, and Bacillus subtilis QST 713. However, for azoxystrobin, Rhizoctonia isolates exhibited variable sensitivity ranging from sensitivity (EC₅₀: <0.09 μg a.i. ml⁻¹) to insensitivity with EC₅₀ values exceeding 5 μg a.i. ml⁻¹. In greenhouse and field trials, tolclofos-methyl and fludioxonil exhibited significantly greater control of stem and black scurf whereas azoxystrobin was the least effective. This work demonstrated variable sensitivity within and among anastomosis groups of R. solani and binucleate Rhizoctonia to different fungicides. Information on fungicide sensitivity of Rhizoctonia isolates is crucial in the development of effective Rhizoctonia control strategies and facilitates monitoring of fungicide insensitive isolates in the pathogen population.

Rhizoctonia solani consists of 13 anastomosis groups (AGs) designated AG1 to 13. AG3-PT is considered the predominant AG in potatoes (4) and is associated with quantitative and qualitative yield losses. Qualitative losses are typically associated with the tuber blemish disease, black scurf. However, atypical tuber blemishes such as elephant hide consisting of corky lesions on the tuber surface (2) have also been attributed to Rhizoctonia. Such atypical blemishes are not considered specific to Rhizoctonia, making direct-cause effect estimates difficult (1). Koch's postulates for the elephant hide symptom and R. solani AG3-PT have not been completed. Recently, growth cracking and scab lesions were observed on potato tubers in South Africa and attributed to a new Streptomyces species (3). These lesions and cracks were similar to elephant hide symptoms attributed to R. solani AG3-PT. Therefore, the cause of the elephant hide symptom in South Africa was investigated further. Symptoms of elephant hide and cracking have been observed on tubers from the Eastern Free State, KwaZulu-Natal, Limpopo, Mpumalanga, North-Eastern Cape, Northern Cape, North West, Sandveld, and Western Free State growing regions. In 2012, three samples of potato tubers (cv. BP1) with elephant hide and cracking were selected for analysis. These samples were collected from Clanwilliam in the Sandveld potato growing region. Tubers were surface sterilized with 1% NaOCl; sections of affected tissue were excised and plated onto potato dextrose agar (PDA). Rhizoctonia-like colonies were identified and after further sub-culturing on PDA, three representative isolates (Rh3, Rh4, and Rh6) of R. solani from each sample were obtained. For each isolate, genomic DNA was extracted and the rDNA ITS region sequenced using ITS1-F and ITS4 (2). The resulting sequences (KF234142, KF234143, and KF234144) were at least 98% identical to other AG3-PT sequences on GenBank (JX27814 and KC157664). To confirm Koch's postulates, pathogenicity tests were conducted with the three isolates. PDA plugs of each isolate were added to 10 g of barley grains which were incubated for 14 days until fully colonized. The barley grains were then used to inoculate disease-free mini-tubers (cv. BP1) in 5l pots containing a sand-clay-pine bark mixture (1:1:1 ratio). Potato plants inoculated with sterile barley grains served as controls. Plants were held for 120 days in a greenhouse at 22°C with light for 12 h a day. Incidence of the elephant hide symptom for isolates Rh3, Rh4, and Rh6 was 58%, 33%, and 37.5%, respectively. Growth cracking and black scurf were also observed with each isolate. R. solani AG3-PT was successfully re-isolated from symptomatic tubers, confirming Koch's postulates. This is the first report of R. solani AG3-PT causing elephant hide in potato tubers in South Africa. Elephant hide caused by R. solani AG3-PT has been reported in tubers from France (2) and the United Kingdom (3), but Koch's postulates were not proven. In this study, Koch's postulates were proven for R. solani AG3-PT causing scab or elephant hide symptom and cracking in potato tubers. R. solani AG3-PT should thus be considered in addition to Streptomyces as a cause of this symptom and control strategies should also consider R. solani AG3-PT. References: (1) G. J. Banville et al. Pages 321-330 in: Rhizoctonia Species: Taxonomy, Molecular Biology, Ecology, Pathology and Disease Control, B. Sneh et al., eds. Kluwer Academic Publishers, Dordrecht, The Netherlands, 1996. (2) M. Fiers et al. Eur. J. Plant. Pathol. 128:353, 2010. (3) R. Gouws and A. McLeod. Plant Dis. 96:1223, 2012. (4) J. W. Woodhall et al. Eur. J. Plant. Pathol. 136:273, 2013.