scholarly journals First Report of Rhizoctonia solani AG 4HG-III Causing Potato Stem Canker in South Africa

Plant Disease ◽  
2014 ◽  
Vol 98 (6) ◽  
pp. 853-853 ◽  
Author(s):  
N. Muzhinji ◽  
J. W. Woodhall ◽  
M. Truter ◽  
J. E. van der Waals

Black scurf and stem canker caused by Rhizoctonia solani Kühn (teleomorph: Thanathephorus cucumeris Frank Donk) are potato diseases of worldwide economic importance (4). R. solani consists of 13 anastomosis groups (AGs) of which AG 3-PT is considered the dominant causal agent of potato diseases globally (1,4). However, other AGs such as AG 2-1, 5, and 8 have been reported to cause potato diseases (1,4). In February 2013, potato stem samples (cv. Mondial) displaying dark brown lesions resembling those caused by Rhizoctonia stem canker were obtained from a commercial field in Limpopo Province, South Africa. Symptomatic tissue was disinfected with 1% NaOCl for 1 min, rinsed in sterile water, and 4-mm stem pieces excised from the margins of symptomatic tissues and plated on 2% water agar supplemented with 20 mg/l of chloramphenicol. Single hyphal tips taken from fungal isolates identified as R. solani based on morphological traits (3) were transferred to potato dextrose agar. DNA was isolated from the resulting cultures and ITS region of rDNA was sequenced as previously described (2). The resulting sequences of three of the isolates, Rh 81, Rh 82, and Rh 83 (KF712285, KF712286, and KF712287), were 99% similar to those of AG 4 HG-III found in GenBank (DQ102449 and AF354077). Therefore, based on molecular methods, these three isolates were identified as R. solani AG4 HG-III. To determine pathogenicity of the AG4 HG-III isolates, certified disease free mini-tubers (Generation 0, cv. Mondial, produced in tunnels) were used in pot trials. PDA plugs of each isolate were added to 10 g of barley grains, which had been sterilized by autoclaving for two consecutive days at 121°C for 30 min, and were incubated for 14 days until fully colonized. Ten colonized barley grains were placed 10 mm above each mini-tuber planted in 5l pots containing sterile potting mixture of sand:clay:pinebark (1:1:1). Ten tubers were inoculated with each isolate. Uninoculated, sterile barley grains were applied to the control treatment. Mini-tubers were grown in a greenhouse maintained at 22°C with light for a 12 h day. After 7 weeks, five plants for each isolate were destructively sampled and assessed for stem canker symptoms. At 120 days after sowing, the remaining five plants per treatment were assessed for blemishes on progeny tubers. The stem canker incidences of plants inoculated with Rh 81, Rh 82, and Rh 83 were 25, 25, and 50%, respectively, whereas no symptoms were observed in control plants. Sclerotia formation and blemishes were not observed on any of the progeny tubers, which might indicate that these strains are only able to infect stems, or that environmental conditions were not suitable for tuber blemish or black scurf development. R. solani AG4 HG-III was consistently re-isolated from symptomatic stems displaying brown lesions, and the identity of the re-isolates were confirmed by molecular tests as previously described, thereby fulfilling Koch's postulates. To our knowledge, this is the first report of R. solani AG4 HG-III causing stem canker on potato in South Africa and worldwide. Knowledge of which AGs are present in crop production systems is important when considering disease management strategies such as crop rotation and fungicide treatments (3). References: (1) C. Campion et al. Eur. J. Plant. Pathol. 109:983, 2003. (2) N. Muzhinji et al. Plant Dis. 98:570, 2014. (3) L. Tsror. J. Phytopathol. 158:649, 2010. (4) J. W. Woodhall et al. Plant. Pathol. 56:286, 2007.

Plant Disease ◽  
2014 ◽  
Vol 98 (4) ◽  
pp. 570-570 ◽  
Author(s):  
N. Muzhinji ◽  
J. W. Woodhall ◽  
M. Truter ◽  
J. E. van der Waals

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.


Plant Disease ◽  
2015 ◽  
Vol 99 (12) ◽  
pp. 1790-1802 ◽  
Author(s):  
N. Muzhinji ◽  
M. Truter ◽  
J. W. Woodhall ◽  
J. E. van der Waals

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.


Plant Disease ◽  
2004 ◽  
Vol 88 (1) ◽  
pp. 83-83 ◽  
Author(s):  
M. Truter ◽  
F. C. Wehner

Rhizoctonia disease (black scurf of tubers and stem canker) of potato (Solanum tuberosum L.) caused by Rhizoctonia solani Kühn was first recorded in South Africa in 1918 (3). Although the sclerotial form on tubers is one of the most common potato diseases in the country, it is not known which anastomosis groups (AGs) of R. solani are involved. Between 1999 and 2001, R. solani was isolated from 28 plant and 56 soil samples collected in 7 (Eastern Free State, Gauteng, KwaZulu-Natal, Limpopo, Mpumalanga, Northern Cape, and Sandveld) of the 14 potato-production regions of South Africa and screened for hyphal anastomosis with tester strains of R. solani AG-1 to AG-10 according to Carling et al. (1). Of the 411 isolates from tubers with black scurf symptoms, 408 were AG-3 and three were AG-5. Symptomless tubers yielded two AG-3 isolates and three AG-5 isolates. Of 39 isolates from symptomatic stems and roots, 32 were AG-3, five were AG-4, and two were AG-5. Of the 127 isolates obtained from soil, 86, 28, 7, 3, and 3 were AG-3, AG-4, AG-5, AG-7, and AG-8, respectively. More than one AG was isolated from five of the seven regions. Virulence of 40 isolates representative of the above AGs was determined in triplicate on sprouts growing from seed tubers of potato cultivar Up-to-Date in a sand/soil mixture as described by Carling and Leiner (2) but using cultures grown in cornmeal/sand instead of colonized agar disks as inoculum. Damage to sprouts (lesions, girdling, and death) was assessed after 28 days at 16 to 28°C according to the 0 to 4 rating scale (2). Chi-square analysis of the data indicated that AG-3 was the most virulent, with isolates from sclerotia on tubers and lesions on stems more aggressive than those from symptomless tubers or soil. AG-4 and AG-5 caused significantly less disease than AG-3, but none of the AG-7 and AG-8 isolates showed any virulence to potato sprouts. References: (1) D. E. Carling et al. Phytopathology 77:1609, 1987. (2) D. E. Carling and R. H. Leiner. Phytopathology 80:930, 1990. (3) E. M. Doidge. S. Afr. Fruit Growers 5:6, 1918.


Plant Disease ◽  
2012 ◽  
Vol 96 (11) ◽  
pp. 1701-1701 ◽  
Author(s):  
J. W. Woodhall ◽  
P. S. Wharton ◽  
J. C. Peters

The fungus Rhizoctonia solani is the causal agent of stem canker and black scurf of potato (Solanum tuberosum). R. solani is a species complex consisting of 13 anastomosis groups (AGs) designated AG1 to 13 (2, 3). Stems of potato (cv. Russet Norkotah) with brown lesions were recovered from one field in Kimberley, Idaho, in August 2011. Using previously described methods (3), R. solani was recovered from the symptomatic stems and one representative isolate (J15) was selected for further characterization. Sequencing of the rDNA ITS region of isolate J15 was undertaken as previously described (3) and the resulting rDNA ITS sequence (HE667745) was 99% identical to sequences of other AG4 HG-II isolates in GenBank (AF354072 and AF354074). Pathogenicity of the isolate was determined by conducting the following experiment. Mini-tubers of cv. Santé were planted individually in 1-liter pots containing John Innes Number 3 compost (John Innes Manufacturers Association, Reading, UK). Pots were either inoculated with J15, an isolate of AG3-PT (Rs08), or were not inoculated. Each treatment was replicated four times. Inoculum consisted of five 10-mm-diameter potato dextrose agar plugs, fully colonized by the appropriate isolate, placed in the compost approximately 40 mm above each seed tuber. Pots were held in a controlled environment room at 21°C with 50% relative humidity and watered as required. After 21 days, plants were assessed for disease. No symptoms of the disease were present in non-inoculated plants. In the Rs08 (AG3-PT) inoculated plants, all stems displayed large brown lesions and 20% of the stems had been killed. No stem death was observed in J15 (AG4 HG-II) inoculated plants. However, brown lesions were observed in three of the four J15 (AG4 HG-II) inoculated plants. These lesions were less severe than in plants inoculated with the Rs08(AG3-PT) inoculated plants and were present in 40% of the main stems. In the J15 (AG4 HG-II) inoculated pots, R. solani AG4 HG-II was reisolated from the five symptomatic stems, thereby satisfying Koch's postulates. To our knowledge, this is the first report of AG4 HG-II causing disease on potatoes in Idaho. AG4 has been isolated from potato previously from North Dakota, although the subgroup was not identified (1). The only previous report where AG4 HG-II was specifically determined to cause disease on potato was in Finland, but the isolate could not be maintained and Koch's postulates were not completed (3). The present study shows that AG4 HG-II can cause stem disease in potatoes, although disease does not develop as severely or as consistently as for AG3-PT. However, as demonstrated with isolates of AG2-1 and AG5, even mild stem infection can reduce tuber yield by as much as 12% (4). AG4 HG-II is a pathogen of sugar beet in Idaho, which was grown previously in this field. This history may have contributed to high levels of soilborne inoculum required to produce disease on potato. References: (1) N. C. Gudmestad et al. Page 247 in: J. Vos et al. eds. Effects of Crop Rotation on Potato Production in the Temperate Zones. Kluwer, Dordrecht, Netherlands, 1989. (2) M. J. Lehtonen et al. Agric. Food Sci. 18:223, 2009. (3) J. W. Woodhall et al. Plant Pathol. 56:286, 2007. (4) J. W. Woodhall et al. Plant Pathol. 57:897, 2008.


Plant Disease ◽  
2012 ◽  
Vol 96 (3) ◽  
pp. 460-460 ◽  
Author(s):  
J. W. Woodhall ◽  
A. R. Belcher ◽  
J. C. Peters ◽  
W. W. Kirk ◽  
P. S. Wharton

Rhizoctonia solani is an important pathogen of potato (Solanum tuberosum) causing qualitative and quantitative losses. It has been associated with black scurf and stem canker. Isolates of the fungus are assigned to one of 13 known anastomosis groups (AGs), of which AG3 is most commonly associated with potato disease (2,4). In August 2011, diseased potato plants originating from Rupert, ID (cv. Western Russet) and Three Rivers, MI (cv. Russet Norkotah) were received for diagnosis. Both samples displayed stem and stolon lesions typically associated with Rhizoctonia stem canker. The presence of R. solani was confirmed through isolation as previously described (4) and the Idaho and Michigan isolates were designated J11 and J8, respectively. AG was determined by sequencing the rDNA internal transcribed spacer (ITS) region using primers ITS5 and ITS4 (3). The resulting sequences of the rDNA ITS region of isolates J8 and J11 (GenBank Accession Nos. HE608839 and HE608840, respectively) were between 97 and 100% identical to that of other AG2-2IIIB isolates present in sequence databases (GenBank Accession Nos. FJ492075 and FJ492170, respectively). Koch's postulates were confirmed for each isolate by carrying out the following protocol. Each isolate was cultured on potato dextrose agar for 14 days. Five 10-mm agar plugs were then placed on top of seed tubers (cv. Maris Piper) in 1-liter pots containing John Innes Number 3 compost (John Innes Manufacturers Association, Reading, UK). Pots were held in a controlled environment room at 18°C with 50% relative humidity and watered as required. After 21 days, plants were removed and assessed for disease. Typical Rhizoctonia stem lesions were observed and R. solani was successfully reisolated from symptomatic material. To our knowledge, this is the first report of AG2-2IIIB causing disease on potatoes in the United States. In the United States, AGs 2-1, 3, 4, 5, and 9 have all been previously implicated in Rhizoctonia potato disease (2). AG2-2IIIB should now also be considered a potato pathogen in the United States. Knowledge of which AG is present is invaluable when considering a disease management strategy. AG2-2IIIB is a causal agent of sugar beet (Beta vulgaris) root rot in Idaho (1). Sugar beet is commonly grown in crop rotation with potato and such a rotation could increase the risk of soilborne infection to either crop by AG2-2IIIB. References: (1) C. A. Strausbaugh et al. Can. J. Plant Pathol. 33:210, 2011. (2) L. Tsror. J. Phytopatol. 158:649, 2010. (3) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, Inc., New York, 1990. (4) J. W.Woodhall et al. Plant Pathol. 56:286, 2007.


Plant Disease ◽  
2013 ◽  
Vol 97 (8) ◽  
pp. 1113-1113 ◽  
Author(s):  
S. Lob ◽  
M. V. Jaspers ◽  
H. J. Ridgway ◽  
E. E. Jones

Phoma black leg or stem canker, caused by Leptosphaeria maculans or L. biglobosa, is an important disease of brassicas, causing significant crop losses in areas such as Europe, Australia, and North America (1). Samples collected in 2011 from canola and forage brassica (swede, kale, and turnip) crops in the main New Zealand growing regions (Southland, Central Otago, Canterbury, Hawkes Bay, and Manawatu) to identify the causal agent(s) of the characteristic stem cankers, found many isolates of L. maculans, which has been reported previously in New Zealand (2), and three isolates identified by colony characteristics as L. biglobosa. Of the latter, two isolates were from canola (Brassica napus) stem cankers from Darfield and Lincoln, Canterbury, and one was from a kale (B. oleracea) stem canker from Lincoln. An isolate (ICMP10665) of similar morphology, from the International Collection of Microorganisms from Plants (ICMP), obtained from a basal rot lesion on a cauliflower (B. oleracea var. botrytis) plant in Levin, New Zealand in 1979, was also evaluated. The initial, incorrect identification of the latter isolate as L. maculans predates the reclassification of L. maculans group B isolates as a new species, L. biglobosa (1). These four isolates produced fluffy white mycelium and a yellow pigment on potato dextrose agar (PDA) after 5 days' growth, and abundant black-brown, globose pycnidia containing cylindrical hyaline conidia after 7 days. In contrast, L. maculans isolates had slower growth and no pigment production (4). Amplification of genomic DNA using species-specific primers LmacR, LmacF, and LbigF (1) generated a PCR product of 444 bp that is typical of L. biglobosa isolates. Sequencing of the PCR product from each of the four isolates showed they were 100% identical to a sequence of L. biglobosa ‘brassicae’ in GenBank (JF740198). To confirm the species identity of the isolates, the rDNA, actin, and β-tubulin gene regions were amplified (1,3). Sequences for the rDNA (568 bp), actin (941 bp), and β-tubulin (410 bp) gene regions were 99% identical to sequences of the same regions of isolates in GenBank for L. biglobosa ‘brassicae’ (AY48997, AY748949.1, and AY748997.1, respectively). The four L. biglobosa isolates were tested for pathogenicity on a canola cultivar commonly grown in New Zealand (Flash). Cotyledons of 10-day-old seedlings (n = 12 seedlings/isolate or control treatment) grown in a potting mix in pots were pricked with a sewing needle, and each wound inoculated with 10 μl of the appropriate conidial suspension (106 conidia/ml) or 10 μl sterilized distilled water for the control treatment. Leaf lesions that developed on the inoculated cotyledons were characteristic of those caused by L. biglobosa, i.e., small and dark with a distinct margin. No pycnidia were produced on the lesions. No lesions developed on the cotyledons of the non-inoculated control plants. The causal agents were confirmed as L. biglobosa by the colony morphology of isolates that grew from surface-sterilized, inoculated leaf lesions plated on PDA amended with 100 μg/ml ampicillin. The fungus was not isolated from control leaf tissue. To our knowledge, this is the first report of L. biglobosa as a pathogen of canola and kale in New Zealand. This finding shows that both causal agents of black leg are present in New Zealand's brassica cropping areas. References: (1) S. Y. Liu et al. Plant Pathol. 55:401, 2006. (2) H. C. Smith and B. C. Sutton. Trans. Brit. Mycol. Soc. 47:159, 1964. (3) L. Vincenot et al. Phytopathology 98:321, 2008. (4) R. H. Williams and B. D. L. Fitt. Plant Pathol. 48:161, 1999.


Plant Disease ◽  
2018 ◽  
Vol 102 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Norman Muzhinji ◽  
James W. Woodhall ◽  
Mariette Truter ◽  
Jacquie E. van der Waals

Understanding the contribution of seed tuber- and soilborne inocula of Rhizoctonia solani AG 3-PT in causing potato disease epidemics is an important step in implementing effective management strategies for the pathogen. A 2-year study was conducted to evaluate the contribution of each source of inoculum using an integrative experimental approach combining field trials and molecular techniques. Two distinct sets of genetically marked isolates were used as seed tuberborne and soilborne inocula in a mark-release-recapture experiment. Disease assessments were done during tuber initiation and at tuber harvest. Both inoculum sources were found to be equally important in causing black scurf disease, whereas soilborne inocula appeared to be more important for root and stolon infection, and seedborne inocula contributed more to stem canker. However, seed tuber-transmitted genotypes accounted for 60% of the total recovered isolates when genotyped using three polymerase chain reaction restriction fragment length polymorphism markers. The changes in population structure of the experimental R. solani population over the course of the growing season and across two growing seasons were investigated using eight microsatellite markers. The populations at different sampling times were somewhat genetically differentiated, as indicated by Nei’s gene diversity (0.24 to 0.27) and the fixation index (FST). The proportion of isolates with genotypes that differed from the inoculants ranged from 13 to 16% in 2013 and 2014, respectively, suggesting the possibility of emergence of new genotypes in the field. Because both soilborne and tuberborne inocula are critical, it is important to ensure the use of pathogen-free seed tubers to eliminate seed tuberborne inoculum and the introduction of new genotypes of R. solani for sustainable potato production in South Africa.


Plant Disease ◽  
2021 ◽  
Vol 105 (1) ◽  
pp. 213
Author(s):  
S. D. Takooree ◽  
H. Neetoo ◽  
V. M. Ranghoo-Sanmukhiya ◽  
S. Hardowar ◽  
J. E. van der Waals ◽  
...  

Plant Disease ◽  
2019 ◽  
Vol 103 (8) ◽  
pp. 2130-2130
Author(s):  
M. R. Murdock ◽  
J. W. Woodhall ◽  
R. Maggard ◽  
S. Keith ◽  
M. Harrington ◽  
...  

Plant Disease ◽  
2013 ◽  
Vol 97 (9) ◽  
pp. 1245-1245 ◽  
Author(s):  
J. W. Woodhall ◽  
B. Lutomirska ◽  
J. C. Peters ◽  
P. S. Wharton

Rhizoctonia solani is a species complex of 13 related but genetically distinct anastomosis groups (AGs). In potato, R. solani can infect the stems, stolons, and roots, resulting in quantitative losses. It can also cause qualitative losses through blemishes occurring on progeny tubers, such as black scurf and elephant hide (corky cracking). Knowledge of the AG in local populations is important because they differ in host range, fungicide sensitivity, and disease severity (2). To determine the AGs present in Poland, 54 tuber samples displaying typical R. solani symptoms were taken from six different fields in 2011. The fields were representative of five different administrative regions of Poland and from at least 10 different varieties. Rhizoctonia was isolated from tubers by placing symptomatic material on to tap water agar amended with streptomycin and penicillin and after 2 to 3 days Rhizoctonia colonies were identified and hyphal tips of these transferred to potato dextrose agar. Rhizoctonia was successfully isolated from 48 tubers displaying black scurf and two tubers displaying elephant hide symptoms. DNA was extracted from Rhizoctonia cultures using a Wizard Food kit (Promega) and the AG was determined using specific real-time PCR assays (1). All Rhizoctonia isolates were determined to be AG3 and this was confirmed for 10 selected isolates by observing hyphal fusion with a known AG3 tester isolate (Rs08) as described previously (3). Pairings were also conducted amongst the 10 Polish isolates, C2 reactions were typically observed indicating numerous vegetative compatible groups are present. This study shows that AG3 is likely to be the predominant AG in potato tubers in Poland. This is similar to other studies in Europe, which have all determined that AG3 accounts for at least 92% of isolates from potato (2,3). AG2-1, 4, and 5 have also been found in tubers worldwide and climate and certain crop rotations can influence the presence of these other AGs in potato tubers (2). However, climate and crop rotations in Poland are similar to other parts of Europe so the predominance of AG3 is expected. AG3 was also isolated from elephant hide symptoms; however, it was more frequently isolated from sclerotia. The ability of AG3 to prolifically produce sclerotia and thereby survive on seed tubers may explain its predominance in potato crops (4). Therefore, studies focusing on the management of Rhizoctonia potato disease in Poland should consider AG3 in the first instance. References: (1) G. E. Budge et al. Plant Pathol. 58:1071, 2009. (2) L. Tsror. J. Phytopathol. 158:649, 2010. (3) J. W. Woodhall et al. Plant Pathol. 56:286, 2007. (4) J. W. Woodhall et al. Plant Pathol. 57:5, 2008.


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