scholarly journals Puccinia sorghi Virulent on Sweet Corn with the Rp1-D Gene in Southern France

Plant Disease ◽  
2001 ◽  
Vol 85 (5) ◽  
pp. 560-560
Author(s):  
J. K. Pataky ◽  
D. C. Plaisted ◽  
D. Scholten ◽  
H. F. de Durand

The Rp1-D gene, which conveys a chlorotic-fleck resistant reaction to Puccinia sorghi, effectively controlled common rust on sweet corn in North America for nearly 15 years. Biotypes of P. sorghi virulent on plants with the Rp1-D gene were widespread in North America for the first time in 1999 and again in 2000 (1,2). Many Rp-resistant sweet corn hybrids that are developed and grown in North America also are grown in Europe, including France where virulence against the Rp1-D gene has not been reported previously. In September 2000, uredinia of common rust were observed on and collected from sweet corn hybrids with the Rp1-D gene in commercial fields and hybrid trials in the Landes and Pyrénées Atlantiques departments of the Aquitaine region of southwestern France. Severity of rust generally was below 5% on these plants except for a few hybrids for which severity was about 20 to 30%. Common rust was not observed on hybrids with the Rp-G gene. Urediniospores were increased as a bulk population on the susceptible sweet corn hybrid Sterling in a greenhouse. Plants with each of 10 single Rp genes (Rp1-A, Rp1-C, Rp1-D, Rp1-E, Rp1-F, Rp1-I, Rp1-K, Rp1-L, Rp1-N, and Rp-G) or each of six compound rust resistance genes (Rp1-D5, Rp1-JC, Rp1-JFC, Rp-GDJ, Rp-GFJ, and Rp-G5JC) were assayed for reactions to this population of P. sorghi. Two to six different sources of seed of each single Rp gene and two different sources of seed of each compound rust resistance gene were replicates with a single pot of 6 to 18 plants grown from a specific seed source. Plants were inoculated three times on successive days by placing 2 or 3 ml of a urediniospore suspension in the whorl of two- to four-leaved seedlings. Reactions were rated 10 days after the last inoculation. Plants without symptoms or with chlorotic-fleck resistant reactions were inoculated again and rated 10 days later. Uredinia did not form on plants with compound rust resistance genes. Plants with the genes Rp1-E, Rp1-I, Rp1-K, and Rp-G also were resistant although a few, very small uredinia (i.e., type-1 uredinia) were observed on a few plants. Plants with the genes Rp1-A, Rp1-C, Rp1-D, Rp1-F, Rp1-L, and Rp1-N were fully susceptible. This pattern of virulence is the same as that observed during the past two years in North American populations of P. sorghi virulent against Rp1-D. Rp-resistance currently available in most sweet corn hybrids will not be effective in France if these virulent biotypes become prevalent. References: (1) J. K. Pataky et al. Plant Dis. 85:165, 2001. (2) M. C. Pate et al. Plant Dis. 84:1154, 2000.

Plant Disease ◽  
2001 ◽  
Vol 85 (2) ◽  
pp. 165-168 ◽  
Author(s):  
Jerald K. Pataky ◽  
Molly C. Pate ◽  
Scot H. Hulbert

Resistance in sweet corn conferred by the Rp1-D gene has controlled common rust, caused by Puccinia sorghi, in North American corn for nearly 15 years. Eleven isolates of P. sorghi virulent on corn with the Rp1-D gene were collected from Rp-resistant corn in 1999 from Wiscon-sin, Illinois, New York, and Minnesota. Isolates were increased on susceptible sweet corn. Urediniospores of nine isolates were bulked. Reactions of individual Rp genes in the rp1 region and reactions of linked combinations of Rp genes in the rp1 region (i.e., compound rust resistance genes) were evaluated against the bulked population of P. sorghi in several greenhouse trials. Reactions of individual and compound Rp genes also were evaluated against individual isolates of P. sorghi. Each trial contained at least two replicates of several lines with Rp genes and one susceptible check. Five to 10 two-leaved seedlings per line were inoculated at least twice with a suspension of urediniospores. Ten days after inoculation, rust reactions were rated:+ = sporulating uredinia, - = no sporulating uredinia, and I = chlorotic or necrotic tissue surrounding small uredinia. Four single genes, Rp1-E, Rp-G, Rp1-I, and Rp1-K, and eight compound genes, Rp1-JFC, Rp1-JC, Rp-GI, Rp-G5, Rp-GDJ, Rp-G5JD, Rp-G5JC, and Rp-GFJ, conferred resistance. Additional characterization of virulence in North American populations of P. sorghi that are avirulent against Rp1-D is necessary to determine if these genes will be as widely effective as the Rp1-D gene has been. Two subpopulations of P. sorghi were detected from the bulked population after it was sequentially cultured for at least five cycles on seedlings with Rp1-C or with Rp1-J. The subpopulation cultured on Rp1-J was avirulent on lines with Rp1-C/L/N, Rp1-B, and Rp1-M; whereas the subpopulation cultured on Rp1-C was virulent on lines with each of these genes. Both subpopulations were virulent on lines with Rp1-D.


Plant Disease ◽  
2000 ◽  
Vol 84 (7) ◽  
pp. 810-810 ◽  
Author(s):  
J. K. Pataky ◽  
T. A. Natti ◽  
E. B. Snyder ◽  
C. J. Kurowski

Several different Rp genes in corn condition chlorotic fleck resistant reactions to Puccinia sorghi. Rp-resistance has been used successfully for the past 15 years to control common rust on sweet corn in North America. Most, but not all, Rp-resistant sweet corn hybrids carry the Rp1-D gene. In August and September 1999, isolates of P. sorghi were collected from Rp-resistant sweet corn grown in Illinois, Wisconsin, Minnesota, Michigan, and New York. This was the first widespread occurrence in North America of P. sorghi virulent on corn with Rp1-D (2). The origin of this population of P. sorghi with a virulence phenotype new to North America is not known. Since many believe Mexico is the source of common rust inocula for the midwestern United States, it is important to discover if this virulence occurs in Mexico. Forty-one Rp-resistant and nine susceptible sweet corn hybrids were planted 8 December 1999 in a nursery near Los Mochis, Mexico, in the state of Sinalao. Rp-resistant hybrids had been effective against common rust in Los Mochis nurseries prior to 1999. Each hybrid was in a single row of about 30 plants. The Los Mochis nursery also included two replicate rows of sweet corn or field corn inbred lines with one of 17 different single Rp-genes or one of 11 different compound genes for rust resistance (1). Plants were exposed to local populations of P. sorghi. Reactions were rated in March 2000. Sporulating uredinia (susceptible reactions) were abundant on all sweet corn hybrids and on inbreds with Rp1-D. Susceptible reactions also were observed on other inbred lines with Rp-genes except for lines with the single genes: Rp1-E, Rp-G, Rp1-I, Rp1-K, and Rp1-L or lines with the compound rust genes: Rp1-GI, Rp1-G5, Rp1-GDJ, Rp1-GFJ, Rp1-G5JC, Rp1-G5JD, and Rp1-JFC. This pattern of virulence is similar to that of P. sorghi isolates collected in the midwestern United States in 1999. Rp-resistance currently available in most sweet corn hybrids grown in the Midwest will not be effective when this population of P. sorghi spreads from Mexico to the United States. Therefore, other sources of rust resistance need to be incorporated into sweet corn hybrids. References: (1) S. H. Hulbert, Annu. Rev. Phytopathol. 35:292, 1997. (2) J. K. Pataky and W. F. Tracy. Plant Dis. 83:1177, 1999.


Plant Disease ◽  
1999 ◽  
Vol 83 (12) ◽  
pp. 1177-1177 ◽  
Author(s):  
J. K. Pataky ◽  
W. F. Tracy

Single, dominant resistance genes have been used successfully for the past 15 years to control common rust, caused by Puccinia sorghi, on sweet corn in the United States. Most sweet corn hybrids grown in the Midwest for mid- to late-season processing have Rp resistance, which is expressed as hypersensitive reactions resulting in chlorotic or necrotic flecks with little or no formation of urediniospores. Many, but not all, Rp-resistant sweet corn hybrids carry the gene Rp1D. Biotypes of P. sorghi in North America have been avirulent on plants with the Rp1D gene, except for an isolate collected in Kansas in 1990 (1). In a sweet corn nursery in Urbana, IL, in 1997, small uredinia of P. sorghi occurred on 27 of 79 Rp-resistant sweet corn hybrids that also were infected severely with southern rust caused by P. polysora (2). During August and September 1999, small uredinia or fully susceptible reactions to common rust were observed on several Rp-resistant sweet corn hybrids grown in an area bounded by Mendota, IL, Ripon, WI, and Le Sueur, MN. Southern rust also was prevalent and frequently severe in the area. Isolates of P. sorghi from Rp-resistant corn were collected during September 1999 from Mendota, Rock Falls, and Dekalb, IL; Sun Prairie, Madison, and Ripon, WI; and Rochester, Stanton, and Le Sueur, MN. Ten two-leaved seedlings of one susceptible sweet corn hybrid and five Rp-resistant hybrids, including hybrids known to carry the gene Rp1D, were inoculated in greenhouse trials. Each location (collection) was a separate trial. Inocula were prepared from several uredinia of P. sorghi per location. One set of seedlings also was inoculated with P. polysora. Susceptible reactions (uredinia with urediniospores) were observed on all inoculated seedlings. Uredinia and urediniospores of P. sorghi and P. polysora from seedlings inoculated in the greenhouse were compared directly. All isolates of P. sorghi were confirmed based on 6- to 7-day latent periods, formation of uredinia on both leaf surfaces, and urediniospores that were mostly spherical, cinnamon colored, and moderately echinulate. This is the first widespread occurrence in North America of a biotype of P. sorghi that is virulent on Rp-resistant sweet corn. References: (1) S. H. Hulbert et al. Plant Dis. 75:1130, 1991. (2) J. K. Pataky et al. Purdue Univ. AES Bull. No. 758:99, 1997.


2009 ◽  
Vol 99 (6) ◽  
pp. 750-758 ◽  
Author(s):  
M. E. Ordoñez ◽  
J. A. Kolmer

Wheat leaf rust caused by Puccinia triticina is widely distributed in the wheat growing regions of the United States and Canada, and is subject to selection for virulence phenotype by leaf rust resistance genes in wheat cultivars. The objective of this study was to determine the number of genetically differentiated groups of P. triticina that are currently present in North America. In total, 148 isolates of P. triticina from the 1980s to 2005 were collected from wheat-growing regions of the United States and Canada and tested for virulence on 20 lines of wheat with single genes for leaf rust resistance and for molecular genotype with 23 simple sequence repeat (SSR) markers. In total, 91 virulence phenotypes and 65 SSR genotypes were found. After removal of isolates with identical virulence and SSR genotypes, 125 isolates were included for further analysis. Bayesian cluster analysis indicated five different groups of isolates based on SSR genotypes that also differed for virulence to leaf rust resistance genes Lr2a, Lr2c, Lr3bg, Lr17, and Lr28. Isolates avirulent to Lr14a and Lr20 that have increased since 2003 had SSR genotypes identical or similar to older isolates in one of the five groups, indicating that these isolates were derived by mutation from the previously existing population of P. triticina. The representative collection of P. triticina isolates had characteristics consistent with an asexual dikaryotic population of genetically differentiated groups of SSR genotypes with high levels of heterozygosity and disequilibrium within which stepwise mutation at avirulence or virulence loci regularly occurs.


Plant Disease ◽  
2000 ◽  
Vol 84 (10) ◽  
pp. 1154-1154 ◽  
Author(s):  
M. C. Pate ◽  
J. K. Pataky ◽  
W. C. Houghton ◽  
R. H. Teyker

For the past 15 years, the Rp1-D gene has controlled common rust on sweet corn in North America. In August and September 1999, isolates of Puccinia sorghi were collected from Rp1-D sweet corn hybrids in Illinois, Wisconsin, Minnesota, Michigan, and New York. This was the first widespread occurrence in the continental United States of P. sorghi virulent on the Rp1-D gene (1). Isolates of P. sorghi collected from Los Mochis, Mexico, in March 2000 had a pattern of virulence similar to the pattern for the isolates collected in the Midwest in 1999 (2). In April and May 2000, small uredinia were observed on Rp1-D sweet corn in Florida and Texas. In Florida, isolates were collected from six different locations within a 13-km radius near Belle Glade. Three isolates were collected each from Rp1-D and non-Rp sweet corn hybrids. Isolates also were collected from two Rp1-D sweet corn hybrids and a non-Rp sweet corn hybrid near Hondo, TX. Inocula of isolates were increased through one uredinial generation in the greenhouse. Several 1-cm2 pieces of leaf tissue with sporulating uredinia were placed in 15 ml of a solution of water and Tween 20. This inoculum was placed in whorls of five two-leaved seedlings of a susceptible hybrid, ‘Primetime.’ Urediniospores from newly formed uredinia were collected 10 days later and used as inocula to assay each isolate. Two isolates from Florida (one each from an Rp1-D and a non-Rp hybrid) were assayed on a non-Rp susceptible check, 20 different single Rp genes, and nine compound Rp genes. Other isolates were assayed on two replicates of a non-Rp susceptible check, a source of Rp1-D, and five single Rp genes that were effective against the isolates collected from the Midwest in 1999 and from Mexico in 2000. Each experimental unit consisted of five plants grown in 10-cm-diameter pots. Plants at the two-leaf stage were inoculated three times within 5 days by filling whorls with a urediniospore suspension. Rust reactions were rated 10 days after the final inoculation. Isolates collected in Florida from non-Rp hybrids were avirulent on Rp1-D but those collected in Texas from non-Rp hybrids were virulent on Rp1-D. Isolates collected in Florida and Texas from Rp1-D hybrids had a similar pattern of virulence as isolates collected from the Midwest in 1999 and from Mexico in March 2000; that is, effective single Rp genes included Rp1-E, Rp-G, Rp1-I, and Rp1-K. A source that we previously believed was Rp1-L now appears to be Rp-G. These are the first reports from Florida and Texas of P. sorghi virulent on Rp1-D, and they are the first occurrences of virulence against Rp1-D in the continental U.S. in 2000. Apparently, P. sorghi with virulence against Rp1-D has become established in an area where common rust inocula for North America overwinters. References: (1) J. K. Pataky and W. F. Tracy. Plant Dis. 83:1177, 1999. (2) J. K. Pataky et al. Plant Dis. 84:810, 2000.


1999 ◽  
Vol 35 (No. 3) ◽  
pp. 85-92
Author(s):  
P. Bartoš ◽  
J. Huszár ◽  
E. Herzová

In 1997–1998 virulence of the leaf rust population was studied on near isogenic Thatcher lines with the genes for resistance Lr1, Lr2a, Lr2b, Lr2c, Lr3, Lr9, Lrll, Lr15, Lr/7, Lr19, Lr21, Lr23, Lr24, Lr26 and Lr28, and on the standard differentials Mala­ koff, Carina, Brevit, Webster, Loros, Mediterranean, Hussar, Democrat and the supplemental cultivar Salzmtinder Bartweizen. All 55 analyzed rust samples were avirulent on Lr9, Lr19, Lr24 and Lr28.On the standard differentials, races 61SaBa, 77SaBa, 77/57SaBa, 2SaBa, 77, 12SaBa, 62SaBa, 6, 6SaBa and 14 were determined. Races 61SaBa and 77SaBa (77/57SaBa) prevailed in both years. Races 6 and 6SaBa were found for the first time. The effectiveness of leaf rust resistance genes in registered cultivars under field conditions in variety trials is discussed.


2010 ◽  
Vol 36 (1) ◽  
pp. 109-114 ◽  
Author(s):  
Hong ZHANG ◽  
Zhi-Long REN ◽  
Yin-Gang HU ◽  
Chang-You WANG ◽  
Wan-Quan JI

Plant Disease ◽  
2013 ◽  
Vol 97 (3) ◽  
pp. 387-392 ◽  
Author(s):  
Mohsen Mohammadi ◽  
Davoud Torkamaneh ◽  
Mehran Patpour

Following emergence of Ug99, the new virulent race of Puccinia graminis f. sp. tritici in Africa, a global effort for identification and utilization of new sources of Ug99-resistant germplasm has been undertaken. In this study, we conducted replicated experiments to evaluate the resistance of Iranian wheat germplasm to the TTKSK lineage of the Ug99 race of P. graminis f. sp. tritici. We also evaluated for presence of stem rust resistance genes (i.e., Sr2, Sr24, Sr26, Sr38, Sr39, Sr31, and Sr1RSAmigo) in wheat cultivars and breeding lines widely cultivated in Iran. Our phenotyping data revealed high levels of susceptibility to Ug99 in Iranian bread wheat germplasm. Our genotyping data revealed that Iranian cultivars do not carry Sr24, Sr26, or Sr1RSAmigo. Only a few salt-tolerant cultivars and breeding lines tested positively for Sr2, Sr31, Sr38, or Sr39 markers. In conclusion, the genetic basis for resistance to Ug99 in Iranian wheat cultivars was found to be vulnerable. Acquiring knowledge about existing resistance genes and haplotypes in wheat cultivars and breeding lines will help breeders, cereal pathologists, and policy makers to select and pyramid effective stem rust resistance genes.


Genome ◽  
2008 ◽  
Vol 51 (11) ◽  
pp. 922-927 ◽  
Author(s):  
P. G. Luo ◽  
X. Y. Hu ◽  
Z. L. Ren ◽  
H. Y. Zhang ◽  
K. Shu ◽  
...  

Stripe rust, caused by Puccinia striiormis Westend f. sp. tritici, is one of the most important foliar diseases of wheat ( Triticum aestivum L.) worldwide. Stripe rust resistance genes Yr27, Yr31, YrSp, YrV23, and YrCN19 on chromosome 2BS confer resistance to some or all Chinese P. striiormis f. sp. tritici races CYR31, CYR32, SY11-4, and SY11-14 in the greenhouse. To screen microsatellite (SSR) markers linked with YrCN19, F1, F2, and F3 populations derived from cross Ch377/CN19 were screened with race CYR32 and 35 SSR primer pairs. Linkage analysis indicated that the single dominant gene YrCN19 in cultivar CN19 was linked with SSR markers Xgwm410, Xgwm374, Xwmc477, and Xgwm382 on chromosome 2BS with genetic distances of 0.3, 7.9, 12.3, and 21.2 cM, respectively. Crosses of CN19 with wheat lines carrying other genes on chromosome 2B showed that all were located at different loci. YrCN19 is thus different from the other reported Yr genes in chromosomal location and resistance response and was therefore named Yr41. Prospects and strategies of using Yr41 and other Yr genes in wheat improvement for stripe rust resistance are discussed.


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