scholarly journals First Report of Puccinia sorghi Virulent on Sweet Corn with the Rp1-D Gene in Florida and Texas

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.

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.


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 ◽  
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 ◽  
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 ◽  
2007 ◽  
Vol 91 (11) ◽  
pp. 1484-1488 ◽  
Author(s):  
Jerald K. Pataky ◽  
M. Andrea Campaña

The Rp1D gene confers a hypersensitive, chlorotic-fleck, resistant reaction to Puccinia sorghi, the casual agent of common rust of corn. About 40% of commercial sweet corn hybrids carry the Rp1D gene. Sine 1999, Rp1D-virulent (D-virulent) isolates of P. sorghi have occurred regularly in populations of P. sorghi in North America. Observations from sweet corn hybrid nurseries and other trials indicate that the frequency of D-virulent isolates affects severity of rust on Rp1D hybrids; however, the frequency of D-virulence at which the Rp1D gene is rendered completely ineffective is not known. The objective of this study was to assess whether common rust severity is reduced by the Rp1D gene in sweet corn hybrids infected by mixtures of D-virulent and Rp1D-avirulent (avirulent) P. sorghi. Forty pairs of Rp1D-resistant and susceptible (rp1d) versions of sweet corn hybrids from six different commercial breeding programs were evaluated in 2003 and 2004 in trials inoculated with one of five different ratios of avirulent:D-virulent inocula: 100:0, 90:10, 80:20, 60:40, or 0:100. When D-virulent P. sorghi was 100% of initial inoculum, common rust was equally severe on Rp1D and rp1d versions of the same hybrid. Thus, the Rp1D gene did not confer partial or residual resistance in these trials. When initial inocula consisted of 40% or less D-virulent P. sorghi, rust was significantly less severe on Rp1D versions than on rp1d versions of the same hybrids. Relationships between rust severity on Rp1D and rp1d versions of hybrids were explained by linear regressions in all trials. Slope coefficients (i.e., rust severity on Rp1D hybrids as a proportion of that on rp1d hybrids) were related to the percentage of D-virulent P. sorghi in the initial inoculum and were 0.21, 0.29, 0.51, 0.64, and 0.93 in 2003 and 0.25, 0.50, 0.67, 0.76, and 1.0 in 2004 for trials inoculated with 0, 10, 20, 40, and 100% D-virulent P. sorghi, respectively. Thus, the Rp1D gene may convey levels of control in proportion to the frequency of virulence in mixed populations of D-virulent and avirulent P. sorghi when the frequency of virulent isolates is less than 40%.


Author(s):  
J. Ingham

Abstract A description is provided for Ramularia alba. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Lathyrus odoratus, the sweet pea. DISEASE: White blight of sweet pea, also called white mould or Cladosporium blight. Leaf spots vary from yellow flecks to buff coloured dead areas, which may be circular or irregular in shape merging gradually into healthy leaf tissue. Leaf spots may merge together affecting most of the leaf and in such cases defoliation may result (30, 41). GEOGRAPHICAL DISTRIBUTION: Europe (Denmark, England, Sweden). North America (Canada: British Columbia, Ontario; USA: California, Massachusetts, New Jersey, New York, Pennsylvania, Texas). TRANSMISSION: By wind dispersal of air-borne conidia.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Dedi Ruswandi ◽  
Yuyun Yuwariah ◽  
Mira Ariyanti ◽  
Muh Syafii ◽  
Anne Nuraini

Multienvironment testing is an important phase to study the interaction of G × E and to select stable hybrids for a broad environment or for a specific environment. To study the interaction of G × E and the stability of earliness and yield of Indonesian new sweet corn hybrids under different locations and seasons in West Java, Indonesia, eighteen hybrids were evaluated in six environments in West Java, Indonesia, and were analysed using parametric and nonparametric stability models, additive main effects and multiplicative interaction (AMMI), and GGE biplots. Results showed that the most promising sweet corn hybrids including hybrids G5 (SR 24 x SR 17) and G11 (SR 31 x SR 17) were identified. The parametric and nonparametric stability parameters and ASV were complement to the AMMI and GGE biplots in selecting stable and adaptable hybrids in terms of earliness and yield. G5 was selected as a high-response hybrid for grain yield to Jatinangor (E1, E2), Lembang (E3, E4), and Wanayasa (E5, E6), as well as earliness to Jatinangor (E2), Lembang (E3, E4), and Wanayasa (E5, E6). G5 sweet corn hybrid, therefore, is suggested to be extensively evaluated on farm and produced for smallholder farmers in West Java, Indonesia.


Weed Science ◽  
2012 ◽  
Vol 60 (4) ◽  
pp. 577-582 ◽  
Author(s):  
Martin M. Williams ◽  
Jerald K. Pataky

Maize dwarf mosaic (MDM) stunts corn growth, delays development, and is the most prevalent viral disease of sweet corn grown in many regions of North America and Europe. Although some weeds escape control in most sweet corn fields, the extent to which MDM influences the weed suppressive ability of the crop is unknown. Field studies were conducted over a 3-yr period to characterize the influence of variable MDM incidence in sweet corn on growth, fecundity, and germinability of wild-proso millet, a common weed in the crop. Treatments included five levels of MDM incidence (0, 25, 50, 75, and 100% of plants infected) in two MDM-susceptible hybrids differing in weed suppressive ability. Previous research showed that hybrid ‘Legacy’ had greater weed suppressive ability than ‘Sugar Buns’. Wild-proso millet biomass and fecundity depended largely on the hybrid in which the weed was growing. Wild-proso millet growing in Sugar Buns weighed 45 to 117% more than wild-proso millet in Legacy. Incidence of MDM in sweet corn affected wild-proso millet biomass and fecundity, but only under high weed population densities. When wild-proso millet was observed at 122 plants m−2, weed biomass increased 9 g m−2 for each additional 10% incidence of MDM of sweet corn. Weed suppressive ability of the competitive and less competitive hybrids were influenced to the same extent by MDM. Coupled with a lack of resistance to MDM in two-thirds of commercial sweet corn hybrids, the disease could be an additional factor perpetuating weed growth and fecundity in sweet corn, particularly in fields with high population densities of wild-proso millet.


2005 ◽  
Vol 19 (2) ◽  
pp. 342-345 ◽  
Author(s):  
Nader Soltani ◽  
Shane Diebold ◽  
Darren E. Robinson ◽  
Peter H. Sikkema

Limited information exists on sweet corn tolerance to postemergence (POST) applications of clopyralid under Ontario growing conditions. Eight sweet corn hybrids were evaluated for tolerance to clopyralid in three field experiments conducted in 2001 and 2002 in Ontario. Clopyralid was applied POST at 200 and 400 g ai/ha, the proposed and twice the proposed registered rate for use in sweet corn in Ontario. Sweet corn response to clopyralid did not vary among the hybrids tested. In 2001, visual injury among hybrids 7 d after treatment (DAT) with clopyralid at 400 g/ha was less than 3%. Subsequent visual injury evaluations at 14 and 28 DAT showed no differences among sweet corn hybrids at either rate of clopyralid evaluated. The application of clopyralid at 200 and 400 g/ ha had no detrimental effect on plant height or marketable yield of any of the eight sweet corn hybrids. On the basis of visual injury, height, and marketable yield response ‘Calico Belle’, ‘CNS 710’, ‘DelMonte 2038’, ‘GG 222’, ‘GG 246’, ‘GH 2684’, ‘Reveille’, and ‘Rival’ are all tolerant to the POST application of clopyralid.


Plant Disease ◽  
2001 ◽  
Vol 85 (12) ◽  
pp. 1278-1284 ◽  
Author(s):  
Noah D. Freeman ◽  
Jerald K. Pataky

Stewart's wilt reactions and yield of a total of 69 sweet corn hybrids were evaluated in trials in 1999 and 2000 in order to determine the level of Stewart's wilt resistance necessary to prevent reduction in yield of sweet corn hybrids. Plants at the 2- to 3-leaf stage were inoculated with Erwinia stewartii using the pinprick method. Stewart's wilt symptoms were rated from 1 to 9, and incidence of systemic infection was determined as a percentage for each experimental unit. Primary ears were harvested about 21 days after midsilk, and yield was measured as ear weight and number of marketable ears. Percent yield was calculated for each hybrid by dividing yield from inoculated treatments by yield from noninoculated treatments and multiplying by 100. Hybrid means for Stewart's wilt ratings in inoculated treatments ranged from 2.0 to 7.3. The relationships between percent yield and Stewart's wilt severity ratings were described best by curvilinear regressions, whereas percent yield decreased linearly with the incidence of systemic infection in 2000. Ear weights of hybrids with ratings below 3 or 3.5 were estimated from the regression equations to be within 95 or 92%, respectively, of those from noninoculated treatments of the same hybrid. The number of marketable ears from hybrids with ratings of 3 or below was estimated from the regression equations to be within 90% of those from noninoculated treatments of the same hybrid. A level of resistance that resulted in Stewart's wilt ratings below 3 or 3.5 corresponded to nonsystemic infection of most plants (i.e., incidence of systemic infection below 5 or 10%, respectively). The adverse effects of Stewart's wilt on ear weight and marketability appeared to be minor for sweet corn hybrids with levels of resistance that prevented or minimized systemic infection.


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