scholarly journals Levels of Stewart's Wilt Resistance Necessary to Prevent Reductions in Yield of Sweet Corn Hybrids

Plant Disease ◽  
2001 ◽  
Vol 85 (12) ◽  
pp. 1278-1284 ◽  
Author(s):  
Noah D. Freeman ◽  
Jerald K. Pataky
Keyword(s):  
Adverse Effects ◽  
Sweet Corn ◽  
Systemic Infection ◽  
Experimental Unit ◽  
Regression Equations ◽  
Corn Hybrids ◽  
Wilt Resistance ◽  
Leaf Stage ◽  
Erwinia Stewartii ◽  
Stewart's Wilt

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.

scholarly journals Relationships Between Reactions of Sweet Corn Hybrids to Stewart's Wilt and Incidence of Systemic Infection by Erwinia stewartii

Plant Disease ◽  
2003 ◽  
Vol 87 (3) ◽  
pp. 223-228 ◽  
Author(s):  
P. M. Michener ◽  
N. D. Freeman ◽  
J. K. Pataky
Keyword(s):  
Growth Stage ◽  
Sweet Corn ◽  
Systemic Infection ◽  
Control Measures ◽  
Growth Stages ◽  
Corn Hybrids ◽  
Systemic Movement ◽  
Erwinia Stewartii ◽  
Stewart's Wilt ◽  
Central Illinois

Relationships between the reactions of sweet corn hybrids to Stewart's wilt and the incidence of natural, systemic infection by Erwinia stewartii differed among trials in which the prevalence of Stewart's wilt differed. Systemic Stewart's wilt infection was assessed for 262, 296, and 245 hybrids planted in seven trials in central Illinois in June and July 1998, 1999, and 2000, respectively. Incidence of systemic infection was calculated in each trial for all hybrids in each of nine categories of Stewart's wilt reactions (i.e., 1 = resistant and 9 = susceptible). When mean incidence was about 5%, incidence ranged from about 1 to 8% on resistant to moderately susceptible hybrids, but incidence was nearly 30% on susceptible hybrids. When mean incidence ranged from 10 to 16%, the relationships between hybrid reactions and incidence were explained by exponential or polynomial regressions. Incidence was less than 10% for hybrids with resistant and moderately resistant reactions, and incidence was greater than 15% for moderately susceptible to susceptible hybrids. When mean incidence was near 50%, the relationship was linear. Incidence was about 18% for resistant hybrids and about 80% for susceptible hybrids. Incidence increased about 8% for each class of hybrid reaction from 1 to 9. The influence of resistance on the development of systemic infection at very early seedling growth stages also was evaluated in six greenhouse trials. A highly resistant hybrid, Bonus, was systemically infected in two of six greenhouse trials when seedlings were inoculated prior to the V3 growth stage; however, systemic infection was not as severe as on a susceptible hybrid, Jubilee. Systemic infection was more severe on Bonus when plants were inoculated at earlier growth stages between VE and V3. The resistant hybrid Bonus was not systemically infected when inoculated after the V4 growth stage except for one greenhouse trial when all Stewart's wilt ratings were higher than usual. Hybrid reactions to Stewart's wilt affected the incidence of systemic infection in field situations and they affected the growth stage at which resistance effectively prevented systemic movement of E. stewartii within plants in greenhouse trials. This information can be used to determine more effectively when to apply other control measures, such as insecticidal seed treatments.

scholarly journals Control of Stewart's Wilt in Sweet Corn with Seed Treatment Insecticides

Plant Disease ◽  
2000 ◽  
Vol 84 (10) ◽  
pp. 1104-1108 ◽  
Author(s):  
J. K. Pataky ◽  
P. M. Michener ◽  
N. D. Freeman ◽  
R. A. Weinzierl ◽  
R. H. Teyker
Keyword(s):  
Host Resistance ◽  
Seed Treatment ◽  
Sweet Corn ◽  
Flea Beetle ◽  
Field Trials ◽  
Seed Treatments ◽  
Corn Hybrids ◽  
Flea Beetles ◽  
Erwinia Stewartii ◽  
Stewart's Wilt

Corn flea beetles, Chaetocnema pulicaria, vector Erwinia stewartii (synamorph Pantoea stewartii), which causes Stewart's bacterial wilt of corn (Zea mays). A seed treatment insecticide, imidacloprid, killed flea beetles and reduced the number of feeding wounds and Stewart's wilt symptoms per leaf in greenhouse studies. The objective of our research was to evaluate the ability of imidacloprid and thiamethoxam seed treatments to control Stewart's wilt on sweet corn hybrids under field conditions with naturally occurring populations of the corn flea beetle. Six field trials were planted at four locations in 1998. Eleven field trials were planted at nine locations in 1999. The treatment design was a factorial of sweet corn hybrids and seed treatments. Stewart's wilt incidence ranged from 0 to 54% in the 1998 trials. Incidence of Stewart's wilt in nontreated plots of the susceptible hybrid Jubilee ranged from 2% at the 8-leaf stage to 77% 1 week after mid-silk in the 1999 trials. Seed treatment insecticides reduced the incidence of Stewart's wilt by ≈50 to 85% relative to nontreated controls. The level of control was ≈75 to 85% in seven trials planted before 1 June 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 4 to 71%. The level of control was ≈50 to 70% in the three trials planted after 1 July 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 44 to 73%. Although comparisons varied, the level of control gained from seed treatment insecticides was similar to the next higher level of host resistance. Seed treatment insecticides appear to control Stewart's wilt during very early growth of corn plants, when foliar applications of insecticides are ineffective and the effectiveness of host resistance varies depending on the proximity of flea beetle feeding sites to the plant's growing point.

scholarly journals Transmission of Erwinia stewartii from Plants to Kernels and Reactions of Corn Hybrids to Stewart's Wilt

Plant Disease ◽  
2002 ◽  
Vol 86 (2) ◽  
pp. 167-172 ◽  
Author(s):  
P. M. Michener ◽  
J. K. Pataky ◽  
D. G. White
Keyword(s):  
Sweet Corn ◽  
F1 Hybrids ◽  
Enzyme Linked Immunosorbent Assay ◽  
Corn Hybrids ◽  
Food Grade ◽  
Kernel Infection ◽  
Dent Corn ◽  
The Mean ◽  
Erwinia Stewartii ◽  
Stewart's Wilt

Stewart's wilt reactions of 98 food-grade, white corn hybrids, 3 yellow dent corn hybrids, and 23 sweet corn hybrids and infection of kernels by E. stewartii were evaluated in 1998, 1999, and 2000. Stewart's wilt symptoms were rated from 1 (no appreciable spread of symptoms) to 9 (dead plants) following inoculation. The mean Stewart's wilt ratings for the food-grade, white corn and yellow dent corn hybrids were 1.9, 2.4, and 2.9 in 1998, 1999, and 2000, respectively. The mean Stewart's wilt ratings for the sweet corn hybrids were 3.8, 4.2, and 4.6 in 1998, 1999, and 2000, respectively. Hybrids with ratings less than 3 were classified as resistant. Hybrids with ratings between 3 and 4.5 were classified as moderate. Hybrids with ratings greater than 4.5 were classified as susceptible. Ears harvested from each row in 1998 and 1999 were assayed for E. stewartii using an enzyme-linked immunosorbent assay (ELISA)-based seed health test. Kernels from 16 hybrids were positive for E. stewartii in 1998. Kernels from 11 hybrids were positive for E. stewartii in 1999. Kernel infection by E. stewartii was affected considerably by the level of host resistance (i.e., reactions of seed parent plants). For hybrids classified as resistant, estimates of kernel infection were 0.024 and 0.0007% in 1998 and 1999, respectively. For hybrids with moderate reactions to Stewart's wilt, estimates of kernel infection were 0.19 and 0.07% in 1998 and 1999, respectively. For hybrids with susceptible reactions to Stewart's wilt, estimates of kernel infection were 11.6 and 7.8% in 1998 and 1999, respectively. Based on high levels of Stewart's wilt resistance in food-grade, white corn hybrids, and low rates of kernel infection by E. stewartii in resistant and moderate hybrids, there is an exceedingly low probability of introducing E. stewartii to areas where it does not occur by transmitting the bacterium in grain of the food-grade, white corn hybrids evaluated in this study. Although all of the kernels harvested in these experiments were produced as grain on open-pollinated F1 hybrids, the rates of kernel infection observed for hybrids with resistant, moderate and susceptible reactions to Stewart's wilt are applicable to seed produced on inbred lines with equivalent Stewart's wilt reactions.

scholarly journals SWEET CORN INBREDS WITH PARTIAL RESISTANCE TO NORTHERN LEAF BLIGHT AND STEWART'S WILT

HortScience ◽  
1990 ◽  
Vol 25 (9) ◽  
pp. 1067a-1067 ◽  
Author(s):  
A. C. Meyer ◽  
J. K Pataky ◽  
J.A. Juvik
Keyword(s):  
Partial Resistance ◽  
Sweet Corn ◽  
Leaf Blight ◽  
Exserohilum Turcicum ◽  
Northern Leaf Blight ◽  
Dent Corn ◽  
Erwinia Stewartii ◽  
Stewart's Wilt ◽  
Corn Inbred ◽  
Moderately Resistant

Approximately 200 sweet corn inbred lines were screened for two years for resistance to northern leaf blight, caused by Exserohilum turcicum, and Stewart's wilt, caused by Erwinia stewartii. Inbreds with the best levels of partial resistance to races 1 and 2 of E. turcicum included IL11d, IL676a, IL677a, IL685d, IL766a, IL767a and IL797a. Inbreds with the best partial resistance to E. stewartii included IL126b, IL676a, IL767a, IL772a, IL774g, IL797a, IL798a and M6011. Several of these resistant and moderately resistant inbreds had common ancestors; however, inspection of pedigrees suggested that resistance was derived from Puerto Rican, Bolivian, and other tropical sources and/or dent corn. Thus, many of the sweet corn inbreds may carry different genes for resistance and can be used for the development of populations with improved resistance.

scholarly journals Rates of Transmitting Erwinia stewartii from Seed to Seedlings of a Sweet Corn Hybrid Susceptible to Stewart's Wilt

Plant Disease ◽  
2002 ◽  
Vol 86 (9) ◽  
pp. 1031-1035 ◽  
Author(s):  
P. M. Michener ◽  
J. K. Pataky ◽  
D. G. White
Keyword(s):  
Sweet Corn ◽  
Natural Infection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Adult Plant ◽  
Plant Seed ◽  
Transmission Rates ◽  
Infected Seed ◽  
Erwinia Stewartii ◽  
Stewart's Wilt ◽  
Corn Hybrid

Rates of transmitting Erwinia stewartii from seed to seedlings were estimated from field grow-outs of seedlings grown from seed infected with E. stewartii. Infected seed were produced in 1998, 1999, and 2000 on a Stewart's wilt-susceptible sweet corn hybrid, Jubilee. Seedlings were inoculated repeatedly with pinprick inoculators and suspensions of E. stewartii were injected into ear shanks of the primary ears of each adult plant. Seed from inoculated plants were harvested and bulked. Single kernels were assayed for E. stewartii to estimate the proportion of kernels infected with E. stewartii. Estimates of E. stewartii-infection were 15.6 ± 4.3, 49.4 ± 3.9, and 12.5 ± 2.4% for seed produced in 1998, 1999, and 2000, respectively. Approximately 61,800 seedlings were grown in DeKalb, IL in 1999 and 83,400 and 60,000 seedlings were grown in Plover WI in 2000 and 2001, respectively, from infected seed lots produced the previous year. Approximately 10,000, 12,200, and 29,400 seedlings of susceptible sweet corn hybrids also were grown each year from commercial seed produced in Idaho where Stewart's wilt does not occur. Based on estimates of kernel infection in each seed lot and plant populations in each grow-out trial, about 9,600, 41,200, and 7,500 seedlings were grown from infected kernels in 1999, 2000, and 2001, respectively. Seedlings at the two- to three-leaf stage were examined for symptoms of Stewart's wilt. Infected plants were confirmed by microscopic observations of bacterial ooze and by enzyme-linked immunosorbent assay. When data were combined from all three trials, 59 of approximately 58,300 seedlings grown from infected seed were infected with E. stewartii based on symptoms of Stewart's wilt and E. stewartii-positive leaf tissue samples. Of these 59 seedlings, 22 probably were infected from seed-to-seedling transmission of E. stewartii and 37 probably were the result of natural infection due to the presence of flea beetles in DeKalb in 1999. Twenty-two infected seedlings from 58,300 infected kernels corresponds to a seed-to-seedling transmission rate of 0.038%. This rate of seed-to-seedling transmission of E. stewartii is substantially lower than seed transmission rates reported in the first half of the twentieth century; however, it is similar to seed-to-seedling transmission rates reported from other recent research.

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
Keyword(s):  
New York ◽  
North America ◽  
Sweet Corn ◽  
Leaf Tissue ◽  
Tween 20 ◽  
Experimental Unit ◽  
Corn Hybrids ◽  
Widespread Occurrence ◽  
Puccinia Sorghi ◽  
Corn Hybrid

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.

scholarly journals Selection for Quantitative Trait Loci Associated with Resistance to Stewart's Wilt in Sweet Corn

2008 ◽  
Vol 98 (4) ◽  
pp. 469-474 ◽  
Author(s):  
J. K. Pataky ◽  
M. O. Bohn ◽  
J. D. Lutz ◽  
P. M. Richter
Keyword(s):  
Sweet Corn ◽  
Mapping Population ◽  
Marker Allele ◽  
Wilt Resistance ◽  
Resistant Lines ◽  
Selection For ◽  
Marker Alleles ◽  
Stewart's Wilt ◽  
Corn Inbred ◽  
Corn Hybrid

The objectives of this research were to identify quantitative trait loci (QTL) for Stewart's wilt resistance from a mapping population derived from a sweet corn hybrid that is highly resistant to Pantoea stewartii and to determine if marker-based selection for those QTL could substantially improve Stewart's wilt resistance in a population derived from a cross of resistant lines and a highly susceptible sweet corn inbred. Three significant QTL for Stewart's wilt resistance on chromosomes 2 (bin 2.03), 5 (bin 5.03), and 6 (bin 6.06/6.07) explained 31% of the genetic variance in a population of 110 F3:4 families derived from the sweet corn hybrid Bonus. The three QTL appeared to be additive in their effects on Stewart's wilt ratings. Based on means of families that were either homozygous or heterozygous for marker alleles associated with the resistance QTL, the QTL on chromosomes 2 and 6 appeared to have dominant or partially dominant gene action, while the QTL on chromosome 5 appeared to be recessive. A population of 422 BC2S2 families was derived from crosses of a sweet corn inbred highly susceptible to Stewart's wilt, Green Giant Code 88 (GG88), and plants from two F3:4 families (12465 and 12467) from the Bonus mapping population that were homozygous for marker alleles associated with Stewart's wilt resistance at the three QTL. Mean Stewart's wilt ratings for BC2S2 families were significantly (P < 0.05) lower for families that were homozygous for the bnlg1902 marker allele (bin 5.03) from resistant lines 12465 or 12467 than for families that were heterozygous at this marker locus or homozygous for the bnlg1902 marker allele from GG88. Resistance associated with this QTL was expressed only if F3:5 or BC2S2 families were homozygous for marker alleles associated with the resistant inbred parent (P1). Marker alleles identified in the F3:5 mapping population that were in proximity to the resistance QTL on chromosomes 2 and 6 were not polymorphic in crosses of GG88 with 12465 and 12467. Selection for other polymorphic marker loci adjacent to these two regions did not improve Stewart's wilt resistance of BC2S2 families.

scholarly journals Influence of Host Resistance on Stewart's Wilt Forecasts and Probability of Exceeding Thresholds for Use of Seed-Treatment Insecticides on Sweet Corn

Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1111-1117
Author(s):  
M. D. Meyer ◽  
J. K. Pataky ◽  
D. K. Joos ◽  
R. W. Esgar ◽  
B. R. Henry
Keyword(s):  
Host Resistance ◽  
Seed Treatment ◽  
Sweet Corn ◽  
Winter Temperature ◽  
Corn Hybrids ◽  
Frequency Distributions ◽  
Economic Thresholds ◽  
The Mean ◽  
Stewart's Wilt ◽  
Wilt Incidence

Many sweet corn (Zea mays) hybrids commercially available today have higher levels of resistance to Stewart's disease (caused by Pantoea stewartii subsp. stewartii) than the cultivars from which Stevens developed the first forecast of this disease in the 1930s. Incorporating levels of host resistance into forecasts of the seedling wilt phase of Stewart's disease (i.e., Stewart's wilt) could improve control decisions for sweet corn which are made prior to planting. Incidence of systemic infection of seedlings was assessed on 27 sweet corn hybrids with a range of reactions to P. stewartii. In total, 741 observations were collected from 1998 to 2009 in 79 field trials at 15 locations throughout Illinois and one each in Kentucky and Delaware. Relative frequency distributions of the incidence of systemic Stewart's wilt were developed for combinations of hybrids with different levels of resistance and ranges of winter temperature from Stewart's wilt forecasts. The probability of exceeding thresholds of 1 or 5% incidence that warrant the use of seed-treatment insecticides on sweet corn grown for fresh market or processing, respectively, was determined from these frequency distributions. Levels of host resistance affected the incidence of systemic seedling wilt within ranges of winter temperatures used by Stewart's wilt forecasts. For moderate and resistant hybrids, frequency distributions of Stewart's wilt incidence and mean incidence ranging from 0.7 to 1.8% did not differ among three winter temperature ranges above –2.8°C. Conversely, distributions of Stewart's wilt incidence on susceptible hybrids differed among each of the four ranges of winter temperature from the Stevens-Boewe forecast (i.e., >0.6, –1.1 to 0.6, –2.8 to –1.1, and <–2.8°C), with mean incidence ranging from 0.5 to 8.5%. Occurrence of Stewart's wilt also differed among trials varying in number of winter months above –4.4°C, the criterion used by the Iowa State forecast of this disease. Levels of host resistance to P. stewartii also affected the occurrence of Stewart's wilt as predicted by the Iowa State method. The probability of exceeding economic thresholds of 1 or 5% incidence of systemic Stewart's wilt depended on levels of host resistance and winter temperature. Stewart's wilt is unlikely to exceed economic thresholds when the mean winter temperature is below –4.4°C. When mean winter temperature was above –2.8°C, the probability of exceeding 1% incidence of systemic Stewart's wilt was 0.59 for susceptible sweet corn hybrids and 0.28 for moderate and resistant hybrids. When mean winter temperature was below –2.8°C, the probability of exceeding 1% incidence of systemic Stewart's wilt was 0.22 for susceptible hybrids and 0.04 for moderate or resistant sweet corn hybrids. The probability of exceeding 5% incidence was less than 0.1, except when the mean winter temperature was above –2.8°C and susceptible hybrids were grown.

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