Influence of Host Resistance and Growth Stage at the Time of Inoculation on Stewart's Wilt and Goss's Wilt Development and Sweet Corn Hybrid Yield

Plant Disease ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 339 ◽  
Author(s):  
Suparyono Suparyono
Plant Disease ◽  
2002 ◽  
Vol 86 (9) ◽  
pp. 1031-1035 ◽  
Author(s):  
P. M. Michener ◽  
J. K. Pataky ◽  
D. G. White

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.


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

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.


2008 ◽  
Vol 98 (4) ◽  
pp. 469-474 ◽  
Author(s):  
J. K. Pataky ◽  
M. O. Bohn ◽  
J. D. Lutz ◽  
P. M. Richter

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.


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

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.


Plant Disease ◽  
2003 ◽  
Vol 87 (3) ◽  
pp. 223-228 ◽  
Author(s):  
P. M. Michener ◽  
N. D. Freeman ◽  
J. K. Pataky

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.


Plant Disease ◽  
2000 ◽  
Vol 84 (8) ◽  
pp. 901-906 ◽  
Author(s):  
Jerald K. Pataky ◽  
Lindsey J. du Toit ◽  
Noah D. Freeman

Maize accessions were evaluated in 1997, 1998, and 1999 to identify additional sources of Stewart's wilt resistance and to determine if reactions differed among accessions collected from various regions of the United States and throughout the world. The distributions of Stewart's wilt reactions rated from 1 (no appreciable spread of symptoms) to 9 (dead plants) were relatively similar among groups of accessions from all regions of the world except for those from the Mid-Atlantic/Ohio River Valley region of the United States, the southern United States, and the northeastern United States. The mean and median Stewart's wilt rating for 1,991 accessions evaluated in 1997 was 4. The mean Stewart's wilt rating for 245 accessions collected from the Mid-Atlantic/Ohio River Valley region was 3.1, which was significantly lower than that for accessions from all other regions. The mean rating for accessions from the southern United States was 3.7, which also was lower than mean ratings for accessions from all other regions. Ratings from trials in 1997 and 1998 were highly correlated (r = 0.87) for 292 accessions and 15 sweet corn hybrid checks evaluated in both years. Of 20 accessions rated below 2 in 1997 and 1998, seven were from Virginia, seven were from the Ohio River Valley or central Corn Belt of the United States, four were from the northern or western Corn Belt of the United States, and two were from Spain. Ratings for these accessions ranged from 1.7 to 3.1 in 1999. Ratings ranged from 2.6 to 3.7 for F1 hybrids of these accessions crossed with one of two susceptible sweet corn inbreds, CrseW30 or Crse16, which were rated 5.7 and 5.4, respectively. Based on the reactions of this collection of germ plasm, it appears that high levels of Stewart's wilt resistance are prevalent only among accessions collected from areas where the disease has been endemic for several years, whereas moderate levels of resistance can be found in accessions collected from nearly everywhere in the world.


Weed Science ◽  
1996 ◽  
Vol 44 (2) ◽  
pp. 339-344 ◽  
Author(s):  
Darren K. Robinson ◽  
David W. Monks ◽  
James D. Burton

LAB 145 138 (LAB) was evaluated as a safener to improve sweet corn tolerance to nicosulfuron applied POST alone or with terbufos applied in the planting furrow or bentazon applied POST. To ensure enhanced injury for experimental purposes, nicosulfuron was applied at twice the registered rate alone or mixed with bentazon at the six- to seven-leaf growth stage of corn previously treated with the highest labeled rate of terbufos 15 G formulation. LAB applied as a seed treatment (ST) or POST at the two- to three-, four- to five-, or six- to seven-leaf growth stages reduced height reduction and yield loss from nicosulfuron applied POST in combination with terbufos applied in-furrow. LAB applied POST at the four- to five-leaf growth stage was most effective in preventing injury from this treatment, with yield reduced only 8% compared with 54% from the nicosulfuron and terbufos treatment. LAB applied POST at the eight- to nine-leaf growth stage did not alleviate injury. With the nicosulfuron, terbufos, and bentazon combination, LAB applied POST at the three- to four- or six- to seven-leaf growth stages decreased height reduction and yield loss caused by this combination, with LAB at the three- to four-leaf growth stage being most effective.


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.


2014 ◽  
Vol 81 (1) ◽  
pp. 139-148 ◽  
Author(s):  
Lindsey Burbank ◽  
Mojtaba Mohammadi ◽  
M. Caroline Roper

ABSTRACTIron is a key micronutrient for microbial growth but is often present in low concentrations or in biologically unavailable forms. Many microorganisms overcome this challenge by producing siderophores, which are ferric-iron chelating compounds that enable the solubilization and acquisition of iron in a bioactive form.Pantoeastewartiisubsp.stewartii, the causal agent of Stewart's wilt of sweet corn, produces a siderophore under iron-limiting conditions. The proteins involved in the biosynthesis and export of this siderophore are encoded by theiucABCD-iutAoperon, which is homologous to the aerobactin biosynthetic gene cluster found in a number of enteric pathogens. Mutations iniucAandiutAresulted in a decrease in surface-based motility thatP. stewartiiutilizes during the early stages of biofilm formation, indicating that active iron acquisition impacts surface motility forP. stewartii. Furthermore, bacterial movementin plantais also dependent on a functional siderophore biosynthesis and uptake pathway. Most notably, siderophore-mediated iron acquisition is required for full virulence in the sweet corn host, indicating that active iron acquisition is essential for pathogenic fitness for this important xylem-dwelling bacterial pathogen.


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