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

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 ◽  
2002 ◽  
Vol 86 (2) ◽  
pp. 167-172 ◽  
Author(s):  
P. M. Michener ◽  
J. K. Pataky ◽  
D. G. White

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.


HortScience ◽  
1990 ◽  
Vol 25 (9) ◽  
pp. 1067a-1067 ◽  
Author(s):  
A. C. Meyer ◽  
J. K Pataky ◽  
J.A. Juvik

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.


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.


Plant Disease ◽  
1998 ◽  
Vol 82 (7) ◽  
pp. 775-780 ◽  
Author(s):  
C. C. Block ◽  
J. H. Hill ◽  
D. C. McGee

Seed transmission of Pantoea stewartii was evaluated by assays of more than 76,000 plants in greenhouse and field grow-out trials. Fourteen P. stewartii-infected seed lots were obtained from two dent corn inbreds and two sweet corn cultivars that were inoculated with either a rifampicin and nalidixic acid-resistant strain (rif-9A) or a wild-type strain (SS104) of P. stewartii. Four additional seed lots were collected from naturally infected inbreds. Percentages of infected kernels ranged from 0.8 to 72%, as determined by agar plating or by individual-kernel enzyme-linked immunosorbent assay (ELISA). Plants grown from this seed were assayed by a stem-printing technique that consisted of cutting and pressing a cross-section of each stem onto agar media. Prints were examined for development of P. stewartii colonies after 24 and 48 h. The transmission rate from seed produced on the inoculated plants was 0.066% (28 of 42,206 plants), based on all seedlings assayed. Transmission was estimated to be 0.14% from infected kernels. The transmission rate from seed produced on naturally infected plants was 0.0029% (1 of 34,924 plants), based on all seedlings, and 0.022% from infected kernels. Seed transmission occurred significantly less often (P = 0.034) from seed produced on naturally infected plants than from seed produced on inoculated plants, probably due to greater kernel damage caused by ear shank inoculation. The rarity of seed transmission of P. stewartii from heavily infected seed lots that would ordinarily be rejected due to poor germination suggests that the likelihood of seed transmission from good quality commercial seed corn is virtually nonexistent.


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 ◽  
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.


Sign in / Sign up

Export Citation Format

Share Document