Resistance in Capsicum pubescens

to Xanthomonas campestris pv. vesicatoria Pepper Race 6

F. Sahin and S. A. Miller, Department of Plant Pathology, The Ohio State University, Ohio Agricultural Research
and Development Center, Wooster 44691

most of these are resistant to copper,

ABSTRACT streptomycin, or both (31). Therefore, new
Sahin, F., and Miller, S. A. 1998. Resistance in Capsicum pubescens to Xanthomonas campestris sources of resistance in pepper need to be
pv. vesicatoria pepper race 6. Plant Dis. 82:794-799. identified.
The objectives of this study were to (i)
One hundred seventy Capsicum spp. germplasm accessions were evaluated as potential sources evaluate Capsicum germplasm for sources
of resistance to X. campestris pv. vesicatoria pepper race 6 (P6). This race has been identified of resistance to X. campestris pv. vesicato-
recently in Ohio and overcomes all three known resistance genes in cultivated pepper. Only C.
ria race P6 and (ii) utilize newly identified
pubescens plant introduction (PI) 235047 was found to be resistant to X. campestris pv. vesica-
toria P6 strains using hypersensitivity and pathogenicity tests. Further studies using PI 235047
resistant pepper germplasm to determine
as a differential line showed that strains classified as X. campestris pv. vesicatoria races P1 and the existence of additional variation in
P3 were heterogeneous in terms of virulence. Strains of X. campestris pv. vesicatoria P1 and P3 virulence among strains of other X. cam-
that were compatible with PI 235047 were reclassified as two new pepper races, designated X. pestris pv. vesicatoria pepper races.
campestris pv. vesicatoria P7 and P8, respectively. According to the new race classification, PI
235047 plants are incompatible with X. campestris pv. vesicatoria pepper races P0, P1, P3, P4, MATERIALS AND METHODS
and P6, but compatible with races P2, P5, P7, and P8. Plant material and growing condi-
tions. Seeds for all PI lines of Capsicum
spp., including 119 accessions of C. an-
nuum and 51 accessions of other Capsicum
Bacterial spot of pepper (Capsicum vesicatoria is economically and technically spp. (C. anomallum, C. baccatum, C. cha-
spp.), caused by Xanthomonas campestris the most practical method for bacterial spot coense, C. chinense, C. frutescens, C. ga-
pv. vesicatoria (proposed to be renamed management (23–25). There is an increas- lapagoense, and C. pubescens) originating
Xanthomonas axonopodis pv. vesicatoria; ing interest in developing pepper cultivars from 40 countries were obtained from the
37), is one of the most destructive pepper with resistance to bacterial spot. However, United States Department of Agriculture-
diseases both in the greenhouse and in the development of disease-resistant cultivars Agriculture Research Station (USDA-
field when environmental conditions are requires the identification and incorpora- ARS) Plant Genetic Resources Conserva-
favorable for the pathogen (8,24,25,33). tion of resistance genes into horticulturally tion Unit, University of Georgia, Griffin
The current management methods for bac- superior and widely acceptable cultivars. (Table 1).
terial spot, including sanitation, chemical Good progress has been made in identifi- A total of 20 seeds from each of the 170
application, cultural practices, and use of cation of suitable sources of disease resis- accessions and the bell pepper cultivar
X. campestris pv. vesicatoria-resistant tance by screening a number of accessions Marengo (X. campestris pv. vesicatoria-
cultivars (10,14,17,23–25,27,29,33,36), are of cultivated pepper species and related susceptible) were sown in commercial peat
not always successful. Contaminated seeds wild species with great genetic diversity mix (Baccto High Density Professional
are the main source of X. campestris pv. (11–13,15,16,20). So far, three genes for Planting Mix, Michigan Peat Co., Hous-
vesicatoria inoculum (3–5,17). However, resistance to bacterial spot, designated Bs1, ton) in new 128-cell plastic flats
seed treatment, which may not completely Bs2, and Bs3, have been identified in three (Landmark Plastics Corp., Akron, OH).
eliminate X. campestris pv. vesicatoria different plant introduction (PI) lines: PI The seedlings were grown on the green-
inoculum if internal seed infection occurs 163192 (C. annuum), PI 260435 (C. cha- house bench until they reached the second
(5), is not always done, for economic rea- coense), and PI 271322 (C. annuum), re- or third true-leaf stage (approximately 3 to
sons as well as potential reduction of seed spectively (11,13,20). 4 weeks). Then 15 seedlings of each acces-
viability. Cost, potential chemical residues Resistance in pepper to strains of X. sion were transplanted into five 25-cm-
on fruit, and resistance among X. campes- campestris pv. vesicatoria is associated diameter plastic pots (three plants/pot)
tris pv. vesicatoria strains are the main with the hypersensitive response (HR; 1,6– containing steamed soil (mixture of 0.43
disadvantages of chemical applications 9,11–13,15,16,18–21,28,30,34). Currently, m3 Wooster silty-loam, 0.43 m3 muck soil,
(2,27,29,33,36). Therefore, use of pepper seven pepper races (P0–P6) have been 0.14 m3 peat moss, and 1.2 kg lime/m3).
cultivars resistant to X. campestris pv. identified among X. campestris pv. vesica- The plants were maintained for 7 days in
toria strains worldwide (8,22,28,29,32,33). the greenhouse (20 to 28°C) after trans-
Corresponding author: S. A. Miller Pepper races are easily identified based on planting. Plants were fertilized once a
E-mail address: miller.769@osu.edu the presence or absence of HR in the X. week with Peter’s 20-20-20 (N-P-K; 454
campestris pv. vesicatoria-susceptible mg/378 ml) and watered as required. Nine
This research was supported by Ataturk Univer- cultivar Early Calwonder (ECW) and its plants from each accession were used to
sity, Erzurum, Turkey, and State and Federal near-isogenic derivative lines, designated test pathogenicity and six plants were used
Funds appropriated to the Ohio Agricultural Re-
search and Development Center (OARDC), The ECW-10R, ECW-20R, and ECW-30R, to test HR elicitation. This experiment was
Ohio State University. OARDC Research Article which contain the resistance genes Bs1, conducted twice. The remaining five seed-
Number 148-97. Bs2, and Bs3, respectively (28). Race P6 lings of the PI accessions and Marengo
strains, first identified in Ohio in 1994 were used as negative controls in the ex-
Accepted for publication 24 March 1998. (32), are able to defeat all of the known periments.
resistance genes in pepper (24,25,32,33). Inoculum preparation. A highly ag-
Publication no. D-1998-0518-01R The number of X. campestris pv. vesicato- gressive strain of X. campestris pv. vesi-
© 1998 The American Phytopathological Society ria P6 strains is increasing in Ohio and catoria pepper race 6, X. campestris pv.

794 Plant Disease / Vol. 82 No. 7

vesicatoria 17b, isolated from pepper in on Marengo. To test for elicitation of an control. The results were recorded as posi-
1994 in Ohio, was used. Strain X. campes- HR, a bacterial suspension (108 CFU/ml), tive or negative based on the presence or
tris pv. vesicatoria 17b was stored frozen prepared as described above, was infil- absence, respectively, of collapsed tissue at
(–80°C) in 15% glycerol and recovered trated into the intercostal area of the leaves the inoculation site within 48 h after infil-
from frozen culture by restreaking onto of two plants of each PI line and Marengo tration. This experiment was conducted
yeast dextrose carbonate agar (YDC) me- by using a 3-cc syringe (Becton Dickinson four times.
dium (26) and incubating at 28°C for 48 h. and Co., Franklin Lakes, NJ) without a Of the 72 X. campestris pv. vesicatoria
The bacteria were washed from the plate hypodermic needle. Sterilized distilled strains tested for HR on PI 235047, 58
with a sterile glass spreader and suspended water was infiltrated into the leaves of were also tested for pathogenicity on this
in sterile distilled water. The bacterial con- plants of all PI lines and Marengo as nega- accession and Marengo. Two plants of
centration was adjusted to approximately tive controls. The inoculated plants were each accession were dip-inoculated with
108 CFU/ml (A600nm = 0.1). This concen- arranged in a completely randomized de- individual strains as described above. Two
tration was used for inoculation and infil- sign on the greenhouse bench and main- plants of each line were dipped in sterile
tration of pepper seedlings. tained for 24 to 48 h at 20 to 28°C. The water as a negative control. The inoculated
Plant inoculation. Nine 5-week-old presence of rapid tissue necrosis at the plants were arranged in a completely ran-
pepper seedlings (three plants/pot) of each inoculation site was recorded within 24 to domized design with two replications of a
accession and Marengo were dipped into 4 48 h after infiltration. This test was re- single plant each per experiment. The in-
liters bacterial suspension in a 5-liter plas- peated at least three times. oculated plants were incubated in a mist
tic container. Five Marengo seedlings, Variation in host specificity, virulence chamber at 90 to 95% RH for 3 days, then
dipped into sterilized distilled water, were and growth in plants. Seventy-two transferred to the greenhouse at 20 to 28°C
used as a negative control in each experi- strains, including all of the known X. cam- for 7 days. The plants were rated for dis-
ment. The inoculated plants were arranged pestris pv. vesicatoria pepper races (P0 to ease severity 10 days after inoculation by
in a completely randomized design and P6), were used. Strains V-19 and V-205, using a scale of 1 to 5, in which 1 = no
incubated in a mist chamber at 90 to 95% and strains 1138, 1140, and 1141 were disease, 2 = a few water-soaked lesions, 3
relative humidity (RH) for 3 days, then obtained from D. F. Ritchie and F. Louws, = many spots with coalescence and slight
transferred to a greenhouse at 20 to 28°C respectively (Department of Plant Pathol- plant wilting, 4 = severe leaf defoliation,
for 7 days. The control plants were incu- ogy, North Carolina State University, Ral- and 5 = plants dead. Average disease se-
bated under the same conditions, but in eigh). The remaining 67 strains were verity values (DSVs) for each of the bacte-
different greenhouses. The plants were isolated from pepper or tomato plants col- rial strains on PI 235047 and Marengo
observed for development of characteristic lected from commercial fields in Ohio plants were calculated from two experi-
bacterial spot symptoms 10 days after in- between 1993 and 1996. All strains were ments. The data were evaluated with
oculation. Plants were rated as positive or tested for HR elicitation on C. pubescens analysis of variance (ANOVA), and differ-
negative based on the presence or absence PI 235047, ECW, ECW-10R, ECW-20R, ences among the treatment means were
of disease symptoms. Pathogenicity was and ECW-30R as described above. The determined by calculating Fisher’s least
evaluated based on symptom development cultivar Marengo was used as a negative significant difference at P = 0.05.

Table 1. Evaluation of Capsicum spp. accessions for resistance to Xanthomonas campestris pv. vesicatoria race P6
Host/PI HRa Diseaseb
Capsicum annuum
102881, 102882, 102883, 103048, 105262, 105444, 105339, 105538, 109252, 109254, 109255, 109469, 123164, 123165, 123166,
123469, 123470, 123471, 124080, 124540, 125801, 125802, 125803, 127445, 131352, 135826, 135873, 135874, 138557, 138558,
138559, 138561, 143886, 148626, 153565, 155349, 159226, 159227, 159228, 159255, 159265, 159278, 162607, 162608, 164556,
164557, 164558, 164561, 164562, 164564, 164565, 164678, 164961, 167062, 167100, 167215, 169102, 169106, 169110, 169115,
169122, 169130, 169131, 169138, 176888, 181732, 181733, 181734, 182646, 184037, 184038, 184039, 187314, 187315, 187325,
188472, 188473, 188474, 249907, 249911, 251622, 257049, 257187, 262172, 262905, 263073, 263074, 263106, 263110, 264662,
267730, 267731, 267733, 275008, 275009, 275011, 281316, 281323, 281327, 281330, 281341, 281400, 281413, 281416, 286419,
289762, 291999, 294452, 297456, 338490, 338974 , 385960, 385961, 390436, 390437, 390970, 390971, 401728, 401729 – +
C. annuum var. glabriusculum
511885, 511886, 511887 – +
C. anomallum
501532 – +
C. baccatum
260434, 273425, 281398, 3700004, 3700005, 413669, 439359, 439360, 439361, 439364, 439369 – +
C. baccatum var. baccatum
215699, 238061, 260533, 260567, 281306 – +
C. baccatum var. pendulum
152217, 152234, 199506, 203522, 213915, 224440, 238062, 241679, 257122, 241674, 159235, 188803 – +
C. baccatum var. praetermissum
260595 – +
C. chacoense
260426, 260427, 260430, 260431, 273429 – +
C. chinense
152222, 152225, 152452, 194879, 200729, 209589 – +
C. frutescens
123474, 159238, 181865, 188479 – +
C. galapagoense
G-1567 – +
C. pubescens
235047 + –
585266 – +
a HR = hypersensitive response; – = HR not elicited; + = HR elicited.
b Disease = presence (+) or absence (–) of symptoms.

Plant Disease / July 1998 795

 Another experiment was conducted in kept on paper towels for 30 min to allow 1). The negative control Marengo plants
the greenhouse to characterize disease the alcohol to evaporate. Then the leaf inoculated with sterilized water also did
resistance in C. pubescens PI 235047 samples were macerated using a ball bear- not show any recognizable symptoms.
plants to X. campestris pv. vesicatoria P6 ing tissue grinder (BioReba AG, Basel, An HR to X. campestris pv. vesicatoria
strains based on bacterial population dy- Switzerland) in a separate plastic bag 17b was elicited in all infiltrated leaves of
namics in inoculated leaves. Two plants (Agdia Inc, Elkhorn, IN) containing 1 ml PI 235047 plants within 24 h after inocula-
each of PI 235047 and Marengo were in- sterile distilled water/g leaf tissue (fresh tion (Table 1, Fig. 2). None of the other
oculated separately with X. campestris pv. weight). Serial 10-fold dilutions were accessions or Marengo developed an HR
vesicatoria 17b (race P6) and X. campes- performed in sterile distilled water and during the 24 to 48-h incubation period
tris pv. vesicatoria 116 (race P1), a virulent 0.1 ml of the appropriate dilutions was after infiltration. HR was not observed on
strain that did not elicit an HR on PI spread onto each of two plates of CKTM leaves of C. pubescens PI 235047 or
235047. Inoculation, incubation, and dis- medium (35). Characteristic X. campes- Marengo plants infiltrated with sterilized
ease assessment were done as described tris pv. vesicatoria colonies were counted distilled water.
above. All of the leaves on two inoculated after the plates were incubated for 4 days Variation in host specificity, virulence
plants of each cultivar were collected after at 28°C. and growth in plants. Of the 72 X. cam-
scoring disease severity. Half of the leaves pestris pv. vesicatoria strains tested, 46
were surface sterilized by dipping into RESULTS (64%) were race P3 (Table 2). The re-
95% EtOH, and the others were dipped Characteristic symptoms of bacterial maining strains were distributed as fol-
into sterile distilled water. The leaves were spot were observed on all Marengo plants, lows: 1 P0, 10 P1, 2 P2, 3 P4, 1 P5, and 10
and all but one of the Capsicum spp. acces- P6. Although 41 strains (60%) elicited an
sions inoculated with X. campestris pv. HR on C. pubescens PI 235047, the re-
vesicatoria race P6, strain 17b. C. pubes- maining 31 strains (40%) were compatible.
cens PI 235047 plants (Fig. 1) did not de- All strains of X. campestris pv. vesicatoria
velop distinguishable symptoms of races P0, P4, and P6 and almost half of the
bacterial spot in either experiment (Table P1 and P3 strains tested were incompati-

Table 2. Hypersensitive response (HR) in Capsicum pubescens PI 235047 plants and average disease
severity (DSV) on PI 235047 and the pepper cultivar Marengo inoculated with strains of different
pepper races of Xanthomonas campestris pv. vesicatoria
DSVa
Strainb Racec HR testd PI 235047 Marengo
V-19 P0 + 1.00 2.75
Xcv-63 P1 + 1.25 3.25
Xcv-118 P1 + 1.00 3.50
Xcv-119a P1 + 1.00 3.75
Xcv-119b P1 + 1.25 4.00
Xcv-120 P1 + 1.75 3.25
Xcv-106a P3 + 1.75 3.75
Xcv-106b P3 + 1.25 3.50
Xcv-107a P3 + 1.00 2.75
Xcv-107b P3 + 1.25 3.50
Fig. 1. Capsicum pubescens PI 235047 plants. Xcv-108 P3 + 1.00 3.75
(A) Flower (purple), (B) fruit (yellow). Xcv-109a P3 + 1.50 3.25
Xcv-109b P3 + 1.50 3.50
Xcv-112 P3 + 1.00 3.25
Xcv-113 P3 + 1.75 2.75
Xcv-121 P3 + 1.25 2.75
Xcv-122a P3 + 1.00 3.50
Xcv-122b P3 + 1.25 3.75
Xcv-122c P3 + 1.25 3.50
Xcv-122d P3 + 1.00 3.00
Xcv-127a P3 + 1.25 3.75
Xcv-127b P3 + 1.00 3.75
Xcv-127c P3 + 1.25 3.25
Xcv-129a P3 + 1.00 3.50
Xcv-129b P3 + 1.00 4.00
Xcv-130 P3 + 1.00 3.50
Xcv-794a P3 + NT NT
Xcv-794b P3 + NT NT
1138 P4 + NT NT
1140 P4 + NT NT
1141 P4 + NT NT
(continued on next page)
a Average disease severity values calculated from two experiments, each with two replications, after
the plants were rated using a 1 to 5 scale where 1 = no disease, 2 = a few water-soaked lesions, 3 =
many spots with coalescence and slight plant wilting, 4 = severe leaf defoliation, and 5 = plants
dead; NT = not tested.
b Xanthomonas campestris pv. vesicatoria strains isolated from pepper or tomato.

Fig. 2. Leaves of Capsicum pubescens PI c Race of the X. campestris pv. Vesicatoria strains were determined by infiltration of bacterial sus-

235047 plants infiltrated with a suspension of pension (108 CFU/ml) into the leaves of pepper differential lines.
Xanthomonas campestris pv. vesicatoria (A) d Strains of X. campestris pv. vesicatoria eliciting a hypersensitive response on PI 235047 plants; + =

race P6 or (B) race P1. (A) Incompatible reac- incompatible (resistant) reaction, – = compatible (susceptible) reaction.
tion, (B) compatible reaction. e ANOVA = analysis of variance; LSD = least significant difference.

796 Plant Disease / Vol. 82 No. 7

ble. All of the P2 and P5 strains were com- (average DSV = 2.8) were significantly pv. vesicatoria P6 strains, only C. pubes-
patible on this accession. less than those of Marengo plants (average cens PI 235047 was resistant. None of the
All of the strains that elicited an HR DSV = 3.5) inoculated with these strains. C. pubescens PI 235047 plants tested
(incompatible) on C. pubescens PI 235047 Without surface sterilization, the aver- showed leaf spot symptoms 10 days after
caused virtually no symptoms on PI age density of X. campestris pv. vesicato- inoculation, while other accessions and
235047 plants after dip-inoculation. All of ria 17b (P6) in PI 235047 leaves was 6 × Marengo plants were highly susceptible.
the X. campestris pv. vesicatoria strains 105 CFU/g, significantly (P = 0.05) less Furthermore, elicitation of HR was ob-
that did not elicit an HR (compatible) on PI than the bacterial density (3.9 × 109 served in C. pubescens PI 235047 plants
235047 caused serious disease on PI CFU/g) in Marengo leaves. After surface within 24 h after infiltration, but not in
235047 plants. The average DSVs for PI sterilization, the average density of X. other PI lines or Marengo plants. This
235047 plants inoculated with X. campes- campestris pv. vesicatoria 17b in PI supports evidence from previous studies
tris pv. vesicatoria strains in the incom- 235047 leaves was 3.55 × 103 CFU/g, also (13,15,16,20) that there is a strong correla-
patible group (DSVs = 1 to 1.75) were significantly less than in Marengo leaves tion between the incompatible interaction
significantly (P = 0.05) less than those (7.2 × 107 CFU/g). The population density of X. campestris pv. vesicatoria strains on
(DSVs = 2.25 to 3.75) for plants inoculated of X. campestris pv. vesicatoria 116 (P1) in pepper and HR elicitation, which can be
with compatible strains (Table 2). Strains non-surface-disinfested PI 235047 and used as a method for screening Capsicum
of X. campestris pv. vesicatoria in both Marengo leaves was 1.4 × 108 and 5.9 × accessions for resistance to the bacterial
groups caused serious disease on cultivar 108 CFU/g, respectively. After surface spot pathogen. In addition, these results
Marengo. While there were some signifi- disinfestation, the population density in PI indicate that C. pubescens PI 235047
cant differences between individual strains 235047 leaves was 6.4 × 107 CFU/g and in plants carry a resistance (R) gene or genes
of X. campestris pv. vesicatoria in viru- Marengo leaves was 6.5 × 107 CFU/g. that presumably correspond to a novel
lence on PI 235047 and Marengo, there These population densities did not differ (unknown) avirulence gene or genes in X.
were no differences between groups in significantly (P = 0.05). campestris pv. vesicatoria P6 strains. Al-
virulence on Marengo (average DSVs for though genetic analyses of resistance in C.
the compatible group = 3.5, incompatible DISCUSSION pubescens PI 235047 and avirulence in X.
group = 3.42). However, the DSVs of PI Of the 170 accessions from eight differ- campestris pv. vesicatoria P6 strains have
235047 plants inoculated with compatible ent Capsicum species evaluated as poten- not been done, it is likely that the resis-
strains of X. campestris pv. vesicatoria tial sources of resistance to X. campestris tance is governed by a single gene, which
we propose to designate Bs4, with the cor-
responding avirulence gene in the pathogen
Table 2. (continued from preceding page) designated avrBs4. Our results, demon-
strating a qualitative response to the patho-
DSVa gen and the presence of an HR in PI
Strainb Racec HR testd PI 235047 Marengo 235047 plants infiltrated with X. campes-
Xcv-131b P6 + NT NT tris pv. vesicatoria P6 strains, provide indi-
Xcv-787 P6 + NT NT rect evidence for single-gene resistance to
Xcv-788 P6 + NT NT bacterial spot in this accession. Further-
Xcv-789 P6 + NT NT more, all three previously identified bacte-
Xcv-790 P6 + NT NT rial spot resistance genes in pepper, Bs1,
Xcv-791 P6 + NT NT Bs2, and Bs3, are single dominant genes
Xcv-792 P6 + NT NT (11,13,15,16,20). Genetic studies are
Xcv-793 P6 + NT NT
Xcv-69 P1 – 3.25 3.50
needed to determine the inheritance of
Xcv-114 P1 – 3.25 4.00 resistance to bacterial spot in this new
Xcv-115 P1 – 3.25 3.50 resistance source.
Xcv-116 P1 – 3.75 3.75 Further evaluation of variation in viru-
Xcv-117 P1 – 2.75 3.25 lence among X. campestris pv. vesicatoria
Xcv-66 P2 – 2.25 4.00 pepper races showed that C. pubescens PI
Xcv-89 P2 – 2.50 3.25 235047 plants are not only incompatible
Xcv-90 P3 – 2.50 3.25
with X. campestris pv. vesicatoria P6
Xcv-91 P3 – 2.75 3.75
Xcv-110a P3 – 3.25 3.75 strains, but also with P0, P4, and half of
Xcv-110b P3 – 2.75 3.75 the P1 and P3 strains tested. The diversity
Xcv-110c P3 – 2.25 3.25 among X. campestris pv. vesicatoria P1 and
Xcv-111 P3 – 3.00 3.75 P3 strains provided evidence that the strains
Xcv-123a P3 – 2.75 3.50 within X. campestris pv. vesicatoria pepper
Xcv-123b P3 – 3.25 2.75 races may not be homogeneous in terms of
Xcv-123c P3 – 2.75 3.25 host specificity and virulence. Although
Xcv-123d P3 – 2.25 2.75
Xcv-124a P3 – 2.75 3.25
pathological diversity among strains of X.
Xcv-124b P3 – 3.00 3.00 campestris pv. vesicatoria pepper races P0,
Xcv-124c P3 – 3.00 3.75 P2, P4, P5, and P6 was not observed, this
Xcv-124d P3 – 3.25 3.25 does not necessarily indicate that the strains
Xcv-124e P3 – 2.75 3.00 within these races were homogeneous, be-
Xcv-125a P3 – 2.75 4.00 cause the number of strains tested was lim-
Xcv-126a P3 – 2.25 3.75 ited. In order to discriminate different patho-
Xcv-126b P3 – 2.75 4.00
genic groups within X. campestris pv.
Xcv-128a P3 – 2.50 4.00
Xcv-128b P3 – 3.00 3.50 vesicatoria races, C. pubescens PI 235047
Xcv-128c P3 – 2.25 3.25 was used as an additional pepper differential
Xcv-128d P3 – 2.50 3.50 line. Therefore, X. campestris pv. vesica-
Xcv-767 P3 – NT NT toria strains were reclassified into races
V-205 P5 – 3.25 3.75 based on HR on pepper differential lines
ANOVAe (P = 0.05) LSD = 0.17 LSD = 0.20 including PI 235047 (Table 3).

Plant Disease / July 1998 797

 Two new X. campestris pv. vesicatoria characterization of additional resistance 11. Cook, A. A., and Guevara, Y. G. 1984. Hyper-
pepper races, designated X. campestris pv. genes in Capsicum spp. and avirulence sensitivity in Capsicum chacoense to race 1
of the bacterial spot pathogen of pepper. Plant
vesicatoria P7 and P8, were identified by genes in X. campestris pv. vesicatoria. Dis. 68:329-330.
splitting from X. campestris pv. vesicatoria 12. Cook, A. A., and Stall, R. E. 1963. Inheri-
ACKNOWLEDGMENTS
race P1 and P3, the strains that were com- We thank L. V. Madden and P. E. Lipps for pro- tance of resistance in pepper to bacterial spot.
patible with PI 235047. Based on the new viding pre-submission reviews, and M. S. Krause Phytopathology 53:1060-1062.
race classification of X. campestris pv. for preparation of the figures. 13. Cook, A. A., and Stall, R. E. 1982. Distribu-
tion of races of Xanthomonas vesicatoria
vesicatoria strains, C. pubescens PI pathogenic on pepper. Plant Dis. 66:388-
235047 plants are incompatible with LITERATURE CITED
1. Adamson, W. C., and Grover, S. Jr. 1983. 389.
strains of X. campestris pv. vesicatoria Inheritance of bacterial spot resistance in 14. Cox, R. S. 1982. Control of bacterial spot of
pepper races P0, P1, P3, P4, and P6. How- pepper. HortScience 18:905-906. tomato in southern Florida. Plant Dis. 66:870.
ever, they are compatible with strains of X. 2. Adaskaveg, J. E., and Hine, R. B. 1985. Cop- 15. Hibberd, A. M., Bassett, M. J., and Stall, R.
per tolerance and zinc sensitivity of Mexican E. 1987. Allelism tests of three dominant
campestris pv. vesicatoria pepper races P2, genes for hypersensitive resistance to
P5, P7, and P8. strains of Xanthomonas campestris pv. vesi-
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Table 3. Proposed race classification of Xanthomonas campestris pv. vesicatoria pepper strains based
plants. Blackwell Scientific Publications, Ox-
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Pepper differential lines 27. Marco, G. M., and Stall, R. E. 1983. Control
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Races ECW ECW-10R Bs1 ECW-20R Bs2 ECW-30R Bs3 PI 235047 Bs4a of Xanthomonas campestris pv. vesicatoria
P0 –b HR HR HR HR that differ in sensitivity to copper. Plant Dis.
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P3 – – HR – HR C., Kearney, B., Bonas, U., Staskawicz, B. J.,
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P5 – HR – – – ships specifying disease resistance in Xan-
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P6 – – – – HR
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P7 – – HR HR – 3:41-47.
P8 – – HR – – 29. Ritchie, D. F., and Dittapongpitch., V. 1991.
a Proposed designation. Copper- and streptomycin-resistant strains
b Compatible interaction. and host differentiated races of Xanthomonas

798 Plant Disease / Vol. 82 No. 7

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