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III. Improving Resistance to Pests

III. Improving Resistance to Pests

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dant pycnidia. Aerial mycelium is white or green in aggressive types and

mycelium in nonaggressive strains varies between white, grey, yellow, or

orange/brown (Delwiche, 1980; Humpherson-Jones, 1983; Hanacziwskyj

and Drysdale, 1984). Only aggressive isolates produce sirodesmins, which

are phytotoxic secondary metabolites (Koch ef al., 1989). Although a

number of workers have successfully crossed isolates of the aggressive

types, no success in mating either aggressive with nonaggressive or nonaggressive with other nonaggressive strains has been obtained to date (Petrie

and Lewis, 1985; Mengistu et al.. 1990). Evidence for pathogenic specialization within the aggressive types of L. maculans has been reported by

Koch et ul. (1991). They distinguished three pathotypes of aggressive

isolates by the reaction of isolates on the cotyledons of the B. napus

cultivars, Westar, Glacier, and Quinta. These were designated pathogenicity group (PG)2, PG3, and PG4, respectively. Nonaggressive isolates were

designated as PG 1.

A large variation for resistance has been reported among oilseed rape (B.

nupus) cultivars and breeding lines (Alabouvette ef al., 1974; Cargeeg and

Thurling, 1980a; Delwiche, 1980; Jonsson, 1974; Kriiger, 1978; Lammerink, 1979; McGee and Petrie, 1978; Rimmer and van den Berg, 1992; Roy,

1978a; Roy and Reeves, 1975; Thurling and Venn, 1977; Wratten, 1977).

Resistance in some lines may be traced back to the French cultivars Major

and Ramses (Roy, 1978a; Wratten, 1977),which possibly have a common

origin in Nain de Hambourg (Rollier, 1978). Resistance in several winter

cultivars developed in Europe was obtained from the variety Jet Neuf

(Renard d ul., 1983). Resistance to blackleg in spring types of B. napus has

been observed in the French cultivar Cresor and in Australian cultivars,

e.g., Maluka. Taparoo, and others. Many Australian cultivars derive their

resistance from Japanese cultivars, e.g., Chisaya, Chikuzen, and Mutu


Little resistance to blackleg disease has been observed in B. rapa accessions. The rather weak resistance that has been observed seems to be

largely restricted to winter forms of the oilseed types (Kutcher, 1990).

Species with the B genome (B. nigru. B. juncea, and B. carinufu) generally

appear to be highly resistant to blackleg disease (Roy, 1978a; Sacristan and

Gerdemann, 1986; Sjodin and Glimelius, 1988), although some susceptibility has been reported in a few accessions. However, the apparent lack of

symptoms in cotyledons and leaves is often associated with subsequent

extensive colonization of root and basal stem tissues (Gugel ef al., 1990;

Ken, 199 I ). Keri observed that over 80% of 250 accessions of B. juncea

inoculated with Canadian isolates of L. maculuns on the cotyledons were

subsequently found to have root infection.

Success in the development of winter rape cultivars with effective resist-



ance to blackleg, e.g., Jet Neuf, indicates that resistance is a heritable

character. Roy and Reeves (1975) found that 25% of the F, population was

resistant in some crosses and that blackleg resistance was readily incorporated from the cultivar Major into the Australian cultivar Wesreo (Roy,


The incorporation of blackleg resistance into rapeseed lines with desirable agronomic qualities is a major objective of breeding programs in

countries where the disease has seriously reduced yields. The inadequacy of

control by cultural practices and chemical means has further emphasized

the necessity of breeding for resistance. Considering the importance of the

disease and the standard practice of breeding for resistance, the paucity of

published data concerning the inheritance of resistance is surprising.

Seedling resistance to blackleg has been investigated by Delwiche ( 1980),

who found that cotyledon resistance of a French winter breeding line was

controlled by a single dominant gene, Lml. A second dominant gene

(Lm2) conferred resistance in another cultivar. Tests for independent inheritance of these two genes were highly significant, indicating linkage.

Inheritance of cotyledon resistance in spring oilseed rape, however, was

controlled by a single recessive gene (Sawatsky, 1989).

After inoculation of seedlings of many genotypes with Australian isolates

of the pathogen, Cargeeg and Thurling (1980a) observed continuous variation in disease reaction, which they considered to be indicative of polygenic

control of resistance. A significant cultivar by isolate interaction occurred.

Comparative studies between resistance observed in the glasshouse and in

the field indicated variation in resistance both among and within cultivars

of B. napus (Cargeeg and Thurling, 1980b).

Sawatsky ( 1989) found resistance in the French spring rape lines (R8314 and R83- 17) to be governed by two genes with dominant alleles, designated Bl-1 and Bl-2. The presence of both dominant alleles (Bl-I, BI-2)

conferred a high level of resistance whereas a single dominant allele (either

(BI-1 bl-1, bl-2 bl-2) or (bl-1 bl-1, 81-2 bl-2) provided intermediate levels of


Seedling resistance observed in both B. juncea and B. carinata lines is

thought to be controlled by genes located on the B genome and considered

to be more effective than seedling resistance in B. napus. Recent work by

Ken ( 1991 ) indicates that resistance in B. juncea is controlled by two genes.

These genes exhibit dominant recessive epistasis. The presence of wild-type

alleles or homozygous recessive alleles at both loci confers resistance.

Interaction between the wild-type resistance gene and the homozygous

recessive at the second locus results in a compatible or susceptible phenotype.

Numerous techniques have been employed to screen breeding materials

of oilseed brassicas for resistance to blackleg in the field, greenhouse, or



growth chamber. Although selection for resistance can be conducted in

blackleg-infested nurseries in the field, only one generation can be evaluated each year. This is probably the best that can be achieved with winter

forms of B. napus (Wittern and Kriiger, 1989, but with summer forms it is

more efficient to use screening procedures in growth chamber tests to

obtain selections from two generations a year.

Various workers have screened plants at different growth stages using

different modes of inoculation. Cotyledon testing has involved application

of drop or spray suspensions of pycnidiospores or ascospores (Williams,

1985; Alabouvette ef al., 1974; Thurling and Venn, 1977; Wittern and

Kriiger, 1985; Cargeeg and Thurling, 1980b). Seedlings have been inoculated by placing fungus-infested oat kernels at the plant base or by incorporating infected kernels in the soil (McGee and Petrie, 1978; Wittern and

Kriiger, 1985). A method devised by Helms and Cruickshank (1979) involved covering seeds with perlite mixed with a pycnidiospore suspension.

Other tests have screened for blackleg resistance at later growth stages.

Older seedlings have been infected by injecting the base of the petiole with

a pycnidiospore suspension (Newman, 1984). The true leaves can also be

inoculated with a pycnidiospore suspension to test for disease response

(Alabouvette ef al., 1974; McGee and Petne, 1978). A method of inoculating stems at the bolting stage with a pycnidiospore suspension has been

used in blackleg resistance screening (Newman and Bailey, 1987).

In order to evaluate which of these varied techniques are useful it is

important that blackleg resistance testing in the greenhouse accurately

represents the disease reaction obtained in field trials. A technique developed by Delwiche ( 1980) involved inoculating cotyledons with a droplet of

pycnidiospore suspension and rating plants 10 days postinoculation. This

test distinguished differences in disease response between four varieties.

However, disease reactions under field conditions were not determined.

Wittern and Kriiger (1985) found only slight differences between five

varieties in various experiments in which cotyledons were inoculated with

droplet or spray suspensions. A poor correlation between field and greenhouse results were observed. Alabouvette et al. (1974) tested the susceptibility of three rapeseed varieties by applying a spray suspension at the

cotyledon stage. Their results indicated a difference between greenhouse

and field classification of varietal susceptibility.

Cargeeg and Thurling (1980b) compared responses to inoculation in the

glasshouse and field. Seedlings were inoculated with an ascospore suspension and tested in four different glasshouse environments. A significant

positive correlation was found between disease scores in two of the glasshouse environments and the field trial for six field selected lines. However,

the correlation between field and glasshouse results of the glasshouse-selected lines was nonsignificant.



Wittern and Kriiger (1985) used ascospore inoculum as droplet or spray

suspensions to infect cotyledons or hypocotyls. The technique in which a

spray suspension of ascospores was applied to cotyledons resulted in the

greatest differences between varieties, whereas the other tests resulted in

only small differences in disease reactions between the different varieties.

Greenhouse and field results did not correspond for this method.

McGee and Petrie (1978) tested disease responses of 18 B. napus and B.

rupu lines in the greenhouse by inoculating plants at the soil level with oat

kernels infested with the blackleg fungus. These lines were also tested

against a population of L. mucufuns in field trials. The correlation between

disease rankings in each test was highly significant. Wittern and Kniger

(1985) obtained severe infection of rapeseed by mixing L. rnucufuns-infected oat kernels in the soil. However, differences in disease between

varieties were slight and greenhouse and field results did not agree. Helms

and Cruickshank (1979) tested cultivars of B. nupus, B. rupa, and B. rapa

ssp. pekinensis growing in inoculated perlite but could not detect any

differences in susceptibility between cultivars based on symptoms found

on cotyledons and hypocotyls.

Newman and Bailey (1987) reported a high correlation between glasshouse seedling tests and field results using a technique in which petioles

were inoculated. However, this method did not detect all resistant types;

field-resistant selections were uniformly susceptible for two sets of selections. Results obtained from mature plants tested at the bolting stage were

inconsistent with field scores in most experiments. W. McNabb and S. R.

Rimmer (unpublished) found a slight modification of this technique to

correlate best with field observations compared to four other methods.

2. White Rust

White rust (also called white blister) is an important disease of cruciferous species in India and Canada. The disease, caused by Albugo cundida

(Pers. ex Hook.) Kuntze, affects primarily B. rupa and B. junceu. It caused

considerable yield losses of B. rapa in western Canada during the 1970s

(Berkenkamp, 1972; Bernier, 1972; Petrie, 1973). The disease on B. rupa

has been controlled with resistance since the registration of the cultivar

Tobin (B. rupu) in 1981. However, a new pathotype of A. cundida, virulent

on Tobin, has developed recently and may have been responsible for heavy

local infections in Alberta (Conn and Tewari, I99 1). Canadian cultivars of

B. nupus are highly resistant to western Canadian isolates of A. cundida in

both field and laboratory studies (Petrie, 1975, 1988; Verma el uf., 1975).

Albugo candida occurs as a number of specific pathotypes that differ in

their pathogenicity to species and to genotypes within species of crucifer-



ous hosts. A number of pathotypes are specific to Brussicu species and

closely related crops. A numerical classification of races or pathotypes

based on pathogenicity and species specificity to a range of cruciferous

hosts (Pound and Williams, 1963) has been used widely for genetic studies

on host resistance.

In North America, at least eight pathotypes of A. cundidu have been

identified and classified based on their compatibility with different cruciferous host species or genera. These include race 1 on R. sutivus, race 2 on

B. junceu (Pound and Williams, 1963), race 7 on B. rupu (Verma et ul.,

1975; Pidskalny and Rimmer, 1985), and race 8 on B. nigru (L.) Koch

(Delwiche and Williams, 1977). It should be noted that although A. cundidu pathotypes are virulent on many genotypes of their homologous host

species, they are also capable of inciting disease on some genotypes of

closely related species (heterologous hosts).

Other as yet uncharacterized isolates have been obtained with pathogenicity on other Brussicu species (see Table V). Pathotypes occur that are

more or less specific to B. rupu (race 7) and to B. junceu (race 2). No

pathotypes are known whose homologous host is B. nupus, although certain genotypes of this species are susceptible to race 7 (Fan et ul., 1983), to

an Indian isolate from B. junceu (Verma and Bhowmik, 1989), and to

isolates from B. oleruceu and B. curinutu (S. R. Rimmer, unpublished

data). Recently, Ethiopian isolates of A. cundidu from B. curinutu have

been obtained and preliminary examination of the pathogenicity of these

isolates indicates that they are virulent on some genotypes of species with

the CC genome.

a. Resistance to Race 2

Alhugo cundidu race 2 mainly infects B. junceu (Pound and Williams,

1963; Pidskalny and Rimmer, 1985; Petrie, 1988), but some genotypes of

other Brussicu spp. are susceptible. Sources of resistance appear to be very

limited. Parui and Bandyopadhyay (1973) found that a strain, Yellow rai

T4, was virtually immune to natural infection by A. cundidu race 2.

Ebrahimi et al. (1976) described the inheritance of resistance to white rust

in the USDA accession PI 3476 18. F, progenies from the crosses between

resistant and susceptible plants gave a disease reaction similar to that of the

resistant parent. However, no data from the F2 have been reported. Bains

and Jhooty ( 1979) screened 150 lines/cultivars of B. junceu against mixed

infections caused by A. cundidu and Peronosporu purusiticu, but no resistance was observed. Failure to identify resistance to A. cundidu race 2 in B.

junceu was also reported by Delwiche and Williams (1974). Tiwari et ul.

( 1988) studied the inheritance of resistance derived from a Russian accession of B. junceu, Vniimk405, to race 2 of A. cundidu. Their data from BC,

Table V

Specificity of Isolates of Al6ugo cundi& to the Main Cultivated Crucifers'



Pathotypes of A. candida and their homologous hosts

Host species

Brassica rapa

Brassica nigra

Brassica oleracea

Brassica juncea

Brassica napus

Brassica carinata

Raphanus sativus






























































(Ac 1)








Data from Petrie (1988), I. R. Crute (personal communication), and S. R. Rimmer (unpublished).

Capital letters refer to species genome.

Ac, Albugo candida; capital letters refer to homologous host genome of isolate.

Race designation after Pound and Williams (1963).

R, resistant; S, susceptible; SIR, most host genotypes susceptible, some resistant; R/S, most host genotypes resistant, some susceptible; ?, uncertain

due to limited testing; *, not applicable-no isolates are known whose homologous host is B. napus.



and F2 populations strongly support a single dominant gene for resistance

in their material.

In addition to B. juncea, A. candida race 2 also attacks some genotypes

of B. rapa, B. nigra, B. napus, and B. carinata (Pound and Williams, 1963;

Petrie, 1988; Verma and Bhowmik, 1989). Because reaction to A. candida

race 2 in B. rapa varies among individual plants, ranging from low to high

infection type, resistance may be governed by both major and minor genes

and quantitatively inherited, according to Edwards and Williams ( 1987).

With a rapid-cycling population of B. rapa (CrGC-I), they found that the

quantitative resistance conditioned by minor genes could be effectively

enhanced by means of mass selection or half-sib family selection. In B.

nigra and B. carinata, resistance to race 2 has been reported to be conferred

by a single dominant gene (Delwiche and Williams, 1974, 1976, 1977).

Verma and Bhowmik (1989) studied resistance in B. napus to an uncharacterized isolate of A. candida from B. juncea (presumably race 2) and

showed that two dominant genes occurred in the resistant parent.

b. Resistance to Race 7

No information concerning the inheritance of resistance of B. rapa to

race 7 has been published. However, the cultivar Tobin contains resistance

to this pathotype, derived from wild Mexican populations of B. rapa. The

rate of population improvement for resistance from one generation to the

next under selection pressure suggests the presence of a single dominant

gene for resistance in this cultivar. Recently, in western Canada, a new

pathotype of race 7 (race 7v) has occurred that overcomes this resistance.

However, resistance to the new pathotype is also present in populations of

cultivar Tobin at low frequency, and by recurrent selection, with both race

7 and race 7v, subpopulations with high frequencies of resistance to both

pathotypes can be obtained in three or four selection cycles.

c. Resistance in Brassica napus

All present Canadian and European cultivars are resistant to the indigenous races of white rust. However, inheritance of resistance to A. candida

in B. napus was investigated by Fan et al. ( 1983) using a resistant Canadian

variety, Regent, and the susceptible Chinese lines, 2282-9 and GCL. The

segregation of F, progenies from both crosses, 2282-9 XRegent and

GCL X Regent, and their reciprocals suggested that resistance was governed by two independent dominant genes. Resistant plants resulted from

the presence of a dominant allele at either of the two loci, and susceptibility

would be expressed when the alleles at both loci were homozygous recessive. In addition, the segregation of some families of the F2 from the

GCL X Regent cross indicated that a third dominant resistant gene occurs



in Regent. The three resistance genes were designated Ac7- 1, Ac7-2, and


F, plants from 2282-9 X GCL and the reciprocal were all susceptible to

white rust. This suggested that the recessive genes camed by 2282-9 and

GCL were allelic. These two Chinese lines were found to be somewhat

different in their reaction to race 7 (Fan et ul., 1983; Liu et ul., 1989),

probably indicative of minor gene effects, 2282-9 generally appearing

slightly more susceptible than GCL. Liu and Rimmer (1992) reported that

this same line, 2282-9, was resistant to an Ethiopian isolate of A. cundidu

from B. curinuta. Canadian cultivars, including Regent and Stellar, were

susceptible to this isolate. An inheritance study using crosses of 2282-9

with a doubled haploidderived line from Stellar indicated that a single

dominant gene for resistance was present in 2282-9.

d. Selection for Resistance

Resistance to white rust can be efficiently selected in the cotyledon or

seedling stages of plant development. Either oospores or zoosporangia can

be used to produce zoospores for inoculum; oospores may be stored almost

indefinitely at room temperature under dry conditions. Germination of

stored oospores can be achieved by incubating on a shaker for 4-5 days

(Verma and Petrie, 1975). Zoosporangia will store for 1 -2 years if collected dry from plants and stored at - 10 to -20°C. Zoosporangia germinate readily in distilled water at 10 to 16°C within 2-4 hr. The zoospores

from germinated oospores or sporangia are used for inoculation. Details of

inoculation techniques and disease assessment based on the interaction

phenotype are described by Williams (1985). Plants that show any symptoms of white rust up to the flowering stage are discarded and the remaining plants are intermated (B. rupu) or selfed (for amphidiploid species, e.g.,

B. junceu).

3. Sclerotinia Stem Rot

Stem rot, caused by Sclerotiniu sclerotiorum (Lib.) de Bary, is a major

yield constraint in many parts of the world, including Canada (Morrall and

Dueck, 1982), Germany (Kriiger and Stoltenberg, 1983), and China (Liu

ef ul., 1990). The same pathogen causes severe disease on many other

dicotyledonous plants, including sunflower, field beans, peas, carrots, and

lettuce (Purdy, 1979). Because of its broad host range, the lack of evidence

for host specificity among isolates of the pathogen, and its sporadic occurrence due to weather conditions, economic control of this disease has been

difficult. Many producers depend on fungicide applications during the

flowering period for control and considerable effort has been directed



toward development of predictive methods to assist producers in determining whether or not fungicide applications would be economical. Sclerotinia sclerotiorum is an example of a broad host range, nonspecialized,

polyphagous pathogen. Parleviet ( 1989) has presented a general discussion

of the problems related to selection for resistance to such pathogens.

Some evidence for variation for resistance to stem rot in oilseed brassicas

has been reported. Brun ef al. (1987b) compared different inoculation

techniques and demonstrated significant differences in stem rot severity

among a number of B. napus accessions. Norin 9, a Japanese accession,

showed good resistance to stem rot. Insertion of toothpicks infested with

mycelium of the pathogen was shown to be a reliable method for evaluation of resistant materials. Sedun et al. (1989) compared the rate of lesion

expansion of stem rot on stems of various Brassica species as a measure of

disease resistance. Lesion expansion was slowest on B. carinata and B.

napus compared to B. nigra, B. juncea, and B. rapa, which showed the

most rapid lesion expansion. An interesting observation was that B. carinata, when inoculated in the leaf axils, frequently exhibited premature

leaf abscission before infection could become established and thus consequently escaped stem rot. Liu ef al. (1990) reported that heritability of

sclerotinia resistance was high in B. napus, controlled by nuclear genes and

unlinked to the low-erucic acid trait.

Infection of oilseed brassicas by S. sclerotiorum depends on the utilization by germinating ascospores of senescing petals as an energy substrate in

order to colonize the stem (Kriiger, 1975; Lamarque, 1983). Disease escape

may thus be possible through the development of apetalous cultivars. An

apetalous mutant of B. napus obtained from G. Buzza (Pacific Seeds Pty.,

Australia) was used to test this hypothesis and was substantially free of

stem rot compared to the normal petalous cultivar Westar (Table VI). Fu

Table VI

Mean Yield, Disease Incidence, and Severity of Sckrotiniu Stem Rot and Range of Severity

on Erusicu napus cv. Westar and an Apetalous Strain of Oilseed Rape in 1987"


or strain



Standard error





Range of


Yield per plot








I .5




f 4.0

f 3.5


f 32.0

" From S. R. Rirnrner (unpublished data).




ef al. (1 990) studied the inheritance of the apetalous character in B. napus

and showed that four recessive genes control this trait. They also observed

that the apetalous lines were unaffected by stem rot. Apart from its potential use in avoidance of infection by S. sclerotiorum, there is reason to

believe that increased yield may be associated with the apetalous trait

(Mendham ef al., 1991). This could be due to the improved light penetrance into the crop and subsequent increase of photosynthesis as substantial light reflectance by petals occurs during flowering of normal types.

The major difficulty in developing cultivars with resistance to stem rot

has been the lack of convenient reliable techniques for selection of resistant

phenotypes among population sizes required for a breeding program. In

those climates where reliable infection levels may be obtained consistently,

the best method is probably field testing and evaluation. This method is

likely to be satisfactory in some parts of China and Europe where cool wet

conditions are usual at flowering time. In Europe, where intensive oilseed

rape production is widespread, the availability of satisfactory fungicide

control has probably inhibited a concerted effort to select for resistance to

this disease. It is perhaps not too surprising then that most progress in

selection for resistance to stem rot has been made in China, where chemical control is unavailable for most farmers due to the expense and lack of

suitable fungicides. Under drier conditions stem rot occurs sporadically

and in these situations (for example, in western Canada) field selection for

resistance has not been effective.

4. Alternuriu Black Spot

Black spot of oilseed rapes (also called dark leaf and pod spot or Alternaria blight) is caused primarily by Alternaria brassicae (Berk.) Sacc.,

although depending on environmental conditions, Alternaria brassicicola

(Schw.) Wilts., Alternaria raphani Groves and Skolko, and Alternaria

alfernata (Fr.) Keissler may also be associated with the disease in some

areas. Aspects of this disease related to breeding for black spot resistance

have recently been reviewed by Singh and Kolte ( 1993). It is important that

a correct diagnosis of the species involved in the etiology of the disease in a

specific situation be determined before embarking on extensive work on

resistance breeding. The present review will focus on black spot caused by

A . brassicae.

Alternaria brassicae is the most prevalent causal agent of this disease on

oilseed Brussica species in most production areas of the world. Yield losses

may range up to 70%, varying from location to location and from year to



year [for references, see Singh and Kolte ( 1991)]. In Alberta, yield losses of

up to 30% have been reported (Tewari and Conn, 1988).

No high levels of resistance to black spot have been reported in cultivated oilseed Brassica species; generally, the rank in order of most to least

susceptible is B. rapa, B. juncea, B. napus, and B. carinata (Bhowmik and

Munde, 1987). Sinapis alba appears to be the most resistant of species

closely related to the oilseed brassicas (Brun et al., 1987a; Dueck and

Degenhardt, 1975; Rai et al., 1976). Chevre et al. ( 1991) reported interspecific transfer of the S. alba resistance into B. napus. This was accomplished

by manual pollination using reciprocal crosses and by somatic hybridization from protoplast fusion. Subsequently, embryo rescue and cytogenetic

analysis resulted in their obtaining B. napus plants with 38 chromosomes

and with resistance to A. brassicae similar to that of S. alba. The genetic

nature of the resistance transfer is currently under investigation. Some

indication that cytoplasm may influence the degree of resistance has been

obtained by Banga et al. (1984), who provided evidence that alloplasmic

lines of B. juncea, with the cytoplasm of B. napus or B. carinata, exhibited

a comparatively higher degree of resistance under field conditions than

euplasmic lines, whereas lines with cytoplasm of B. rapa were more susceptible.

Some variation for pathogenicity among isolates of A . brassicae occurs

but no isolates by host genotype interactions have been reported (Mridha,

1983). Although A. brassicae has been reported to produce a host-specific

toxin, destruxin B (Bains and Tewari, 1987), no evidence that the toxin is

specific to particular genotypes within any Brassica species has been

presented. Host-specific toxins are normally defined by their interaction

with specific genotypes within a species, e.g., AK-toxin produced by the

Japanese pear pathotype of A. alternata is specifically toxic only to cultivars of Japanese pear that are susceptible to the fungus [see Scheffer (1989)

for a discussion of this concept]. Alternuria brassicae produces a number of

destruxins (Buchwaldt and Jensen, 1991) that are toxic to plants from a

number of genera of dicotyledons. Though the sensitivity of species to

destruxin B is correlated with their relative susceptibility to infection by the

pathogen, the absence of genotypes specifically sensitive to the toxin suggests that the destruxins should be considered as host-selective toxins

(Buchwaldt and Green, 1992). Though this may seem a rather fine distinction, the implications of this for in vitro selection for resistance to black

spot employing these toxins may be considerable (see Section V1,B).

Tewari and colleagues have shown that other more distantly related

cruciferous species may be very resistant to black spot (Tewari et al., 1987;

Conn et al., 1988). Eruca sativa exhibited a hypersensitive-like reaction to

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