**7. Inheritance of resistance to** *L. maculans*

Genetic inheritance studies revealed that resistance to *L. maculans* is complex. Resistance is either described as qualitative (also referred as monogenic/seedling/race-specific resistance/ vertical resistance) or quantitative (also referred as polygenic/adult plant/race non-specific resistance/horizontal resistance) in *Brassica*.

#### **7.1. Qualitative resistance**

are commonly used for evaluating resistance to *L. maculans*. However, disease severity is much more difficult to estimate than disease incidence, due to the G x E interactions and unreliable and inconsistent estimation of canker lesions, even within the same genotype, particularly when infection is not uniform. The use of increased sample size (25 to 50 plants/genotype) and reliable and congenial growing conditions for the disease development will allow better

Assessment of blackleg resistance under field conditions is usually performed by exposing the plants to a mixed population of *L. maculans* races, which can make the detection of racespecific *R*-genes difficult. No relationship between the degree of cotyledon-lesion develop‐ ment at the seedling stage and crown canker development in mature plants was observed in the intercross population derived from Maluka/Niklas [36]. This study concluded the limited value of the cotyledon test in screening for adult plant blackleg resistance. Similarly a lack of correlationbetweencotyledon(seedling)resistance andstem(adultplant)resistance in*B. napus* andBgenome sourceshas alsobeenreported[37].Recently, apoor correlationbetweenseedling and field reactions was reported in the DH from Skipton/Ag-Spectrum which could have been due to the prevalence of different pathotypes under field conditions as contrary to cotyledon test, where often a specific isolate is used for phenotyping [32]. In order to mimic field condi‐ tions and increase reliability of disease development, an ascospore shower test [38] has been usedforgermplasmevaluationandvarietalrelease inAustralia.Inthis test, stubblewithmature pseudothecia is sprayed with distilled water until run-off, producing 'ascospore shower'. The infected plants can then be assessed for resistance at both the cotyledon and adult plant stages. Thismethodhas shownahighcorrelationwithcankerlesions scoredunderfieldconditions [39].

**6. Natural genetic variation for resistance to** *L. maculans*

The introgression of blackleg resistance (*R*) genes into *B. napus* germplasm for blackleg disease management is one of the major objectives of breeding programs aiming to release cultivars in disease-prone areas. Genetic variation for resistance to *L. maculans* exists within *B. napus* germplasm [39, 40, 41]. Some other Brassica species such as *B. rapa*, *B. juncea*, *B. nigra* (black mustard; 2n = 2x = 16, genome BB) and *B. carinata* (Abyssinian or Ethiopian mustard; 2n = 34, genome BBCC), as well as other crucifers such as *Sinapis arvensis* have been reported to carry resistance [42-53]. Some of these sources were utilised in transferring resistance into *B. napus* breeding lines and cultivars. A continuous variation for blackleg resistance in a world-wide collection of *B. rapa* genotypes was reported [54]. None of genotypes were completely suscep‐ tible or completely resistant to either *L. maculans* pathotypes used. However, some *B. rapa* accessions that were either highly resistant or completely susceptible were identified (Raman et al., unpublished) in a set of differential cultivars currently being used in Australia [39].

It has been reported that all B genome Brassica species; *B. nigra, B. carinata* and *B. juncea* carry complete resistance to *L. maculans* which remains effective throughout the life of the plant [40], however susceptible *B. juncea* cultivars have also been identified [55] demonstrating that complete resistance is not a feature of all B genomes. Some B genome resistance genes have been introgressed into *B. napus* lines. [47, 56-59]. Earlier studies have shown that C genome

estimation of canker lesions.

88 Plant Breeding from Laboratories to Fields

Monogenic inheritance was reported in several spring and winter cultivars of *B. napus* such as Cresor, Maluka, Dunkeld, Maluka, Skipton, and Major [32, 63-67]. Eighteen major genes for resistance to *L. maculans*; *Rlm1* to *Rlm11*, *RlmS*, *LepR1* to *LepR4*, *BLMR1* and *BLMR2*, have been identified in Brassica species; *B. rapa*, *B. napus*, *B. juncea* and *B. nigra* [31, 32, 40, 45, 68-73]. Six of them, *Rlm1*, *Rlm2*, *Rlm3*, *Rlm4*, *Rlm7* and *Rlm9* were identified in *B. napus*, all of them except *Rlm2* were clustered genetically on chromosome A07 [74]. *Rlm2* was mapped on chromosome A10 [45]. The *Rlm5* and *Rlm6* were identified in *B. juncea*; *Rlm8* and *Rlm11* in *B. rapa*, and *Rlm10* was identified in *B. nigra*. Four resistance genes; *LepR1*, *LepR2*, *LepR3*, and *LepR4* were introgressed into *B. napus* from *B. rapa* subsp. *sylvestris* (Table 1).




**Species Locus \*Population Phenotyping**

Darmor/Samourai (133

DH)

90 Plant Breeding from Laboratories to Fields

*B. juncea Rlm6* Recombinant lines

*B. napus Rlm7* 2311.1/Darmor

*B. napus Rlm9* Darmor-bzh/Yudal (132 DH)

*B. nigra Rlm10* Addition lines

*B. rapa* ssp. *sylvestris*

*B. rapa* ssp. *sylvestris*

*B. rapa* ssp. *sylvestris*

(221 F2)

*B. napus Rlm3* Maxol/S006 (140DH) Cotyledon

*B. napus Rlm4* Quinta/Score (110F2) Cotyledon

(*B. napus-B. juncea*)

(Darmor/Junius)

*LepR2* 6279/3027 (DHP96) Cotyledon

Topas (DH16516)/ Surpass400

*LepR4* 16S/PAS12//16S (BC3S2)

(1513 F3BC2)

(1513 F3BC2)

Westar (susceptible)

*B. napus BLMR1* Surpass400/Westar

*B. napus BLMR2* Surpass400/Westar

*B. napus LmFr1* Cresor (resistant)/

*LepR1* 6270/Springfield (DHP95)

*B. napus LepR3* Surpass400/Westar (N-o-1)-BC

**stage**

inoculation

inoculation

inoculation

Stem canker

test

Cotyledon and field

Glacier/Yudal (BC189) Cotyledon

Skipton/Ag-Spectrum Cotyledon and

**Marker type**

Cotyledon, Field RAPD Bulked

RAPD Bulked segregant analysis

RAPD Bulked segregant analysis

RAPD Bulked segregant analysis

SSR Whole genome mapping

> Bulked segregant analysis

> segregant analysis

> segregant analysis

Whole genome mapping

RAPD/ RFLP

Cotyledon RAPD Bulked

Cotyledon RAPD Bulked

RAPD

SSR, SCAR

SRAP, SNP

SRAP, SNP

RFLP Whole genome analysis

RFLP Whole genome analysis

RFLP Whole genome analysis

SSR A1 and A10 chromosome specific mapping

> A10 chromosome specific mapping

SSR A genome

specific marker analysis

Selective genotyping

Selective genotyping

Cotyledon test Isozyme

Cotyledon inoculation and field resistance

inoculation and field resistance

Cotyledon inoculation

Cotyledon inoculaton

Cotyledon inoculation Disease nursery (field)

Cotyledon inoculation

Cotyledon inoculation

Field/artificial inoculation

**Mapping strategy**

segregant analysis

**chromosome Linked markers/interval Reference**

A7 M08.1200, M08.600, P02.700 74

A7 M08.1200 (10cM), 74

A7 Q12.750 (7cM) 74

O15.1360 (`33 cM)

B8 OPG02.800, OPT01 47

A7 T12.650 (4cM) 74, 85

A7 T12.650/C02.1375 74

B4 OPA11.1200, OPC19.3300 83, 84

A10 (N10) pN21b, pR34b, pN53b 31

sR12281a (2.2 cM) sN2428Rb (0.7 cM)

A10 (N10) Ind10-12 79

sR9571a (8.3 cM)

A10 (N10) 80E24a (0.1 cM) 70

A10 (N10) R278 (1.2 cM) 70

cDNA011/cDNA110 64

A6 sN2189b (8.8cM)

Linkage group 6 (A7)

A2 (N2) pR4b, pO85h, pW180b, pN181a, pW207a

BRMS075 (`0.7 cM) 32

74

31

69

77

A7 C02.1375 (3.6 cM)/

**Table 1.** Molecular mapping of qualitative genes for resistance to *Leptosphaeria maculans* in *Brassica.*\* BC: Backcross population, DH: Doubled haploid population. # loci not mapped with molecular markers to date.

Recently, two genes *BLMR1* and *BLMR2* in Surpass 400; an Australian cultivar developed from an interspecific cross between wild *B. rapa* subsp. *sylvestris* (resistant) from Sicily and *B. oleracea* subsp. *alboglabra* were identified [70, 76]. However, *LepR1* to *LepR4* genes are thought not be related with *Rlm* genes on the basis of their map locations, except for *Rlm2* and *LepR3*, which are phenotypically different [31, 69, 77]. It appears that loci *LepR3*, *BLMR1* and *BLMR2* localised on chromosome A10 control resistance to *L. maculans* in Surpass 400. However, Van de Wouw et al. [73] demonstrated that two independently segregating *L. maculans* avirulence (Avr) genes, *AvrLm1* corresponding to *Rlm1* (on chromosome A7) and *AvrLmS*, are responsible for inducing resistance in this cultivar. Subsequently, Larkan *et al.* [78] investigated the interaction of *AvLm1* and *AvLmS* isolates with *B. napus* populations segregating for the resistance genes *Rlm1* (from the French cultivar Quinta) and *LepR3* (from Surpass 400). This study reported that (i) *AvrLm1* interacts in a gene-for-gene manner with both *Rlm1* and *LepR3*, (ii) *AvrLmS* is not responsible for triggering the *LepR3* mediated defence response, (iii) Surpass 400 does not contain *Rlm1,* and (iv) *Rlm1* and *LepR3* may be the same genes located in two distinct loci or may have evolved as two functional genes. Recently, *LepR3* has become the first functional *B. napus* resistance gene to be cloned and was shown to encode a receptor-like protein. Additionally, *LepR3*-transgenic *B. napus* and *AvrLm1*-transgenic *L. maculans* were used to demonstrate that *AvrLm1* conveys avirulence to *LepR3*. The shared genomic location of *LepR3* and *BLMR1* also suggested that these were the same gene [79]. Several other genes such as *LmR1, ClmR1, LmFr1, cRLMm, cRLMrb, aRLMrb,* and *LEM1* have also been identified using uncharacterised isolates, which are thought to be allelic to known *R*-genes [45, 68, 74]. Qualitative resistance conferred by single major genes is usually dominant and expressed at the seedling growth stage. Qualitative *R*-genes explain majority of phenotypic variation for blackleg resistance at adult plant stage [32, 74]. However, digenic mode of inheritance has also been reported in *B. napus and B. juncea* populations [40, 80].

#### **7.2. Quantitative resistance**

Quantitative inheritance for field resistance has been reported in segregating populations derived from *B. napus*, *B. juncea* and their hybrid derivatives [30, 32, 65, 80, 86]. Some of the QTLs identified are given in Table 2. Quantitative genetic analysis revealed that significant non-additive genetic variance for all measures of disease severity indicated the presence of strong dominance/epistasis at loci controlling blackleg resistance [36]. In the literature, the term 'QTL' as a quantitative locus has been used even when a large percent of genotypic variation is explained by the major locus. In classical genetics, QTL refers to genes that have, low heritability, non-Mendelian and quantitative accumulative effects. The majority of genetic analyses have utilised doubled-haploid (DH) populations, which are not suitable to infer modes of inheritance. Advanced intercross populations are required to interpret such phe‐ nomena, as used in [74].



Recently, two genes *BLMR1* and *BLMR2* in Surpass 400; an Australian cultivar developed from an interspecific cross between wild *B. rapa* subsp. *sylvestris* (resistant) from Sicily and *B. oleracea* subsp. *alboglabra* were identified [70, 76]. However, *LepR1* to *LepR4* genes are thought not be related with *Rlm* genes on the basis of their map locations, except for *Rlm2* and *LepR3*, which are phenotypically different [31, 69, 77]. It appears that loci *LepR3*, *BLMR1* and *BLMR2* localised on chromosome A10 control resistance to *L. maculans* in Surpass 400. However, Van de Wouw et al. [73] demonstrated that two independently segregating *L. maculans* avirulence (Avr) genes, *AvrLm1* corresponding to *Rlm1* (on chromosome A7) and *AvrLmS*, are responsible for inducing resistance in this cultivar. Subsequently, Larkan *et al.* [78] investigated the interaction of *AvLm1* and *AvLmS* isolates with *B. napus* populations segregating for the resistance genes *Rlm1* (from the French cultivar Quinta) and *LepR3* (from Surpass 400). This study reported that (i) *AvrLm1* interacts in a gene-for-gene manner with both *Rlm1* and *LepR3*, (ii) *AvrLmS* is not responsible for triggering the *LepR3* mediated defence response, (iii) Surpass 400 does not contain *Rlm1,* and (iv) *Rlm1* and *LepR3* may be the same genes located in two distinct loci or may have evolved as two functional genes. Recently, *LepR3* has become the first functional *B. napus* resistance gene to be cloned and was shown to encode a receptor-like protein. Additionally, *LepR3*-transgenic *B. napus* and *AvrLm1*-transgenic *L. maculans* were used to demonstrate that *AvrLm1* conveys avirulence to *LepR3*. The shared genomic location of *LepR3* and *BLMR1* also suggested that these were the same gene [79]. Several other genes such as *LmR1, ClmR1, LmFr1, cRLMm, cRLMrb, aRLMrb,* and *LEM1* have also been identified using uncharacterised isolates, which are thought to be allelic to known *R*-genes [45, 68, 74]. Qualitative resistance conferred by single major genes is usually dominant and expressed at the seedling growth stage. Qualitative *R*-genes explain majority of phenotypic variation for blackleg resistance at adult plant stage [32, 74]. However, digenic mode of inheritance has also

Quantitative inheritance for field resistance has been reported in segregating populations derived from *B. napus*, *B. juncea* and their hybrid derivatives [30, 32, 65, 80, 86]. Some of the QTLs identified are given in Table 2. Quantitative genetic analysis revealed that significant non-additive genetic variance for all measures of disease severity indicated the presence of strong dominance/epistasis at loci controlling blackleg resistance [36]. In the literature, the term 'QTL' as a quantitative locus has been used even when a large percent of genotypic variation is explained by the major locus. In classical genetics, QTL refers to genes that have, low heritability, non-Mendelian and quantitative accumulative effects. The majority of genetic analyses have utilised doubled-haploid (DH) populations, which are not suitable to infer modes of inheritance. Advanced intercross populations are required to interpret such phe‐

> **Chromosome**

**LOD# score**

**%Genetic variance (R2)#**

A1 2.5-5.6 14-16 Not known (-) 86\*

**Additive effect**

**Reference**

been reported in *B. napus and B. juncea* populations [40, 80].

**7.2. Quantitative resistance**

92 Plant Breeding from Laboratories to Fields

nomena, as used in [74].

**Stubble, Location**

*B. napus,* Lake Bolac, Australia

**Flanking markers**

E34M15\_S190/ E35M53\_S416

**Mapping Population**

Av-Sapphire/ Westar10


**Table 2.** Significant QTLs associated with blackleg resistance (scored as Internal infection due to canker development at adult plant stage) identified from mapping populations, \* QTL with consistent effect, # range of LOD and R2 varied with method of regression analysis (simple and composite interval mapping).\* refers to predicted markers from supplementary figures ESM7-10 shown in Kaur et al [81]

#### **8. Gene-for gene interactions**

Host resistance genes (*R*-genes) interact in paired combination with pathogen avirulence (*Avr*) genes to condition resistance [89]. Two types of interactions may occur; compatible and incompatible. Compatible interaction occurs when there is an absence of an effective host defence response, due to a lack of a resistance allele in host (*r*) or an allele for virulence (*avr*) at the corresponding pathogen locus. An incompatible interaction occurs when there is no disease development due to the presence of both an effective host resistance allele (*R*) with an allele for *Avr* at the corresponding pathogen locus [90]. Biochemically, gene-for-gene interac‐ tions have been interpreted as the interaction of a race-specific pathogen elicitors with either cultivar-specific plant receptors or alternatively with a cultivar-specific signal transduction compounds [91]. Differential interaction between specific *R*-genes in the host (Brassica) and corresponding *Avr* genes of the pathogen *(L. maculans)* was first studied at the seedling stage using a cotyledon inoculation test in *B. napus* [92] and subsequently verified [57]. Qualitative and quantitative resistance differ with respect to host-pathogen interaction, as the latter does not appear to (but not proven) follow the gene-for gene hypothesis, being more effective against diverse pathogen populations (non-race specific). While quantitative resistance normally provides partial resistance to the pathogen and it is less likely to be rapidly overcome by shifting pathogen populations.

At least ten *Avr* genes have been identified in *L. maculans*, many of which map to two gene clusters; *AvrLm1-AvrLm2-AvrLm6* and *AvrLm3-AvrLm4-AvrLm7-AvrLepR1* ([71, 72, 86, 87]. Four of the *Avr* genes; *AvrLm1, AvrLm6, AvrLm4-7* and *AvrLm11* have been cloned. It has shown that although *AvrLm1* and *AvrLm6* are physically clustered together in the *L. maculans* genome, they are not allelic forms of a single gene [85, 96]. However, *AvrLm4* and *AvrLm7* are allelic variants of a single *Avr* gene that corresponds to the two resistance genes; *Rlm4* and *Rlm7* [71, 85]. It has also been demonstrated that *AvrLm1* interacts with two distinct resistance loci; *Rlm1* and *LepR3*, though these loci are located on different chromosomes (A7 and A10, respectively) [78]. The cloning and characterisation of additional Brassica *R*-genes and *L. maculans* Avr genes will lead to a better understanding of how these functional redundancies developed. In the recent years, understanding of *L. maculans/Brassica* interactions has increased our ability to deploy appropriate *R*-genes in new cultivars and manage blackleg disease with the increased knowledge of the distribution of *Avr* alleles in *L. maculans* populations [27, 94, 98]. Currently, it seems that the genes involved in race-specific resistance and polygenic non-specific resist‐ ance are distinct. A better understanding of the mechanisms underlying quantitative resistance would help our understanding of the relationships between quantitative and major resistance genes [99].

## **9. Alien gene introgression for blackleg resistance**

**Mapping Population** **Stubble, Location**

94 Plant Breeding from Laboratories to Fields

Wagga, Australia

*B. napus*, ATR Beacon stubble, Wagga, Australia

supplementary figures ESM7-10 shown in Kaur et al [81]

**8. Gene-for gene interactions**

by shifting pathogen populations.

**Flanking markers**

*Xbrms319- Xbrms176*

*Xcb10172- BnFLC10*

*Xbrms287a-Xcb10034*

*c03*

*Xol10-c10/Xna12-*

*Xpbcessrna13/ Xol13-d02a*

*Xem1-bg23-89/ Xol12-e03*

*Xol12-f11/ Xpbcessrbr21* **Chromosome**

**LOD# score**

**%Genetic variance (R2)#**

A9 2.9 5.0 Skipton

A10b 2.2 6.2 Skipton

C2a 6.8 16.6 Skipton

C3 4.2 24.5 Skipton

C6 6.1 14.5 Ag-Spectrum

A1a 6.1 26.1 Ag-Spectrum

**Table 2.** Significant QTLs associated with blackleg resistance (scored as Internal infection due to canker development at adult plant stage) identified from mapping populations, \* QTL with consistent effect, # range of LOD and R2 varied with method of regression analysis (simple and composite interval mapping).\* refers to predicted markers from

Host resistance genes (*R*-genes) interact in paired combination with pathogen avirulence (*Avr*) genes to condition resistance [89]. Two types of interactions may occur; compatible and incompatible. Compatible interaction occurs when there is an absence of an effective host defence response, due to a lack of a resistance allele in host (*r*) or an allele for virulence (*avr*) at the corresponding pathogen locus. An incompatible interaction occurs when there is no disease development due to the presence of both an effective host resistance allele (*R*) with an allele for *Avr* at the corresponding pathogen locus [90]. Biochemically, gene-for-gene interac‐ tions have been interpreted as the interaction of a race-specific pathogen elicitors with either cultivar-specific plant receptors or alternatively with a cultivar-specific signal transduction compounds [91]. Differential interaction between specific *R*-genes in the host (Brassica) and corresponding *Avr* genes of the pathogen *(L. maculans)* was first studied at the seedling stage using a cotyledon inoculation test in *B. napus* [92] and subsequently verified [57]. Qualitative and quantitative resistance differ with respect to host-pathogen interaction, as the latter does not appear to (but not proven) follow the gene-for gene hypothesis, being more effective against diverse pathogen populations (non-race specific). While quantitative resistance normally provides partial resistance to the pathogen and it is less likely to be rapidly overcome

C1 4.2 11.5 Ag-Spectrum

**Additive effect**

**Reference**

Deployment of *R*-genes has been used as the most cost-effective and environmentally sound measure for disease control in various crops since a century ago when first *R*-genes were identified [100]. Conventional plant breeding methodologies have played an important role in gene introgression for disease resistance, especially in easily-crossed genetic back‐ grounds. As a result several cultivars rated for resistance to *L. maculans* now dominate commercial cultivation worldwide. There has been a continuous threat of 'breakdown' of resistance, especially when a resistant cultivar is grown extensively on large acreages over long period of time. For example, 'breakdown' of resistance in cultivar Surpass 400 occurred within three years of its release [101, 102] due to the evolution and spread of more virulent strain of *L. maculans*. 'Breakdown' of resistance implies that the resistance has not changed rather the pathogen population has shifted/been selected for virulence. The effectiveness of *Rlm1* in France was also greatly reduced from 1997 to 2000 following wide deployment of *Rlm1* varieties, effectively selecting for enrichment of the virulent *avrLm1* allele in *L. maculans* populations [34]. Interestingly, a similar enrichment for the virulent *avrLm1* allele was documented after the 'breakdown' of *LepR3* resistance in Australia [103]. Due to the threat of current resistance being rendered ineffective by shifting *L. maculans* populations, new effective sources of resistance are constantly in demand. In order to enlarge genetic variation for resistance to *L. maculans*, interspecific and intergeneric donor sources have been utilised. This has been achieved by conventional sexual crossing [44, 52, 75, 104] or via laboratory tools such as somatic hybridization [105], and embryo culture. Roy [52] crossed *B. juncea* and *B. napus* to introgress genes for blackleg resistance but none of the interspecific hybrids achieved the same level of *B. juncea* resistance as the donor parent. Wide hybrids (interspe‐ cific, intergeneric or intertribal) have also been produced either by sexual crossing fol‐ lowed by embryo culture or by somatic hybridisation as a result of protoplast fusion to transfer genes for blackleg resistance [106, 107]. Previous studies have reported hybrids between *B. napus* and *Arabidopsis thaliana*, belonging to different tribes; the Brassiceae and Sisymbrieae, respectively [108]. These hybrids were further utilized for identifying genetic regions associated with blackleg resistance [49]. Two regions localised on chromosome 3 of *A. thaliana* were shown to be linked with resistance to *L. maculans*.

Crouch *et al.* [75] transferred genes for resistance to *L. maculans* derived from *B. rapa* subsp. *sylvestris* into *B. napus*, using a resynthesised amphidiploid, as a result of hybridisation between *B. rapa* subsp. *sylvestris* and *B. oleracea* subsp. *alboglabra*. As a result, several cultivars derived from the re-synthesized *B. napus* lines were released for commercial cultivation in Australia such as Surpass 400, Surpass 404CL, Surpass 501TT, Surpass 603CL, Hyola 43, and Hyola 60. The *R*-genes *LepR1*, *LepR2* and *LepR4* have also been introgressed into *B. napus* via conventional interspecific crosses [75, 109]. Introgression of genes for resistance to *L. maculans* from *Sinapis arvensis*, *Coincya momensis* and *B. juncea* into *B. napus* was attempted [110]. Hybrid derivatives of *B. napus* and *S. arevensis*, and *B. napus* and *C. momensis* showed a high levels of resistance at the seedling (cotyledon) and/or adult plant stages. The offspring from asymmetric hybrids between *B. napus* and *B. nigra, B. juncea* and *B. carinata* were analysed for the presence of B genome markers and resistance to *L. macu‐ lans* [111]. This study revealed that resistance is conserved in one triplicate region in the B genome. Often, the majority of wide-hybrid derivatives exhibit unwanted traits and low frequencies of recombination between the different species which complicate the develop‐ ment of *B. napus* cultivars resistant to *L. maculans* by traditional breeding [43, 47]. Link‐ age drag due to suboptimal/undesired genes can be eliminated using the application of high density genome-wide molecular markers such as SNPs [112]. However, Rouxel and Balesdent [93] cautioned that before important breeding efforts are devoted to introgres‐ sion of resistance genes from distant species into Brassica, there is a need thoroughly to evaluate their genetic control, putative redundancy and potential durability in the field.

Using transgenic technology, *R*-genes from other organisms can also be transferred irrespec‐ tive of natural barriers to crossing. However, it is possible that transferred genes may not always contribute novel resistance specificities to the transgenic crop. Although several approaches have been used to induce host resistance in plants [113, 114] no major breakthrough has been made for an efficient management of blackleg disease. For example, Hennin *et al.* [115] demonstrated the expression of *Cf9* gene, which confers *Avr9*-dependant resistance to *Cladosporium fulvum* in tomato, along with co-expression of *Avr9* produced increased resistance to *L. maculans* in transgenic *B. napus* plants. Manipulation of plant defense responses is resource-expensive [116] and may be deleterious to the plant. Plants need to be selected for both appropriate expression of beneficial defense responses and avoidance of unnecessary ones [117], making artificially-induced constitutive expression of these responses an imprac‐ tical solution to engineering resistance.
