Bacterial Wilt

Ralstonia solanacarum is a species complex that causes bacterial wilt in tomato. The pathogen has been classified into five races, six biovars, and four phylotypes (Denny 2006). Strains of R. solanacearum are highly variable in their aggressiveness and cause variable severity of disease on tomatoes (Jaunet and Wang 1999). Therefore, it is important to use a well-characterized strain for resistance mapping studies. Sources of resistance to bacterial wilt in tomato have been identified primarily in cultivated tomatoes (Scott etal. 2005b). Classical genetic studies suggested a few major genes together with several minor genes conditioned resistance to bacterial wilt in tomato. Among the resistance sources, mapping has focused on L285 and Hawaii 7996, particularly the latter (Table 12). This is because of its durability at multiple locations and against diverse strains (Scott et al. 2005b). Mapping loci from Hawaii 7996 focused on populations derived from a cross with WVa700. A region on chromosome 6 linked to TG180 and TG240, which possibly contained two QTLs (Mangin etal. 1999), was associated with resistance against different pathogen strains and in different environments

Table 12. Molecular markers linked with resistance to bacterial canker, bacterial speck, bacterial spot, and bacterial wilt in tomatoes

Resistance source

Strain or Race

Mapping populationa

QTL and markers in flanking region (shown in parentheses)13

Reference

Bacterial canker caused by C. michiganensis subsp. michiganensis

LA2157 Cm542 F2 of Solentos :

S. peruvianum

LA2157

LA407

S. habrochaites

A300, A226 and C290 belonged to predominant genetic groups

64 IBLs; F2 of selected IBLs carrying Rcm2.0 or Rcm5.1 crossed with Ohio 86120 for map positioning

Bacterial speck caused by Pseudomonas syringae pv. tomato

Rio Grande-PtoR S. lycopersicum Rio Grande-76R

Strain PTll (raceO)

Strain Tl (race 0)

Bacterial spot caused by Xanthomonas species

Hawaii 7998 (H7998) Race Tl S. lycopersicum

Race Tl

LA716 S. pennellii Money Maker (MM) S. lycopersicum

Race T3

Strains contained avrBs4 that could induce hypersensitive responses on cultivated tomatoes

F2 of Rio Grande-PtoR and Rio Grande F2 of a cross between a prf mutant (prß>to/prß>to) and Rio Grande (Prfpto/Prfpto)

H7998 x (H7998 LA 716)

F2 of Ohio 88119 : : H7998; ABLs and IBLs for linkage confirmation

F, of H 7998 x LA716

Three QTLs on chromosome 5 (TG363), 7 (TG61), 9 (TG254) with additive and co-dominant effects; SCAR markers based on TG61 on chr 7 were developed Rcm2.0 on chromosome 2 (TG537 to TG091; 4.4 cM); Rcm5.1 on chromosome 5 (CT202 to TG358; 2.2 cM) with additive effects and additive-by-additive epistatic gene interactions

Pto on chromosome 5 co-segregated with TG538

Prf is 0.12 cM from Pto; physically Prf lies between Pto (24 Kb from Prf) and Fen (500 bp from Prf)

Three non-dominant and independent QTLs, i.e.

rx-1 (TG236) and rx-2 (TGI 57) on chromosome 1 and rx-3 (TG351) on chromosome 3

Rx3 (Rx3-Ll, CosOH73,

TOM49) on chromosome 3

contributed to reduced bacterial population (25%)

and field resistance (41%)

A single dominant gene, Xv4 (TG599 to TG134) on chromosome 3 conferred HR

Bs4 co-segregated with TG432 on chromosome 5

van Heusden et al. 1999

Kabelka et al. 2002; Coaker and Francis 2004

Martin et al. 1993b Salmerón et al. 1996

Yu et al. 1995 Yang et al. 2005b

Astua-Monge et al. 2000 Ballvora et al. 2001

a F2:3: F2 derived F3 families b Names of QTL or resistance genes are indicated in bold

Table 12. (continued)

Resistance source

Strain or Race

Mapping populationa

QTL and markers in flanking region (shown in parentheses)13

Reference

PI 114490

S. lycopersicum

Bacterial wilt caused by Ralstonia solanacearum

L285 UW364 (race 1, biovar 4)

S. lycopersicum

Hawaii 7996 GMI8217 (race 1, bvl)

S. lycopersicum

166IBL derived from OH 9242 (FL 7600 : : PI 114490)

71 F2 of a cross between L285 and CLN286BC1F2-25-14-7 F2 of H7996 x WVa700

F2 and F2:3 ofH7996 : : WVa700

F2:3 andRIL ofH7996 : WVa700

F2:3 andRIL ofH7996 : WVa700

A common region on chromosome 11 (SSR637, TOM 196, TOM 144) conferred resistance to races T2, T3, and T4

Three QTLs on chromosome 6 (CT184), 7 (TG51b), 10 (CT225b)

Three QTL on chromosomes 4 (TG268), 6 (TG118; a major QTL), and 11 (GP162)

Six QTL on chromosomes 3 (GP226), 4 (K12 to GP165), 6 (TG178 to TGI 18 to TG73), 8 (CD40), 10 (CP105), and 11 (D6b to O10); Temporal analysis supports the presence of two QTL on chromosome 6 linked to TGI 80 and TG240 Five QTL on chromosomes 2 (GP504), 6 (TG73; Cf2), 8 (CT135) and 12 (TG564); QTL linked to TG564 were associated with 70% of total variation Three QTL on chromosomes 6 (Bwr-6; TG73), 8 (Bwr-8; CD40 to CT135), and 12 (Bwr-12; TG564) Three QTLs on chromosomes 3 (Bwr-3; TG515), 4 (Bwr-4; CD73) and 6 (Bwr-6; TG73)

Yang et al. 2005a

Danesh et al. 1994

Thoquet et al. 1996a

Thoquet et al. 1996b; Mangin et al. 1999

Wang et al. 2000

Carmeille et al. 2006 Carmeille et al. 2006

(Thoquet et al. 1996a, b; Wang et al. 2000; Carmeille et al. 2006). QTLs found within other chromosomal locations were not consistent over experiments, and terms such as strain-specific (Wang et al. 2000) or phylotype-specific (Carmeille et al. 2006) have been proposed. With the availability of a permanent mapping population, i.e., RIL population of Hawaii 7996 x WVa700, specificity of QTL can be verified. No known markers are suitable for MAS to transfer resistance from Hawaii 7996 to susceptible cultivars. This is mainly due to the low polymorphism between Hawaii 7996 and WVa700, which could possibly be solved by developing SNP markers.

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