C20

QUASI-ISOGENIC TOMATO LINES CARRYING MI ARE USEFUL TOOLS FOR THE GENETIC ANALYSIS OF BACTERIAL WILT RESISTANCE ON CHROMOSOME 6

Deberdt P1., Olivier J3., Laterrot H2., Moretti A2., Grimsley N3., Darrasse A1., Prior P1.

1 INRA-URPV, Laboratoire de Phytobactériologie, BP 515, 97165, Pointe à Pitre Cedex, Guadeloupe (FWI).
2 INRA, Station d’Amélioration des Plantes Maraîchères, Domaine Saint-Maurice, BP 94, 84143 Montfavet Cedex, France.
3 Laboratoire de Biologie Moléculaire de Relations Plantes-Microorganismes, CNRS-INRA, B.P. 27 Auzeville, 31326 Castanet-Tolosan, France.


As a soil inhabitant, Ralstonia solanacearum is codistributed with polyspecific nematodes populations in tropical and sub-tropical areas. These organisms often have synergistic effects on wilt symptoms, especially on tomato. Additional wounding of the root system by nematodes is generally reported to increase the severity of bacterial wilt (BW), probably because it facilitates bacterial entry. Recently, galling was reported as the primarily synergistic determinant increasing BW severity (Deberdt et al, 1996). Resistance in certain tomato varieties is controlled by numerous quantitative resistance loci (QRL), including the major effect (20 to 50%) of a QRL located on tomato chromosome 6 (Danesh et al., 1994; Thoquet et al., 1996). In previous breeding programmes (Acosta et al., 1994) pairing the Mi root knot nematode resistance gene with BW resistance resulted in a reduction of the parental level of resistance to BW. We hypothesized that introgressing Mi from the wild related species Lycopersicon peruvianum (on chromosome 6) led to the loss of the BW resistance allele(s) on chromosome 6, because these genes may be closely linked. However tomato lines selected for both Mi and BW resistance might be useful material for production and for the genetic mapping of the BW resistance locus (or loci) in this region of the genome.

Disease incidence was assessed following infection with race 1 (Bvs 1 and 3) strains of R. solanacearum differing in aggressiveness. Tomato genotypes consisted in two different quasi-isogenic polygenic resistant lines (QIPRL):

- QIPRL 1; Caraïbo and Carmido (Mi from Ontario 7620 x [Caraibo]6), and

- QIPRL 2; CRA 66 and Cranita (Mi from Anahu x [CRA 66 ]4).

Carmido carries a smaller region of introgressed Lycopersicon peruvianum DNA than Cranita. These QIRPLs are thus nearly homozygous for the BW resistant parent, but are heterozygous around the Mi gene. The segregation of Mi and BW resistance was investigated using progenies which were collected from these two QIRPLs. Individuals homozygous for Mi- and Mi+ were selected using the REX-R1 codominant marker (Williamson et al., 1994) and F3s were produced to assess their level of resistance to BW, compared with parental resistant lines not carrying Mi.The location of BW resistance allele(s) will be determined by RFLP marker analysis of the F2 plants, by definition of the length of DNA introgressed from L. peruvianum, and by further analysis of certain F3 lines.

Preliminary results from tests done in a greenhouse (low environmental constraints) and in the field show that Cranita lost 20 to 45 % of the parental resistance of CRA 66, depending of the R. solanacearum strain used. In the greenhouse, Carmido consistently shows the same level of resistance as Caraïbo with those strain tested in the greenhouse, but is not as resistant in the field when environmental constraints increase. These results suggest that two loci for resistance to wilt may be located on chromosome 6, and that the Mi introgression region in Carmido is not allelic with at least one locus in Caraïbo that affects the expression of resistance.

Acosta J.C. et al. 1964 - Proc. Amer. Soc. Hort. Sci. 84: 455-462

Danesh D. et al. 1994 - Molecular Plant-Microbe Interactions 7, 464-471.

Deberdt P. et al. 1996 - Proceeding of IIIrd International Nematology Congress, July 7-12 1996, Guadeloupe

Thoquet P. et al. 1996 - Molecular Plant-Microbe Interactions 9, 826-836 / 837-842.

Williamson V. et al. 1994 - Theorical and Applied Genetic 87, 757-763.

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