Evaluation of bacterial wilt resistance in tomato lines nearly isogenic for the Mi gene for resistance to root-knot

Resistance to bacterial wilt, caused by #Ralstonia solancearum, in tomato lines CRA 66 and Caraïbo is reported to be decreased by root-knot nematode galling and by introduction of the #Mi gene for nematode resistance. The #Mi gene is located on tomato chromosome 6, which also carries a major quantitative trait locus (QTL) for resistance to bacterial wilt. Bacterial wilt resistance was evaluated in F3-progenies derived from two crosses between near-isogenic lines Caraïbo x Carmido and CRA 66 x Cranita, differing for small and large introgressions from #Lycopersicon peruvianum that carry the #Mi gene, respectively. These introgressed regions were mapped using RFLP markers. Plants homozygous Mi+/Mi+ (susceptible to the nematode) and homozygous Mi/Mi (resistant) for the #Mi gene were selected in F2 and used to produce F3 progenies. Parents and F3-lines with Mi/Mi had resistance to bacterial wilt reduced by 30% in Caraïbo x Carmido and by 15% in CRA 66 x Cranita. Caraïbo and Carmido were demonstrated to be isolines and the small introgression from #L. peruvianum resulted in loss of the QTL for bacterial wilt resistance, which is probably allelic or linked in repulsion to the #Mi gene. In contrast, resistance to bacterial wilt segregated in the F3 lines from the cross CRA 66 x Cranita, giving families varying in resistance between the levels shown by the parents. Consequently, two hyopotheses were considered : (i) after only four backcrosses, the parents were not isolines and the genes for resistance to bacterial wilt from CRA 66 were still segregating, and (ii) the parents were isolines and variation in resistance to bacterial wilt in F3 was due to recombination events among the large "L. peruvianum$ introgressed chromosome region from Cranita. (Résumé d'auteur

Inheritance of partial resistance against Colletotrichum lindemuthianum in Phaseolus vulgaris and co-localization of quantitative trait loci with genes involved in specific resistance

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Genetic and cytogenetic mapping of DMI1, DMI2, and DMI3 genes of Medicago truncatula involved in Nod factor transduction, nodulation, and mycorrhization

The DMI1, DMI2, and DMI3 genes of Medicago truncatula, which are required for both nodulation and mycorrhization, control early steps of Nod factor signal transduction. Here, we have used diverse approaches to pave the way for the map-based cloning of these genes. Molecular amplification fragment length polymorphism markers linked to the three genes were identified by bulked segregant analysis. Integration of these markers into the general genetic map of M. truncatula revealed that DMI1, DMI2, and DMI3 are located on linkage groups 2, 5, and 8, respectively. Cytogenetic studies using fluorescent in situ hybridization (FISH) on mitotic and pachytene chromThe DMI1, DMI2, and DMI3 genes of Medicago truncatula, which are required for both nodulation and mycorrhization, control early steps of Nod factor signal transduction. Here, we have used diverse approaches to pave the way for the map-based cloning of these genes. Molecular amplification fragment length polymorphism markers linked to the three genes were identified by bulked segregant analysis. Integration of these markers into the general genetic map of M. truncatula revealed that DMI1, DMI2, and DMI3 are located on linkage groups 2, 5, and 8, respectively. Cytogenetic studies using fluorescent in situ hybridization (FISH) on mitotic and pachytene chromosomes confirmed the location of DMI1, DMI2, and DMI3 on chromosomes 2, 5, and 8. FISH-pachytene studies revealed that the three genes are in euchromatic regions of the genome, with a ratio of genetic to cytogenetic distances between 0.8 and 1.6 cM per ¿m in the DMI1, DMI2, and DMI3 regions. Through grafting experiments, we showed that the genetic control of the dmi1, dmi2, and dmi3 nodulation phenotypes is determined at the root level. This means that mutants can be transformed by Agrobacterium rhizogenes to accelerate the complementation step of map-based cloning projects for DMI1, DMI2, and DMI3

Gene gain and loss during evolution of obligate parasitism in the white rust pathogen of Arabidopsis thaliana

Biotrophic eukaryotic plant pathogens require a living host for their growth and form an intimate haustorial interface with parasitized cells. Evolution to biotrophy occurred independently in fungal rusts and powdery mildews, and in oomycete white rusts and downy mildews. Biotroph evolution and molecular mechanisms of biotrophy are poorly understood. It has been proposed, but not shown, that obligate biotrophy results from (i) reduced selection for maintenance of biosynthetic pathways and (ii) gain of mechanisms to evade host recognition or suppress host defence. Here we use Illumina sequencing to define the genome, transcriptome, and gene models for the obligate biotroph oomycete and Arabidopsis parasite, Albugo laibachii. A. laibachii is a member of the Chromalveolata, which incorporates Heterokonts (containing the oomycetes), Apicomplexa (which includes human parasites like Plasmodium falciparum and Toxoplasma gondii), and four other taxa. From comparisons with other oomycete plant pathogens and other chromalveolates, we reveal independent loss of molybdenum-cofactor-requiring enzymes in downy mildews, white rusts, and the malaria parasite P. falciparum. Biotrophy also requires ‘‘effectors’’ to suppress host defence; we reveal RXLR and Crinkler effectors shared with other oomycetes, and also discover and verify a novel class of effectors, the ‘‘CHXCs’’, by showing effector delivery and effector functionality. Our findings suggest that evolution to progressively more intimate association between host and parasite results in reduced selection for retention of certain biosynthetic pathways, and particularly reduced selection for retention of molybdopterinrequiring biosynthetic pathways. These mechanisms are not only relevant to plant pathogenic oomycetes but also to human pathogens within the Chromalveolata