Meiotic pairing was studied at metaphase I in three different cv. Chinese Spring × rye hybrid combinations (5B deficient, 3D deficient, and normal ABDR) to establish the arm homoeology of wheat and rye chromosomes. The majority of individual wheat chromosomes and their arms, as well as the arms of chromosomes 1R and 5R, were identified by means of C-banding. The results on pairing relationships support the genome reallocation of chromosomes 4A and 4B. The short arms of wheat chromosomes belonging to homoeologous groups 1, 3, 5, and 6 and of chromosome pairs 4A–4D and 7A–7D showed full pairing homoeology as well as the long arms of wheat chromosomes of groups 1, 3, 6, and 7 and of chromosome pairs 4A–4D and 5B–5D. Chromosomes 2A, 2B, and 2D were homoeologous, but the homoeologies of their arms were not identified. Reduced homoeologies of the 4BL arm to 7AS and 7DS, of the 5AL arm to 4AL and 4DL, and of the 7BS arm to 5BL and 5DL were identified. Arms 4BL, 5AL, and 7BS are involved in a double translocation that arose during the evolution of common wheat. The homoeology relationships of chromosome arm 4BS were not identified since this arm seldom paired. The homoeologous pairing pattern between wheat chromosomes was characterized by a remarkable predominance of A–D associations, altered only by structural changes in groups 4 and 5. Chromosome arm 1RL showed full pairing homoeology to 1AL, 1BL, and 1DL, while 5RL was homoeologous to 5AL and partially homoeologous to 4AL and 4DL. It is concluded that 5RL carries a translocated segment from 4RL. Key words: homoeologous pairing, translocations, wheat evolution, C-banding.

The objective of this research was to determine the quantitative trait loci (QTLs) controlling phenological traits (days to flowering, days to end of flowering, days to harvest as green pod, and days to maturity), seed size traits (seed length, seed height, seed width, and seed weight), and seed quality traits (water absorption, and coat proportion), in common bean. A population of 104 F(7) recombinant inbred lines (RILs) derived from an inter-gene pool cross between Xana, and Cornell 49242, was used to develop a genetic linkage map including 175 AFLPs, 27 microsatellites, 30 SCARs, 33 ISSRs, 12 RAPDs, 13 loci codifying for seed proteins, and the four genes Fin,fin (growth habit); Asp,asp (seed coat shininess); P,p (seed color); and I,i (resistance to bean common mosaic virus). The map has a total length of 1,042 cM distributed across 11 linkage groups aligned to those of the core linkage map of bean using common molecular markers as anchor points. The QTL analyses were carried out over three environments using the mean environment data with composite interval mapping. Thirty-one QTLs for ten traits were found to be significant in at least one environment and in the mean environment data, the number of significant QTLs identified per trait ranging from two to five. Twenty-seven of these QTLs mapped forming clusters in eight different chromosomal regions. The rationale for this clustered mapping and the possible relationship between some QTLs for phenological traits and the genes Fin and I are discussed.

BackgroundBean anthracnose is caused by the fungus Colletotrichum lindemuthianum (Sacc. & Magnus) Lams.- Scrib. Resistance to C. lindemuthianum in common bean (Phaseolus vulgaris L.) generally follows a qualitative mode of inheritance. The pathogen shows extensive pathogenic variation and up to 20 anthracnose resistance loci (named Co-), conferring resistance to specific races, have been described. Anthracnose resistance has generally been investigated by analyzing a limited number of isolates or races in segregating populations. In this work, we analyzed the response against eleven C. lindemuthianum races in a recombinant inbred line (RIL) common bean population derived from the cross Xana × Cornell 49242 in which a saturated linkage map was previously developed.ResultsA systematic genetic analysis was carried out to dissect the complex resistance segregations observed, which included contingency analyses, subpopulations and genetic mapping. Twenty two resistance genes were identified, some with a complementary mode of action. The Cornell 49242 genotype carries a complex cluster of resistance genes at the end of linkage group (LG) Pv11 corresponding to the previously described anthracnose resistance cluster Co-2. In this position, specific resistance genes to races 3, 6, 7, 19, 38, 39, 65, 357, 449 and 453 were identified, with one of them showing a complementary mode of action. In addition, Cornell 49242 had an independent gene on LG Pv09 showing a complementary mode of action for resistance to race 453. Resistance genes in genotype Xana were located on three regions involving LGs Pv01, Pv02 and Pv04. All resistance genes identified in Xana showed a complementary mode of action, except for two controlling resistance to races 65 and 73 located on LG Pv01, in the position of the previously described anthracnose resistance cluster Co-1.ConclusionsResults shown herein reveal a complex and specific interaction between bean and fungus genotypes leading to anthracnose resistance. Organization of specific resistance genes in clusters including resistance genes with different modes of action (dominant and complementary genes) was also confirmed. Finally, new locations for anthracnose resistance genes were identified in LG Pv09.

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A genetic map of common bean was constructed using 197 markers including 152 RAPDs, 32 RFLPs, 12 SCARs, and 1 morphological marker. The map was established by using a F 2 population of 85 individuals from the cross between a line derived from the Spanish landrace Andecha (Andean origin) and the Mesoamerican genotype A252. The resulting map covers about 1,401.9 cM, with an average marker distance of 7.1 cM and includes molecular markers linked to disease resistance genes for anthracnose, bean common mosaic virus, bean golden yellow mosaic virus, common bacterial blight, and rust. Resistance to races 6, 31, 38, 39, 65, and 357 of the pathogenic fungus Colletotrichum lindemuthianum (anthracnose) was evaluated in F 3 families derived from the corresponding F 2 individuals. The intermediate resistance to race 65 proceeding from Andecha can be explained by a single dominant gene located on linkage group B1, corresponding to the Co-1 gene. The recombination between the resistance speciWcities proceeding from A252 agrees with the assumption that total resistance to races 6, 31, 38, 39, 65, and 357, is organized in two clusters. One cluster, located on B4 linkage group, includes individual genes for speciWc resistance to races 6, 38, 39, and 357. The second cluster is located on linkage group B11 and includes individual genes for speciWc resistance to races 6, 31, 38, 39, and 65. These two clusters correspond to genes Co-3/Co-9 and Co-2, respectively. It is concluded that most anthracnose resistance Co-genes, previously described as single major genes conferring resistance to several races, could be organized as clusters of diVerent genes conferring race-speciWc resistance.