Genetic mapping of a major dominant gene for resistance to Ralstonia solanacearum in eggplant.

Resistance of eggplant against Ralstonia solanacearum phylotype I strains was assessed in a F(6) population of recombinant inbred lines (RILs) derived from a intra-specific cross between S. melongena MM738 (susceptible) and AG91-25 (resistant). Resistance traits were determined as disease score, percentage of wilted plants, and stem-based bacterial colonization index, as assessed in greenhouse experiments conducted in Réunion Island, France. The AG91-25 resistance was highly efficient toward strains CMR134, PSS366 and GMI1000, but only partial toward the highly virulent strain PSS4. The partial resistance found against PSS4 was overcome under high inoculation pressure, with heritability estimates from 0.28 to 0.53, depending on the traits and season. A genetic map was built with 119 AFLP, SSR and SRAP markers positioned on 18 linkage groups (LG), for a total length of 884 cM, and used for quantitative trait loci (QTL) analysis. A major dominant gene, named ERs1, controlled the resistance to strains CMR134, PSS366, and GMI1000. Against strain PSS4, this gene was not detected, but a significant QTL involved in delay of disease progress was detected on another LG. The possible use of the major resistance gene ERs1 in marker-assisted selection and the prospects offered for academic studies of a possible gene for gene system controlling resistance to bacterial wilt in solanaceous plants are discussed.

Bacterial wilt resistance in tomato, pepper, and eggplant: genetic resources respond to diverse strains in the Ralstonia solanacearum species complex.

Bacterial wilt, caused by strains belonging to the Ralstonia solanacearum species complex, inflicts severe economic losses in many crops worldwide. Host resistance remains the most effective control strategy against this disease. However, wilt resistance is often overcome due to the considerable variation among pathogen strains. To help breeders circumvent this problem, we assembled a worldwide collection of 30 accessions of tomato, eggplant and pepper (Core-TEP), most of which are commonly used as sources of resistance to R. solanacearum or for mapping quantitative trait loci. The Core-TEP lines were challenged with a core collection of 12 pathogen strains (Core-Rs2) representing the phylogenetic diversity of R. solanacearum. We observed six interaction phenotypes, from highly susceptible to highly resistant. Intermediate phenotypes resulted from the plants' ability to tolerate latent infections (i.e., bacterial colonization of vascular elements with limited or no wilting). The Core-Rs2 strains partitioned into three pathotypes on pepper accessions, five on tomato, and six on eggplant. A "pathoprofile" concept was developed to characterize the strain clusters, which displayed six virulence patterns on the whole set of Core-TEP host accessions. Neither pathotypes nor pathoprofiles were phylotype specific. Pathoprofiles with high aggressiveness were mainly found in strains from phylotypes I, IIB, and III. One pathoprofile included a strain that overcame almost all resistance sources.

Identification of QTLs for Ralstonia solanacearum race 3-phylotype II resistance in tomato.

Resistance against a Ralstonia solanacearum race 3-phylotype II strain JT516 was assessed in a F(2:3) and a population of inbred lines (RIL), both derived from a cross between L. esculentum cv. Hawaii 7996 (partially resistant) and L. pimpinellifolium WVa700 (susceptible). Resistance criteria used were the percentage of wilted plants to calculate the AUDPC value, and bacterial colonization scores in roots and stem (hypocotyl and epicotyl) assessed in two independent greenhouse experiments conducted during the cool and hot seasons in Réunion Island, France. Symptoms were more severe during the cool season trials. Heritability estimates in individual seasons ranged from 0.82 to 0.88, depending on resistance criterion. A set of 76 molecular markers was used for quantitative trait loci (QTL) mapping using the single- and composite- interval mapping methods, as well as ANOVA. Four QTLs, named Bwr- followed by a number indicating their map location, were identified. They explained from 3.2 to 29.8% of the phenotypic variation, depending on the resistance criterion and the season. A major QTL, Bwr-6, and a minor one, Bwr-3, were detected in each season for all resistance criteria. Both QTLs showed stronger effects in the hot season than in the cool one. Their role in resistance to R. solanacearum race 3-phylotype II was subsequently confirmed in the RIL population derived from the same cross. Two other QTLs, Bwr-4 and Bwr-8, with intermediate and minor effects, respectively, were only detected in the hot season, demonstrating that environmental factors may strongly influence the expression of resistance against the race 3-phylotype II strain JT516. These QTLs were compared with those detected in the RIL population against race 1-phylotype I strain JT519 as well as those detected in other previous studies in the same genetic background against other race 1-phylotype I and II strains. This comparison revealed the possible occurrence of some phylotype-specific resistance QTLs in Hawaii 7996.

Genetic mapping of maize stripe disease resistance from the Mascarene source.

Maize stripe virus (MStV) is a potentially threatening virus disease of maize in the tropics. We mapped quantitative trait loci (QTLs) controlling resistance to MStV in a maize population of 157 F(2:3) families derived from the cross between two maize lines, Rev81 (tropical resistant) and B73 (temperate susceptible). Resistance was evaluated under artificial inoculations in replicated screenhouse trials across different seasons in Réunion Island, France. Composite interval mapping was employed for QTL detection with a linkage map of 143 microsatellite markers. Heritability estimates across seasons were 0.96 and 0.90 for incidence and severity, respectively, demonstrating a high genotypic variability and a good control of the environment. Three regions on chromosomes 2L, 3 and 5, with major effects, and another region on chromosome 2S, with minor effects, provided resistance to MStV in Rev81. In individual seasons, the chr2L QTL explained 60-65% of the phenotypic variation for disease incidence and 21-42% for severity. The chr3 QTL, mainly associated with incidence and located near centromere, explained 42-57% of the phenotypic variation, whereas the chr5 QTL, mainly associated with severity, explained 26-53%. Overall, these QTLs explained 68-73% of the phenotypic variance for incidence and 50-59% for severity. The major QTLs on chr2 and 3 showed additive gene action and were found to be stable over time and across seasons. They also were found to be included in genomic regions with important clusters of resistance genes to diseases and pests. The major QTL on chr5 appeared to be partially dominant in favour of resistance. It was stable over time but showed highly significant QTL x season interactions. Possible implications of these QTLs in different mechanisms of resistance against the virus or the insect vector are discussed. The prospects for transferring these QTLs in susceptible maize cultivars and combining them with other resistances to virus diseases by conventional or marker-assisted breeding are promising.

Evaluation of Maize Inbreds for Maize stripe virus and Maize mosaic virus Resistance: Disease Progress in Relation to Time and the Cumulative Number of Planthoppers.

ABSTRACT Five tropical maize lines were tested and compared with the susceptible control line B73 for resistance to Maize stripe virus (MStV) and Maize mosaic virus (MMV), both propagatively transmitted by the planthopper Peregrinus maidis (Homoptera: Delphacidae). Resistance to each virus was evaluated separately by artificial inoculations with planthoppers viruliferous for either one virus or the other. Disease incidence and symptom severity progression were quantified in relation to time and the cumulative number of planthoppers. Line Hi40 was found to be susceptible to MStV and highly resistant to MMV. Generally, no MMV symptoms developed on Hi40, even under intense inoculation pressure by a large number of viruliferous planthoppers. Line Rev81 showed a partial but strong resistance to MStV, which mainly reduced disease incidence. Nevertheless, this resistance to MStV was the highest ever reported and held up, even when challenged by large numbers of planthoppers. The percentage of infected plants in line Rev81 never exceeded 30 to 40% in our experiments. Moderate levels of resistance to MStV, and to a lesser extent MMV, were found in lines 37-2, A211, and Mp705. However, resistance in these lines was completely overcome using a large number of insects transmitting either of the two viruses. These results suggest that different types of resistance to MMV and MStV are available in maize lines from Caribbean and Mascarene germ plasm. The expression of virus-specific resistance identified in Hi40 and Rev81 lines was not affected by intense inoculation pressure. In contrast, the moderate resistance in 37-2, A211, and Mp705 was partially effective against both viruses but not at high inoculation pressure. These different types of resistance, when present in the same genotype, could provide protection against both viruses.

Surface plasmon polaritons and their role in the enhanced transmission of light through periodic arrays of subwavelength holes in a metal film.

We present results of the transmitted, reflected, and absorbed power associated with the enhanced transmittance of light through a silver film pierced by a periodic array of subwavelength holes. Comparing experimentally acquired dispersion curves under different polarization conditions shows that the transmission features of the array are consistent with p-polarized resonant modes of the structure. By exploring the regime in which no propagating diffracted orders are allowed, we further show that the transmittance maxima are associated with both reflectance minima and absorption maxima. These new results provide strong experimental evidence for transmission based on diffraction, assisted by the enhanced fields associated with surface plasmon polaritons.

Genetic mapping of maize streak virus resistance from the Mascarene source. II. Resistance in line CIRAD390 and stability across germplasm.

The streak disease has a major effect on maize in sub-Saharan Africa. Various genetic factors for resistance to the virus have been identified and mapped in several populations; these factors derive from different sources of resistance. We have focused on the Réunion island source and have recently identified several factors in the D211 line. A second very resistant line, CIRAD390, was crossed to the same susceptible parent, B73. The linkage map comprised 124 RFLP markers, of which 79 were common with the D211×B73 map. A row-column design was used to evaluate the resistance to maize streak virus (MSV) of 191 F(2:3) families under artificial infestation at two locations: Harare (Zimbabwe) and in Réunion island. Weekly ratings of resistance were taken and disease incidence and severity calculated. QTL analyses were conducted for each scoring date and for the integration over time of the disease scores, of incidence, and of severity. Heritability estimates (71-98%) were as high as for the D211×B73 population. Eight QTLs were detected on chromosomes 1, 2, 3, 5 (two QTLs), 6, 8, and 10. The chr1-QTL explained the highest proportion of phenotypic variation, about 45%. The QTLs on chromosomes 1, 2, and 10 were located in the same chromosomal bin as QTLs for MSV resistance in the D211×B73 population. In a simultaneous fit, QTLs explained together 43-67% of the phenotypic variation. The QTLs on chromosomes 3, 5, and 6 appeared to be specific for one or the other component of the resistance. For the chr3-QTL, resistance was contributed by the susceptible parent. There were significant QTL × environment interactions for some of the variables studied, but QTLs were stable in the two environments. They also appeared to be stable over time. Global gene action ranged from partial dominance to overdominance, except for disease severity. Some additional putative QTLs were also detected. The major QTL on chromosome 1 seemed to be common to the other sources of resistance, namely Tzi4, a tolerant line from IITA, and CML202 from CIMMYT. However, the distribution of the other QTLs within the genome revealed differences in Réunion germplasm and across these other resistance sources. This diversity is of great importance when considering the durability of the resistance.