Genetic analysis of late blight resistance in a new RIL population of tomato derived from LB-resistant Solanum pimpinellifolium accession PI 270443

Late blight (LB), caused by Phytophthora infestans, is one of the most devastating diseases of tomato (Solanum lycopersicum) worldwide. Aggressive pathogen isolates resistant to fungicides have driven research in favour of finding new sources of host resistance for tomato breeding. Recently, we reported S. pimpinellifolium accession PI 270443 exhibiting LB resistance stronger than all commercial LB-resistant tomato cultivars. The purpose of this study was to examine the inheritance of LB resistance conferred by this accession. An interspecific cross was made between PI 270443 and a LB-susceptible tomato breeding line and advanced to F₁₀ generation. A total of 166 F₉ and corresponding F₁₀ recombinant inbred lines (RILs) were evaluated for response to LB in four replicated greenhouse experiments. Estimates of heritability (h²) of LB resistance, determined by parent–offspring (F₉:F₁₀) correlation analysis, ranged from 0.66 to 0.81, with an average of 0.76. The moderately high h² of LB resistance in PI 270443 suggests the utility of this accession for tomato breeding. Molecular mapping and RNA-sequencing efforts are underway to identify genes underlying LB resistance in PI 270443.     

Genetic analysis of resistance to tomato late blight in Solanum pimpinellifolium accession PI 163245

Late blight (LB), caused by Phytophthora infestans, is one of the most devastating diseases of tomato (Solanum lycopersicum) worldwide. Due to the emergence of new and aggressive P. infestans isolates, identifying new genetic resistance to LB is a priority in tomato breeding. Recently, we reported the identification of several Solanum pimpinellifolium accessions with strong LB resistance. In this study, we investigated the utility of resistant accession PI 163245 for tomato breeding by examining heritability (h²) of resistance and the response to selection for resistance. Estimates of h² based on F₂ : F₃ and F₃ : F₄ parent : offspring correlation analyses averaged 0.79 and 0.94, respectively, suggesting the heritable nature of LB resistance in PI 163245. Analysis of response to selection for resistance from F₂ to F₄ generations indicated a realized h² of 0.63, confirming the utility of this resistance in tomato breeding. Two methods of estimating the minimum number of loci involved indicated the presence of one major resistance locus. Currently, genetic mapping and breeding efforts are underway to further confirm the viability of this accession for improving tomato LB resistance.     

Selective genotyping to identify late blight resistance genes in an accession of the tomato wild species <Emphasis Type="Italic">Solanum pimpinellifolium</Emphasis>

Late blight (LB), caused by the oomycete Phytophtohra infestans, is one of the most destructive diseases of tomato (Solanum lycopersicum) and other Solanaceae species. Current disease control and prevention strategies are not sufficient to control the disease in tomato. Recent germplasm screening experiments led to the identification of a new source of resistance (PI 270443) in the tomato wild species S. pimpinellifolium. This study was conducted to identify genomic regions associated with LB resistance in this accession. A large F₂ population (n = 986) derived from a cross between PI 270443 and a LB-susceptible tomato breeding line (NCEBR-2) was screened for LB resistance using a highly aggressive isolate of P. infestans. Twenty-five of the most resistant and 29 of the most susceptible, but surviving F₂ individuals were identified based on disease evaluations conducted in the F₂ and F₃ progeny populations. The selected individuals were genotyped with 153 DNA markers located across the 12 tomato chromosomes. A selective genotyping approach led to the identification of two genomic regions on tomato chromosomes 1 and 10 associated with LB resistance in PI 270443. Identification of two genomic regions associated with resistance was consistent with a previous estimate of the number of LB resistance genes in this accession. Research is currently underway to fine map the two resistance genes and incorporate them into new tomato breeding lines and hybrid cultivars.     

Genetic analysis of late blight resistance in Solanum pimpinellifolium accession PI 270441: Heritability and response to selection

Late blight (LB), caused by Phytophthora infestans, is a destructive disease of tomato (Solanum lycopersicum) worldwide. Currently, there are few commercial cultivars of tomato with resistance to LB, and the disease is mainly controlled by heavy use of fungicides. Due to the emergence of fungicide‐resistant pathogen isolates, there is a concerted effort to identify new genetic sources of resistance and breed new resistant cultivars. A recent screening identified several new tomato accessions with strong resistance to LB. Here, we report on the genetic basis of LB resistance in S. pimpinellifolium accession PI 270441, as determined by generation means analysis and analysis of response to selection, using populations derived from crosses with LB‐susceptible breeding line Fla. 8059. Heritability of LB resistance ranged from 0.76 to 0.78, and the minimum number of genes was estimated 1—few. These results suggest that transfer of LB resistance from PI 270441 to the cultivated tomato should be feasible via a traditional backcross breeding approach. Genetic mapping studies are underway to identify molecular markers associated with resistance in this accession.     

Response of accessions within tomato wild species,Solanum pimpinellifolium to late blight

Late blight (LB), caused by the oomycete Phytophthora infestans, is one of the most devastating diseases of the cultivated tomato (Solanum lycopersicum) worldwide. Most commercial cultivars of tomato are susceptible to LB. Previously, three major LB resistance genes (Ph‐1, Ph‐2, Ph‐3) were identified and incorporated into a few commercial cultivars of tomato. Reduced effectiveness and potential breakdown of the resistance genes has necessitated identification, characterization and utilization of new sources of resistance. We evaluated the response of 67 accessions of the wild tomato species, S. pimpinellifolium to LB, under multiple field and greenhouse (GH) conditions and compared them with six control genotypes. Sixteen accessions were identified with strong LB resistance in both field and GH experiments. However, 12 accessions exhibited resistance similar to a control line which was homozygous for Ph‐2 + Ph‐3. Genotyping accessions with molecular markers for Ph‐2 and Ph‐3 were not conclusive, indicating that resistance in these accessions could be due to these or other resistance genes. Strong correlations were observed between field and GH disease response and between foliar and stem infection.     

Parent-offspring correlation estimate of heritability for early blight resistance in tomato, Lycopersicon esculentum Mill.

This study estimated the heritability (h ²) of early blight (EB) resistance in filial progeny of a cross between a susceptible (`NC84173';mid-season maturity) and a resistant (`NC39E'; late-season maturity)tomato breeding lines. It addition, it examined the potential of identifying progeny with mid-season maturity and EB resistance. A total of 162F₂ plants were grown under field conditions in 1998 and evaluated for disease symptoms three times during the season, and the area under the disease progress curve (AUDPC) and final percent defoliation (disease severity) were determined. The F₂ plants were self-pollinated and F₃ seeds produced. The 162 F₃ progeny families, consisting of 20 plants per family, were grown in a replicated field trial in 1999 and evaluated for EB resistance (final percent defoliation) and plant maturity(days to 50% ripe fruit). The distributions of the final percent defoliation values in the F₂ and F₃ generations indicated that resistance from `NC39E' was quantitative in nature. Estimates of h <sup>2</sup> for EB resistance, computed as the correlation coefficients between F<sub>3</sub>progeny family means and F<sub>2</sub> individual plant values, ranged from0.65 to 0.71, indicating that EB resistance of `NC39E' was heritable. Across F₃ families, a negative correlation (r = –0.46, p< 0.01) was observed between disease severity and earliness in maturity, indicating that plant maturity affected disease severity. However, several F₃ families were identified with considerable EB resistance and mid-season maturity, indicating that resistance from `NC39E' might be useful for the development of commercially acceptable EB resistant tomato cultivars. This revised version was published online in August 2006 with corrections to the Cover Date.     

Heritability of early blight resistance in a Lycopersicon esculentum×Lycopersicon hirsutum cross estimated by correlation between parent and progeny

Sixteen‐hundred BC₁ plants of a cross between an early blight (EB) susceptible tomato (Lycopersicon esculentum Mill.) breeding line (‘NC84173’ maternal and recurrent parent) and a resistant accession (‘PI126445’) of the tomato wild species Lycopersicon hirsutum Humb. and Bonpl. were grown in a field in 1998. This population was segregating (among other traits) for growth habit, self‐incompatibility and earliness in maturity. To eliminate confounding effects of these factors on disease evaluation and h² estimation, plants that were self‐incompatible, indeterminate and/or late‐maturing were eliminated. The remaining plants (146), which were self‐compatible and determinate (sp./sp.) in growth habit, with early‐ to mid‐season maturity, were evaluated for EB resistance and self‐pollinated to produce BC₁S₁ seed. The 146 BC₁S₁ progeny families, consisting of 30 plants per family, were grown in a replicated field trial in 1999 and evaluated for EB resistance and plant maturity. For each of the 146 BC₁ plants and corresponding BC₁ families, the area under the disease progress curve (AUDPC) and final disease severity (final percentage defoliation) were determined and used to measure disease resistance. The distributions of the AUDPC and final percentage defoliation values in the BC₁ and BC₁S₁ generations indicated that resistance from ‘PI126445’ was quantitative in nature. Estimates of h² for EB resistance, computed by correlation between BC₁S₁ progeny family means and BC₁ individual plant values, ranged from 0.69 to 0.70, indicating that EB resistance of ‘P1126445’ was heritable. Across BC₁S₁ families, a small, but significant, negative correlation (r = ‐0.26, P < 0.01) was observed between disease resistance and earliness in maturity. However, several BC₁S₁ families were identified with considerable EB resistance and reasonably early maturity. These families should be useful for the development of commercially acceptable EB‐resistant tomato lines.     

Response of tolerant breeding lines of tomato, Lycopersicon esculentum, originating from three different sources (L. peruvianum, L. pimpinellifolium and L. chilense) to early controlled inoculation by tomato yellow leaf curl virus (TYLCV)

Selection of tomato plants supposedly tolerant to tomato yellow leaf curl virus (TYLCV), based solely on the absence of symptoms in an infested field can be misleading. An inoculation routine was therefore established to avoid escapes and to overcome difficulties associated with the age of the plant at the time of infection. The inoculation routine was applied to a selection of resistant/tolerant individuals generated through a diallel F¹ cross and to F² segregating populations originating from three wild tomato species described as tolerant to TYLCV: Lycopersicon peruvianum EC 104395, Lycopersicon pimpinellifolium Hirsute and Lycopersicon chilense LA 1969. Clear differences were observed between susceptible symptomatic and tolerant symptomless tomato genotypes, indicating that the uncertainty resulting from escapes, from different levels of inoculum, and from the time of inoculation, can be eliminated. The genes involved in tolerance provided different levels of protection; combinations of various tolerant sources and levels in a single genotype gave a higher level of tolerance. Differences in level of protection were found between genes from the same source and between sources; none of the sources tested had complete dominance. The results obtained with the F² segregating population showed that tolerance from L. pimpinellifolium is controlled by one major gene, that from L. chilense by two genes, and that from L. peruvianum by three genes with no dominant effect. The combination of sources for resistance can thus have positive or negative synergistic effects, or no effect. We suggest that a maximal level of tolerance can be obtained by the additive effect of the partly dominant genes from L. pimpinellifolium and L. chilense.     

Pyramiding of genes conferring resistance to Tomato yellow leaf curl virus from different wild tomato species

Tomato (Solanum lycopersicum) production in tropical and subtropical regions of the world is limited by the endemic presence of Tomato yellow leaf curl virus (TYLCV). Breeding programmes aimed at producing TYLCV‐resistant tomato cultivars have utilized resistance sources derived from wild tomato species. So far, all reported breeding programmes have introgressed TYLCV resistance from a single wild tomato source. Here, we tested the hypothesis that pyramiding resistances from different wild tomato species might improve the degree of resistance of the domesticated tomato to TYLCV. We have crossed TYLCV‐resistant lines that originated from different wild tomato progenitors, Solanum chilense, Solanum peruvianum, Solanum pimpinellifolium, and Solanum habrochaites. The various parental resistant lines and the F₁ hybrids were inoculated in the greenhouse using viruliferous whiteflies. Control, non‐inoculated plants of the same lines and hybrids were exposed to non‐viruliferous whiteflies. Following inoculation, the plants were scored for disease symptom severity, and transplanted to the field. Resistance was assayed by comparing yield of inoculated plants to those of the control non‐inoculated plants of the same variety. Results showed that the F₁ hybrids between the resistant lines and the susceptible line suffered major yield reduction because of infection, but all hybrids were more resistant than the susceptible parent. All F₁ hybrids resulting from a cross between two resistant parents, showed a relatively high level of resistance, which in most cases was similar to that displayed by the more resistant parent. In some cases, the hybrids displayed better levels of resistance than both parents, but the differences were not statistically significant. The F₁ hybrid between a line with resistance from S. habrochaites and a line with resistance from S. peruvianum (HAB and 72‐PER), exhibited the lowest yield loss and the mildest level of symptoms. Although the resistance level of this F₁ hybrid was not statistically different from the level of resistance displayed by the 72‐PER parent itself, it was statistically better than the level of resistance displayed by the F₁ hybrids between 72‐PER and any other resistant or susceptible line.     

Evaluation of the Ph‐3 gene‐specific marker developed for marker‐assisted selection of late blight‐resistant tomato

Late blight caused by Phytophthora infestans is one of the most destructive diseases of tomato (Solanum lycopersicum L.) that mainly occurs in cool and wet environments. With the spread of the A2 mating type and new clonal lineages, fewer fungicides provide effective control of the disease, which has increased its worldwide threat. Host resistance could contribute significantly to sustainable disease control. Ph‐3 is a race‐specific late blight resistance gene commonly used in commercial tomato breeding. Availability of precise and easy to use gene‐based markers would facilitate selection. In this study, a Ph‐3 on‐gene cleaved amplified polymorphic sequence (CAPS) marker, Ph3.gsm/HincII, was developed based on the published gene sequence of Ph‐3. The effectiveness of the marker was evaluated along with other published Ph‐3 markers using an F₉ recombinant inbred line (RIL) population derived from NC 23E‐2(93) × L3708. Markers Ph3.gsm/HincII and TG328/BstNI accurately genotyped the RIL population for Ph‐3. In addition, Ph3.gsm/HincII was able to differentiate variable susceptible alleles. This reliable codominant DNA marker would be very useful in marker‐assisted selection, particularly for resistance gene pyramiding.     

Genetic basis of physiological traits related to salt tolerance in tomato, Lycopersicon esculentum Mill.

Genetic relationships between salt tolerance and expression of various physiological traits during vegetative growth in tomato, Lycopersicon esculentum Mill., were investigated. Parental, F₁, F₂ and backcross progeny of a cross between a salt tolerant (PI174263) and a salt sensitive tomato cultivar (‘UCT5’) were evaluated in saline solutions with electrical conductivity of 0.5 (non-stress) and 20 dS/m (salt stress). Absolute growth, relative growth, tissue ion content, leaf solute potential and the rate of ethylene evolution were measured. Growth of both parents was reduced under salt stress; however, the reduction was significantly less in PI174263 than ‘UCT5’, suggesting greater salt tolerance of the former. Under salt stress, leaves of PI174263 accumulated significantly less Na⁺ and Cl^? and more Ca²⁺ than leaves of ‘UCT5’. Across parental and progeny generations, growth under salt stress was positively correlated with leaf Ca²⁺ content and negatively correlated with leaf Na⁺ content. In contrast, no correlation was observed between growth and either leaf solute potential or the rate of ethylene evolution under salt stress. Generation means analysis indicated that under salt stress both absolute and relative growth and the Na⁺ and Ca²⁺ accumulations in the leaf were genetically controlled with additivity being the major genetic component. The results indicated that the inherent genetic capabilities of PI174263 to maintain high tissue Ca²⁺ levels and to exclude Na⁺ from the shoot were essential features underlying its adaptation to salt stress and that these features were highly heritable. Thus, tissue ion concentration may be a useful selection criterion when breeding for improved salt tolerance of tomato using progeny derived from PI174263.     

Inheritance of resistance to fruit rot (Phytophthora parasiticaDast.) in tomato (Lycopersicon esculentum Mill.)

Summary Fruit rot disease caused by Phytophthora parasiticaDast. is a limiting factor in tomato production in Himachal Pradesh. 30 to 60 per cent fruits are damaged by this disease. Crosses were made between EC 54725 (Lycopersicon pimpinellifolium), a small tyuited type, resistant to fruit rot and four highly susceptible tomato commercial cultivars (Gola, Sioux, S12, and Lalmani). Studies of F₁'s, F₂'s and back crosses indicated that EC 54725 carries a dominant gene imparting resistance to fruit rot.     

Screening recently identified whitefly/spider mite‐resistant wild tomato accessions for resistance to Tuta absoluta

The tomato leaf miner (Tuta absoluta) is a serious pest of tomato (Solanum lycopersicum) in the tropics and subtropics. Previous World Vegetable Center studies identified selected accessions of S. galapagense, S. cheesmaniae and S. pimpinellifolium that were resistant to whitefly (Bemisia tabaci Genn.) and spider mite (Tetranychus urticae Koch). Here, we evaluated these accessions for resistance to T. absoluta based on the number of eggs from choice bioassays, and larval mortality and adults emerged percentages in no‐choice feeding bioassays at WorldVeg Eastern and Southern Africa (WorldVeg) and the International Centre for Insect Physiology and Ecology (icipe). At WorldVeg, S. galapagense VI063177 exhibited high resistance in both choice and no‐choice bioassays. There was strong negative correlation between larval mortality and adults emerged percentages in the no‐choice feeding bioassays. Results from the icipe experiments were consistent with those of the WorldVeg screening, except for S. pimpinellifolium accession VI030462 , which was susceptible at icipe. Tuta absoluta is rapidly spreading and the resistance sources reported here will be valuable in breeding tomato varieties resistant to this insect and others.     

Genetics of resistance to early blight (Alternaria solani Sorauer) in tomato (Lycopersicon esculentum L.)

The genetic nature of early blight resistance in tomato was studied in three crosses at seedling and adult plant stages. A six generation mean analysis of the cross Arka Saurabh (susceptible) × IHR1939 (resistance) and its reciprocal cross revealed that the resistance to early blight was conferred by recessive polygenes at both seedling and adult plant stages. This polygenic early blight resistance revealed the importance of additive and additive × additive gene effects at seedling stage and higher magnitude of dominance and dominance× dominance gene effects at adult plant stage. Evaluation of parents, F₁, F₂ and backcross generations of IHR1816 (resistance) × IHR1939 (resistance) revealed that the early blight resistance genes in IHR1816 (Lycopersicon esculentum NCEBR-1) and IHR1939 (Lycopersicon pimpinellifolium L4394) are independent. This revised version was published online in July 2006 with corrections to the Cover Date.     

Inheritance of resistance to Pyrenophora teres f. teres in spring barley

The inheritance of seedling resistance to a Swedish isolate of Pyrenophora teres f. teres was investigated in four resistance sources of spring barley. Accessions CI 2330, CI 5791, CI 5822 and CI 9779 were used as resistance sources, and the cultivar ‘Alexis’ was used as a susceptible parent in different crosses. From the disease reaction in the F₁, F₂ and F₃ generations it was concluded that the resistance was governed by the same two complementary genes in CI 5791, CI 822 and CI 9776. One of these genes was present in CI 2330. The first three cultivars were highly resistant to the isolate used in this investigation. These results, when combined with earlier studies, suggest that CI 5791, CI 5822 and CI 9776 may be of great value as sources of resistance to barley net blotch. Spearman's rank correlation between the disease reaction of F₂ plants and their F₃ progeny was highly significant (r = 0.75; P ≥ 0.001) It is suggested that selection in the F₂ generation is effective. In a backcross breeding scheme, single plant reactions in F₁ or F₂ need to be confirmed in later generations.     

Genetics of Cyst Nematode Resistance in Soybean PIs 467312 and 507354

Soybean Cyst nematode (SCN) Heterodera glycines Ichinohe is the most serious pest of soybean [Glycine max (L.) Merr.] in the world and genetic resistance in soybean cultivars have been the most effective means of control. Nematode populations, however, are variable and have adapted to reproduce on resistant cultivars over time due mainly to the narrow genetic base of SCN resistance in G. max. The majority of the resistant cultivars trace to two soybean accessions. It is hoped that new sources of resistance might provide durable resistance. Soybean plant introductions PI 467312 and PI 507354, are unique because they provide resistance to several nematode populations, i.e. SCN HG types 0, 2.7, and 1.3.6.7 (corresponding to races 3, 5, and 14) and HG types 2.5.7, 0, and 2.7 (corresponding to races 1, 3, and 5), respectively. The genetic basis of SCN resistance in these PIs is not yet known. We have investigated the inheritance of resistance to SCN HG types 0, 2.7, and 1.3.6.7 (races 3, 5, and14) in PI467312 and the SCN resistance to SCN HG types 2.5.7 and 2.7 (races 1 and 5) in PI 507354. PI 467312 was crossed to ‘Marcus’, a susceptible cultivar to generate F₁ hybrids, 196 random F₂ individuals, and 196 F_2:3 families (designated as Pop 467). PI 507354 and the cultivar Hutcheson, susceptible to all known SCN races, were crossed to generate F₁ hybrids, 225 random F₂ individuals and 225 F_2:3 families (designated as Pop 507). The F_2:3 families from each cross were evaluated for responses to the specific SCN HG types in the greenhouse. Chi-square (χ²) analyses showed resistance from PI 467312 to HG types 2.7, and 1.3.6.7 (races 5 and 14) in Pop 467 were conditioned by one dominant and two recessive genes (Rhg rhg rhg) and resistance to HG type 0 (race 3) was controlled by three recessive genes (rhg rhg rhg). The 225 F_2:3 progenies in Pop 507 showed a segregation of 2:223 (R:S) for response to both HG types 2.5.7 and 2.7 (corresponding to races 1 and 5). The Chi-square analysis showed SCN resistance from PI 507354 fit a one dominant and 3 recessive gene model (Rhg rhg rhg rhg). This information will be useful to soybean breeders who use these sources to develop SCN resistant cultivars. The complex inheritance patterns determined for the two PIs are similar to the three and four gene models for other SCN resistance sources known to date.     

Introgression of phenoxy herbicide resistance from Raphanus raphanistrum into Raphanus sativus

Phenoxy herbicides such as 2,4‐dichlorophenoxy acetic acid (2,4‐D) and 4‐chloro‐2‐methylphenoxy acetic acid (MCPA) are selective herbicides used extensively in agriculture for weed control. Wild radish (Raphanus raphanistrum) is a problem weed across the globe and heavily infests crop fields in Australia. Phenoxy herbicides are used to selectively control dicot weeds, including wild radish. As a result of selection, phenoxy‐resistant wild radish populations evolved in Western Australia. In this research, introgression of phenoxy resistance from wild radish to cultivated radish (Raphanus sativus) was investigated following classical breeding procedures. F₁ progeny were generated by crossing MCPA‐resistant R. raphanistrum and MCPA‐susceptible R. sativus. F₁ hybrids were screened for MCPA resistance. The MCPA‐resistant F₁ hybrids were used to produce three generations of backcross progeny. Genetic analyses of F₁ and backcross progeny demonstrated introgression of the MCPA‐resistant trait from wild radish to cultivated radish. Implications of phenoxy resistance introgression into cultivated radish include potential development of herbicide‐tolerant radish cultivars or other members of the Brassicaceae family.     

A novel source of resistance to the two-spotted spider mite in Lycopersicon pimpinellifolium (Jusl.) Mill.: its genetics as affected by interplot interference

We have previously found an accession of Lycopersicon pimpinellifolium (Jusl.) Mill. (`TO-937') that appeared to resist attack by the two-spotted spider mite (Tetranychus urticae Koch). L. pimpinellifolium is a very close relative of the cultivated tomato (Lycopersicon esculentum Mill.) and thereby a potential source of desirable traits that could be introgressed to the crop species. The objective of this study was to investigate the genetics of the resistance present in `TO-937'. Resistance to infestation by the spider mite was quantified in 24-plant plots of L. pimpinellifolium accessions `TO-937' and `PE-10', L. pennellii accession `PE-45', L. esculentum cultivars `Moneymaker', `Roma' and `Kalohi' (reported to be partially resistant: Stoner & Stringfellow, 1967), and the interspecific F₁ cross, L. esculentum `Moneymaker' × L. pimpinellifolium `TO-937'. Only `TO-937', the F<sub>1</sub>, and`PE-45' were found to be resistant. Resistance of `TO-937' was complete when evaluated in two small greenhouses completely planted with `TO-937' so as to simulate the genotypic homogeneity usual in commercial crops. Generations (P₁, P₂, F₁, F₂, BC₁P₁, and BC₁P₂) of a P₁ (susceptible) × P₂ (resistant) cross (`Moneymaker' × `TO-937') were studied for resistance in a single-plant per plot design. Resistance of `TO-937' was inherited with complete dominance and appeared to be controlled by either two or four genes according to whether segregation in the F₂ or the BC₁P₁, respectively, were considered. However, calculation of the number of genes involved in the resistance was complicated by negative interplot interference due to the high frequency of resistant genotypes within most of the generations. This revised version was published online in July 2006 with corrections to the Cover Date.     

Inheritance of resistance to the peach root‐knot nematode (Meloidogyne floridensis) in interspecific crosses between peach (Prunus persica) and its wild relative (Prunus kansuensis)

The peach root‐knot nematode, Meloidogyne floridensis (MF), infects majority of available nematode‐resistant peach rootstocks which are mostly derived from peach (Prunus persica) and Chinese wild peach (P. davidiana). Interspecific hybridization of peach with its wild relative, Kansu peach (P. kansuensis), offers potential for broadening the resistance spectrum in standard peach rootstocks. We investigated the inheritance of resistance to MF in segregating populations of peach (‘Okinawa’ or ‘Flordaguard’) × P. kansuensis. A total of 379 individuals from 13 F₂ and BC₁F₁ families were challenged with a pathogenic MF isolate “MFGnv14” and were classified as resistant (R) or susceptible (S) based on root galling intensity. Segregation analyses in F₂ progeny revealed the involvement of a major locus with a dominant or recessive allele determining resistance in progeny segregating 3R:1S and 1R:3S, respectively. Testcrosses with a homozygous‐susceptible peach genotype (‘Flordaguard’ or ‘UFSharp’) confirmed P. kansuensis as a source of new resistance and the heterozygous allelic status of P. kansuensis at the locus conferring resistance to MF. We propose a single‐locus dominant/recessive model for the inheritance of resistance.     

Genetic Relationships Among Four Pepper Genotypes Resistant to Phytophthora capsici

According to our previous investigations, resistance to Phytophthora capsid in Capsicum annuum genotypes, ‘Line 29’, ‘PI201232’, ‘PI201234’ and Serrano Criollo de Morelos 334 (‘SCM334’), seems to be controlled by three genes. In order to determine the genie relationships between these four sources of resistance, three experiments were conducted which included the four genotypes, their F₁s, F₂s, F3s and BC₁ generations together with the susceptible pepper genotype ‘Morron INI A 224’. Inoculations were made, when plants had 4—6 leaves, by irrigating the culture substrate with a zoospore suspension of P. capsici isolate ‘Bl’. Though the four genotypes showed percentages of resistance close to a 100%, none of them actually reached this level in the three experiments. ‘SCM334’ was the most resistant genotype, transmitting a high level of resistance to its F₁, F₂ and BQ generations. ‘Line 29’ was more resistant than ‘PI201232’ and ‘PI201234’. However, the F₁ F₂ and BQ generations of these three lines showed similar degrees of resistance. The four genotypes seem to have one of the three genes postulated for their resistance in common. All genes displayed a similar level of resistance, except the specific genes of ‘SCM334’, the effect of which was slightly higher. Several working procedures are suggested for breeding programmes.