Beet Cyst Nematode Resistance Research Articles

No Pairwise Interactions of GmSNAP18, GmSHMT08 and AtPR1 with Suppressed AtPR1 Expression Enhance the Susceptibility of Arabidopsis to Beet Cyst Nematode.

GmSNAP18 and GmSHMT08 are two major genes conferring soybean cyst nematode (SCN) resistance in soybean. Overexpression of either of these two soybean genes would enhance the susceptibility of Arabidopsis to beet cyst nematode (BCN), while overexpression of either of their corresponding orthologs in Arabidopsis, AtSNAP2 and AtSHMT4, would suppress it. However, the mechanism by which these two pairs of orthologous genes boost or inhibit BCN susceptibility of Arabidopsis still remains elusive. In this study, Arabidopsis with simultaneously overexpressed GmSNAP18 and GmSHMT0 suppressed the growth of underground as well as above-ground parts of plants. Furthermore, Arabidopsis that simultaneously overexpressed GmSNAP18 and GmSHMT08 substantially stimulated BCN susceptibility and remarkably suppressed expression of AtPR1 in the salicylic acid signaling pathway. However, simultaneous overexpression of GmSNAP18 and GmSHMT08 did not impact the expression of AtJAR1 and AtHEL1 in the jasmonic acid and ethylene signaling pathways. GmSNAP18, GmSHMT08, and a pathogenesis-related (PR) protein, GmPR08-Bet VI, in soybean, and AtSNAP2, AtSHMT4, and AtPR1 in Arabidopsis could interact pair-wisely for mediating SCN and BCN resistance in soybean and Arabidopsis, respectively. Both AtSNAP2 and AtPR1 were localized on the plasma membrane, and AtSHMT4 was localized both on the plasma membrane and in the nucleus of cells. Nevertheless, after interactions, AtSNAP2 and AtPR1 could partially translocate into the cell nucleus. GmSNAP18 interacted with AtSHMT4, and GmSHMT4 interacted with AtSNAP2. However, neither GmSNAP18 nor GmSHMT08 interacted with AtPR1. Thus, no pairwise interactions among α-SNAPs, SHMTs, and AtPR1 occurred in Arabidopsis overexpressing either GmSNAP18 or GmSHMT08, or both of them. Transgenic Arabidopsis overexpressing either GmSNAP18 or GmSHMT08 substantially suppressed AtPR1 expression, while transgenic Arabidopsis overexpressing either AtSNAP2 or AtSHMT4 remarkably enhanced it. Taken together, no pairwise interactions of GmSNAP18, GmSHMT08, and AtPR1 with suppressed expression of AtPR1 enhanced BCN susceptibility in Arabidopsis. This study may provide a clue that nematode-resistant or -susceptible functions of plant genes likely depend on both hosts and nematode species.

Opposite Beet Cyst Nematode Infection Phenotypes of Transgenic Arabidopsis Between Overexpressing GmSNAP18 and AtSNAP2 and Between Overexpressing GmSHMT08 and AtSHMT4.

The rhg1-a GmSNAP18 (an α-SNAP) and Rhg4 GmSHMT08 are two major cloned genes conferring soybean cyst nematode resistance in Peking-type soybeans, but the application of α-SNAPs and SHMTs in cyst nematode management remains elusive. In this study, GmSNAP18 and GmSHMT08, together with their orthologs in Arabidopsis, AtSNAP2 (an α-SNAP) and AtSHMT4, were individually transformed into Arabidopsis Col-0 to generate the transgenic lines, and the growth of transgenic plants, beet cyst nematode (BCN) infection phenotypes, and AtSNAP2, AtSHMT4, and AtPR1 expression patterns were analyzed using Arabidopsis-BCN compatible interaction system, in addition with protein-protein interaction assay. Pulldown and BiFC assays revealed that GmSNAP18 and GmSHMT08 interacted with AtSHMT4 and AtSNAP2, respectively. Plant root growth was not impacted by overexpression of GmSNAP18 and AtSNAP2. However, overexpression of GmSHMT08 and AtSHMT4 both increased plant height, additionally, overexpression of GmSHMT08 decreased rosette leaf size. Overexpression of GmSNAP18 and GmSHMT08 both suppressed AtPR1 expression and significantly enhanced BCN susceptibility, while overexpression of AtSNAP2 and AtSHMT4 both substantially boosted AtPR1 expression and remarkably enhanced BCN resistance, in transgenic Arabidopsis. Overexpression of GmSNAP18 reduced, while overexpression of AtSNAP2 unaltered AtSHMT4 expression. Overexpression of GmSHMT08 and AtSHMT4 both suppressed AtSNAP2 expression in transgenic Arabidopsis. Thus, different expression patterns of AtPR1 and AtSHMT4 are likely associated with opposite BCN infection phenotypes of Arabidopsis between overexpressing GmSNAP18 and AtSNAP2, and between overexpressing GmSHMT08 and AtSHMT4; and boosted AtPR1 expression are required for enhanced BCN resistance in Arabidopsis. All these results establish a basis for extension of α-SNAPs and SHMTs in cyst nematode management.

Generation and Identification of the Number of Copies of Exogenous Genes and the T-DNA Insertion Site in SCN-Resistance Transformation Event ZHs1-2.

Soybean cyst nematode (SCN, Heterodera glycines Ichinohe) causes an estimated economic loss of about USD 3 billion each year in soybean (Glycine max L.) production worldwide. Overexpression of resistance genes against SCN provides a powerful approach to develop SCN resistance cultivars in soybean. The clarification of molecular characterization in transformation events is a prerequisite for ecological risk assessment, food safety, and commercial release of genetically modified crops. Here, we generated transgenic events harboring the BCN (beet cyst nematode) resistance Hs1pro−1 gene using the Agrobacterium-mediated method in soybean, evaluated their resistance to SCN infection, and clarified the molecular characterization of one of the transformation events. Five independent and stable inheritable transformation events were generated by an Agrobacterium-mediated transformation method. SCN resistance tests showed the average number of developed females per plant and female index (FI) in T4 ZHs1-1, ZHs1-2, ZHs1-3, ZHs1-4, and ZHs1-5 transformation events were significantly lower than that in the nontransgenic control. Among these, the ZHs1-2 transformation event had the lowest number of developed females per plant and FI. Southern hybridization showed the exogenous target Hs1pro−1 gene was inserted in one copy and the Bar gene was inserted two copies in the ZHs1-2 transformation event. The exogenous T-DNA fragment was integrated in the reverse position of Chr02: 5351566–5231578 (mainly the Bar gene expression cassette) and in the forward position of Chr03: 17083358–17083400 (intact T-DNA, including Hs1pro−1 and Bar gene expression cassette) using a whole genome sequencing method (WGS). The results of WGS method and Southern hybridization were consistent. All the functional elements of exogenous T-DNA fragments were verified by PCR using specific primer pairs in the T5 and T6 ZHs1-2 transformation events. These results demonstrated that the overexpression of Hs1pro−1 gene enhanced SCN resistance, and provide an important reference for the biosafety assessment and the labeling detection in transformation event ZHs1-2.

BvcZR3 and BvHs1pro-1 Genes Pyramiding Enhanced Beet Cyst Nematode (Heterodera schachtii Schm.) Resistance in Oilseed Rape (Brassica napus L.).

Beet cyst nematode (Heterodera schachtii Schm.) is one of the most damaging pests in sugar beet growing areas around the world. The Hs1pro-1 and cZR3 genes confer resistance to the beet cyst nematode, and both were cloned from sugar beet translocation line (A906001). The translocation line carried the locus from B. procumbens chromosome 1 including Hs1pro-1 gene and resistance gene analogs (RGA), which confer resistance to Heterodera schachtii. In this research, BvHs1pro-1 and BvcZR3 genes were transferred into oilseed rape to obtain different transgenic lines by A. tumefaciens mediated transformation method. The cZR3Hs1pro-1 gene was pyramided into the same plants by crossing homozygous cZR3 and Hs1pro-1 plants to identify the function and interaction of cZR3 and Hs1pro-1 genes. In vitro and in vivo cyst nematode resistance tests showed that cZR3 and Hs1pro-1 plants could be infested by beet cyst nematode (BCN) juveniles, however a large fraction of penetrated nematode juveniles was not able to develop normally and stagnated in roots of transgenic plants, consequently resulting in a significant reduction in the number of developed nematode females. A higher efficiency in inhibition of nematode females was observed in plants expressing pyramiding genes than in those only expressing a single gene. Molecular analysis demonstrated that BvHs1pro-1 and BvcZR3 gene expressions in oilseed rape constitutively activated transcription of plant-defense related genes such as NPR1 (non-expresser of PR1), SGT1b (enhanced disease resistance 1) and RAR1 (suppressor of the G2 allele of skp1). Transcript of NPR1 gene in transgenic cZR3 and Hs1pro-1 plants were slightly up-regulated, while its expression was considerably enhanced in cZR3Hs1pro-1 gene pyramiding plants. The expression of EDS1 gene did not change significantly among transgenic cZR3, Hs1pro-1 and cZR3Hs1pro-1 gene pyramiding plants and wild type. The expression of SGT1b gene was slightly up-regulated in transgenic cZR3 and Hs1pro-1 plants compared with the wild type, however, its expression was not changed in cZR3Hs1pro-1 gene pyramiding plant and had no interaction effect. RAR1 gene expression was significantly up-regulated in transgenic cZR3 and cZR3Hs1pro-1 genes pyramiding plants, but almost no expression was found in Hs1pro-1 transgenic plants. These results show that nematode resistance genes from sugar beet were functional in oilseed rape and conferred BCN resistance by activation of a CC-NBS-LRR R gene mediated resistance response. The gene pyramiding had enhanced resistance, thus offering a novel approach for the BCN control by preventing the propagation of BCN in oilseed rape. The transgenic oilseed rape could be used as a trap crop to offer an alternative method for beet cyst nematode control.

Registration of Sugar Beet Germplasm Lines CN921‐515 and CN921‐516 with Sugar Beet Cyst Nematode Resistance from Beta vulgaris subsp. maritima

CN921‐515 (Reg. No. GP‐295, PI 669447) and CN921‐516 (Reg. No. GP‐296, PI 669448) sugar beet (Beta vulgaris L.) germplasm lines, with sugar beet cyst nematode (SBCN) resistance derived from Beta vulgaris subsp. maritima L. (Bvm), were developed and released by the USDA‐ARS at Salinas, CA, in cooperation with the Beet Sugar Development Foundation in Denver, CO. CN921‐515 and CN921‐516 are multigerm, green hypocotyl, self‐fertile, partially inbred lines extracted from genetic‐male‐sterile facilitated, random‐mated lines. Greenhouse SBCN screening of individual plants and progeny tests indicate each is likely homozygous resistant. CN921‐306 is the progenitor population and was developed from multiple composite crosses involving >40 Bvm accessions. Therefore, the original wild beet accession that contributed sugar beet cyst nematode resistance to these lines is not known, nor are the allelic relationships with recently released CN12‐446, CN12‐770, and CN72‐652. CN921‐515 and CN921‐516 have a higher frequency of SBCN resistance (higher number of resistant individuals per line) than CN921‐306. CN921‐515 and CN921‐516 also have an increased number of rhizomania‐resistant individuals compared with CN921‐306.

Genetic behavior of resistance to the beet cyst nematode (Heterodera schachtii Schm) in radish (Raphanus sativus L.)

The genetic nature of resistance to the beet cyst nematode (BCN) (Heterodera schachtiiSchm) in oil radish was investigated. A segregating population consisted of 245 F2individuals derived from self-pollinated single F1 plant of the radish cross ‘Pegletta X Siletta nova’ was used. Four oil radish populations and one Brassica napus cv. “Madora” as susceptible control were examined for the resistance to the BCN. The number of cysts found on the root system of radish plants and the attached soil were used for resistance criteria. The results showed that all F1 plants appeared in the resistance parent classes, which reflected the dominant behavior of the resistant gene(s). A bimodal distribution was observed for the F2 population. The F2 individuals distributed in two discreet phenotype classes, complying with the assumption of monogenic dominant inheritance of the BCN resistance in oil radish. Key words: Genetic behavior, Raphanus sativus, dominant gene(s), Heterodera schachtiiSchm.

Cloning and sequence diversity analysis of GmHs1 pro-1 in Chinese domesticated and wild soybeans

Soybean cyst nematode (SCN) (Heterodera glycines Ichinohe) is the most important pathogen in soybean production worldwide and causes substantial yield losses. An apparent narrow genetic base of SCN resistance was observed in current elite soybean cultivars, and searching for novel SCN resistance genes as well as novel resistance sources rather than focusing on the two important genes rhg1 and Rhg4 has become another major objective in soybean research. In the present paper we report a 1,477 bp Hs1pro-1 homolog, named GmHs1pro-1. This gene was cloned from soybean variety Wenfeng 7 based on information for Hs1pro-1, a beet cyst nematode resistance gene in sugar beet. It has two domains, Hs1pro-1_N and Hs1pro-1_C, both of which are believed to confer resistance to nematodes. Of the 1,477 bp sequence in GmHs1pro-1, an open reading frame of 1,314 bp, encoding a protein with 437 amino acids, was flanked by a 5′-untranslated region of 27 bp and a 3′-untranslated region of 135 bp. Fourteen single-nucleotide polymorphisms (SNPs) were observed in 44 soybean accessions including 23 wild soybeans, 8 landraces, and 13 soybean varieties (or lines), among which 5 in wild soybeans and 3 in landrace accessions were unique. Sequence diversity analysis on the 44 soybean accessions showed π = 0.00168 and θ = 0.00218 for GmHs1pro-1; landraces had the highest diversity, followed by wild soybeans, with varieties (or lines) having the lowest. Although we did not detect a significant effect of selection on GmHs1pro-1 in the three populations, sequence diversity, unique SNPs, and phylogenetic analysis indicated a slight domestication bottleneck and an intensive selection bottleneck. High sequence diversity, more unique SNPs, and broader representation across the phylogenetic tree in wild soybeans and landraces indicated that wild collections and landrace accessions are invaluable germplasm for broadening the genetic base of elite soybean varieties resistant to SCN.

Broadening the genetic base of sugar beet: introgression from wild relatives

The development of sugar beet as an economically important field crop coincided with our increased understanding of modern genetic principles. It was developed in the late 1700s from white fodder beet; therefore, the genetic base of sugar beet is thought to be narrower than many open-pollinated crops. The wild sea beet is the progenitor of all domesticated beet and cross compatible with cultivated beet (domestic and cultivated are given subspecies level in the same species). The breeding system of sugar beet is complex and the crop is biennial, which lengthens the generation time to almost 1 year. A genetic-cytoplasmic male sterility (CMS) system is utilized for commercial hybrid production. Early breeding objectives were to improve the concentration and extractability of sucrose and little emphasis was placed on host–plant resistance to insect, nematode, and disease pests. As production areas expanded, these pests limited production, sometimes severely. The first systematic attempts to screen exotic and wild beet germplasm for disease resistance were initiated early in the 20th century. Many undesirable traits from wild beet were reportedly introgressed with the selected disease resistance and it was only in the late 1900s that the use of wild beet genetic resources became common place in public breeding programs. In North America, a pivotal development in utilizing the genetic resources available for sugar beet breeding was the formation in 1983 of the Sugarbeet Crop Germplasm Committee (CGC). Since the Sugarbeet CGC identified enhancing the commercial sugar beet germplasm pool as a high priority, there has been an aggressive evaluation of the National Plant Germplasm System (NPGS) Beta collection. This collection now has more than 2500 accessions from within the genus Beta. In 2002, it was estimated that close to 25,000 evaluation data points (descriptors × accessions evaluated) describing the collection were available in the Genetic Resources Information Network (GRIN) database. Over 3000 evaluations described levels of resistance of sugar beet and wild beet accessions to 10 major disease and insect pests of sugar beet. As soon as the evaluation data are collected, they are used to select the sources for the pre-breeding programs. There is a lag time in sugar beet of␣8–15 years between starting a germplasm development program and releasing the first germplasm, but successes of this program are available in the germplasm released to the commercial breeders. Resistance genes from wild beet for rhizomania and beet cyst nematode resistance have been commercialized.

Identification of a putative cation transporter gene from sugar beet ( Beta vulgaris L.) by DDRT-PCR closely linked to the beet cyst nematode resistance gene Hs1pro-1

The beet cyst nematode ( Heterodera schachtii Schm.) is a widespread pest that causes agronomic losses in sugar beet cultivation. Since no nematode resistance genes have been found in Beta vulgaris L. cultivars, a chromosomal fragment from Beta procumbens has been bred into cultivated sugar beet in order to provide resistance to Heterodera schachtii. The introgressed translocation carries the nematode resistance gene Hs1 pro-1 and may also contain genes that are linked to the defense response and/or signal transduction. A novel cDNA designated Bp23 was isolated from the translocation in this work by comparing resistant and susceptible sugar beets of a segregating F 2 population by differential display. Bp23 shows similarity to Arabidopsis thaliana BAC clones and to diverse plant ESTs with similarity to the Escherichia coli cation transporter ChaC. The open reading frame could encode a hydrophilic protein of 25 kDa that is similar to cation transporters and has a presumptive K + selective motif at the N-terminus.

The use of bulked segregant analysis to accumulate RAPD markers near a locus for beet cyst nematode resistance in Beta vulgaris

AbstractBulked segregant analysis (BSA) was used to accumulate RAPD markers near the beet cyst nematode resistance locus Hslpro‐1 of sugar beet (Beta vulgaris L.). Graphical genotypes constructed from RFLP data were utilized to select F2 individuals in (1) the construction of pools of plants used in the initial screening for polymorphisms, and (2) the selection of individual plants used to confirm the potential linkage. The pooled DNA samples were screened for polymorphisms using 668 RAPD primers. Forty‐four candidate markers potentially linked to the region were analysed further using 14 segregating individuals. Close linkage was confirmed for 17 of the markers. Four of the RAPD markers were assigned map coordinates within the RFLP map. Three of these markers extended the RFLP map by 3cM. Altogether, the 8cM target interval contains 10 RFLP and 17 RAPD markers, corresponding to an average marker density of 0.3cM in the Hslpro‐1 region.

Molecular and morphological characterization of monosomic additions in Beta vulgaris, carrying extra chromosomes of B. procumbens or B. patellaris.

DNA fingerprinting with three repetitive DNA sequences (OPX2, PB6-4 and Sat-121) was carried out on a set of 10 monosomic additions of Beta procumbens and 75 anonymous B. patellaris-derived monosomic additions in B. vulgaris, for characterization of the alien chromosomes at the DNA level. The probes are Procumbentes-specific and distributed over all chromosomes. Morphological characteristics were also used for the classification of B. patellaris monosomic addition families and for comparison with the morphology of the addition families of B. procumbens. DNA fingerprinting revealed unique patterns for almost all individual addition chromosomes of B. procumbens. However, it was concluded that chromosomes 1 and 6 of B. procumbens may be identical with the only difference that the chromosome referred to as 6 carries a susceptible allele for beet cyst nematode (BCN) resistance. In contrast, it was concluded that the two addition types with chromosome 2 are carrying different chromosomes of B. procumbens, so that one of them was renumbered to become the new chromosome 6. DNA fingerprinting of 75 anonymous B. patellaris-derived monosomic additions facilitated the identification and characterization of the alien chromosomes and the grouping of these additions into nine different groups. Several of these groups could be divided in two sub-groups on the basis of small differences in banding patterns. The results of the DNA fingerprinting led to the conclusion that B. patellaris most likely is an allotetraploid. It was also deduced that the BCN gene(s) in this species are homozygous and located on chromosome 1, while the pair of homoeologous chromosomes does not carry such BCN gene(s). Because of the allotetraploid nature of B. patellaris, preferential association occurs between the two homologous chromosomes containing the allele(s) for BCN resistance. Each group of B. patellaris addition families united by DNA fingerprinting had comparable morphological characteristics. Some of these morphological traits appeared to be chromosome-specific and were very useful for primary classification of the addition families. However, the present study showed that these morphological traits are not adequate for the identification of all alien chromosomes without the aid of additional markers. Because of similarities observed between molecular characteristics or the effects on plant morphology of several chromosomes of B. procumbens and B. patellaris it was concluded that B. procumbens could have been involved in the evolutionary history of B. patellaris.

Isolation and characterization of RAPD-based markers linked to the beet cyst nematode resistance locus (Hs1 pat-1) on chromosome 1 of B. patellaris

A beet cyst nematode (BCN)-resistant telosomic addition of B. patellaris chromosome 1 in B. vulgaris was used to isolate 6 RAPD markers linked to the BCN resistance locus Hs1 (pat-1). Southern analysis showed that the analyzed RAPD products contain either low-, middle or high-repetitive DNA. The relative positions of the random amplified polymorphic DNA (RAPD) markers and of the restriction fragment length polymorphism (RFLP) loci corresponding to the low-repetitive RAPD products were determined by deletion mapping using a panel of seven nematode-resistant B. patellaris chromosome-1 fragment additions. One RAPD marker, OPB11800, was found to be present in two copies on the long arm telosome of B. patellaris chromosome 1. These copies are closely linked to the BCN resistance gene and flank the gene on both sides. On the basis of the nucleotide sequence of OPB11800, sequence-tagged site (STS) primers were developed that amplify specific fragments derived from the two OPB11800 loci. These STS markers can be used in the map-based cloning of the BCN gene, as they define start and finishing points of a chromosomal walk towards the Hs1 (pat-1) locus. Two copies of the middle-repetitive OPX21100 marker were mapped in the same interval of the deletion mapping panel as the resistance gene locus and thereby belong to the nearest markers as yet found for the BCN gene in B. patellaris.

Long-range organization of a satellite DNA family flanking the beet cyst nematode resistance locus (Hs1) on chromosome-1 of B. patellaris and B. procumbens

New members of a satellite DNA family (Sat 121), specific for wild beets of the section Procumbentes of the genus Beta, were isolated. Sequence analysis showed that the members of Sat-121 fall into two distinct classes. The organization of Sat-121 in the vicinity of a beet cyst nematode (Heterodera schachtii Schm.) resistance locus (Hs1) in B. patellaris and B. procumbens was investigated by pulsed-field gel electrophoresis (PFGE) using DNA from a series of resistant monosomic fragment additions, each containing an extra chromosome fragment of B. patellaris chromosome-1 (pat-1) in B. vulgaris. In this way several clusters of Sat-121 flanking the Hs1 (pat-1) locus were identified. In nematode resistant diploid introgressions (2n=18), which contain small segments of B. procumbens chromosome-1 (pro-1) in B. vulgaris, only two major Sat-121 clusters were detected near the Hs1 (pro-1) locus.

Construction of a YAC library from a Beta vulgaris fragment addition and isolation of a major satellite DNA cluster linked to the beet cyst nematode resistance locus Hs1 pat−1

A YAC library was constructed from the Beta vulgaris fragment addition AN5-203b. This monosomic fragment addition harbors an approximate 12-Mbp fragment of B.patellaris chromosome 1 accomodating the Hs1 (pat-1) conferring resistance to the beet cyst nematode (Heterodera schachtii). The YAC library consists of 20,000 YAC clones having an average size of 140 kb. Screening with organelle-specific probes showed that 12% of the clones contain chloroplast DNA while only 0.2% of the clones hybridizes with a mitochondrial specific probe. On the basis of a sugar beet haploid genome size of 750 Mbp this library represents 3.3 haploid genome equivalents. The addition fragment present in AN5-203b harbors a major satellite DNA cluster that is tightly linked to the Hs1 (pat-1) locus. The cluster is located on a single 250-kb EcoRI restriction fragment and consists of an estimated 700-800 copies of a 159-bp core sequence, most of which are arranged in tandem. Using this core sequence as a probe, we were able to isolate 1 YAC clone from the library that contains the entire 250-kb satellite DNA cluster.

Pre-Breeding for Nematode Resistance in Beet

Pre-breeding for partial resistance to the beet cyst nematode (BCN), Heterodera schachtii, included repeated mass selection in descendants of Beta vulgaris subsp. maritima accession BMH and preliminary studies on inheritance and mechanism of this resistance. The selection in accession BMH and in progenies of a cross with fodder beet resulted in rather high levels of partial resistance. The mean numbers of cysts per plant for the BMH selections and for progenies of a cross with fodder beet were 20-40070 and 15-30%, respectively, of those of the susceptible control varieties. The progenies of crosses between accession BMH and sugar beet were less advanced, and additional selection for bienniality may have decreased the progress in selection for BCN resistance. The resistant materials showed a wide variation in cyst size, and many of the cysts were considerably smaller than those on the susceptible control varieties. This phenomenon will reduce the multiplication rate of the nematodes. The numbers of cysts in progenies of pair crosses between accession BMH and cultivated materials generally were slightly below the mid-parent values. The results are discussed in the light of pre-breeding strategies and the possible application of marker-facilitated selection procedures.

PRELIMINARY SCREENING OF OILSEED RAPE FOR BEET CYST NEMATODE RESISTANCE

Annals of Applied BiologyVolume 108, Issue S1 p. 152-153 PRELIMINARY SCREENING OF OILSEED RAPE FOR BEET CYST NEMATODE RESISTANCE S.A. Bowen, S.A. Bowen Department of Science, Luton College of Higher Education, Park Square, Luton, Beds., LU1 3JU.Search for more papers by this authorG.W. Storey, G.W. Storey Department of Science, Luton College of Higher Education, Park Square, Luton, Beds., LU1 3JU.Search for more papers by this authorK. Evans, K. Evans Rothamsted Experimental Station, Harpenden, Herts., AL5 2JQ.Search for more papers by this author S.A. Bowen, S.A. Bowen Department of Science, Luton College of Higher Education, Park Square, Luton, Beds., LU1 3JU.Search for more papers by this authorG.W. Storey, G.W. Storey Department of Science, Luton College of Higher Education, Park Square, Luton, Beds., LU1 3JU.Search for more papers by this authorK. Evans, K. Evans Rothamsted Experimental Station, Harpenden, Herts., AL5 2JQ.Search for more papers by this author First published: April 1986 https://doi.org/10.1111/aab.1986.108.s1.152Citations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume108, IssueS1April 1986Pages 152-153 RelatedInformation