Publications by authors named "Martin Wubben"

[the guava root-knot nematode (RKN)] is an emerging plant-parasitic nematode that poses a threat to Upland cotton () production in the southeastern United States. Like other RKN spp., has a wide host range and proven ability to overcome resistance sources that have helped protect crops from other spp.

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Cotton () resistance to root-knot nematode (RKN) () is controlled by quantitative trait loci (QTLs) on chromosomes 11 (CHR11) and 14 (CHR14). The individual contributions of these QTLs to resistance are not completely understood. We developed near isogenic lines susceptible at both loci (null), having CHR11 or CHR14 alone, and having both QTLs (CHR11/CHR14).

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The reniform nematode () is a sedentary semi-endoparasitic species that is pathogenic on many row crops, fruits, and vegetables. Here, the authors present a draft genome assembly of . using small- and large-insert libraries sequenced on the Illumina GAIIx and MiSeq platforms.

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MAGIC population sequencing and virus-induced gene silencing identify Gh_D02G0276 as a novel root-knot nematode resistance gene on chromosome 14 in Upland cotton. The southern root-knot nematode [RKN; Meloidogyne incognita (Kofoid & White)] remains the primary yield-limiting biotic stress to Upland cotton (Gossypium hirsutum L.) throughout the southeastern USA.

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The reniform nematode ( Linford and Oliveira) is a semi-endoparasitic nematode that is a pathogen of numerous major crops such as cotton and soybean. Here, the authors present transcriptome assemblies of the egg, second-stage juvenile (J2), J3, vermiform adult, and sedentary female life stages of this important plant pathogen. The reniform nematode ( Linford and Oliveira) is a semi-endoparasitic nematode that is a pathogen of numerous major crops such as cotton and soybean.

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In crop research programs that implement transgene-based strategies for trait improvement it is necessary to distinguish between transgene homozygous and hemizygous individuals in segregating populations. Direct methods for determining transgene zygosity are technically challenging, expensive, and require specialized equipment. In this report, we describe a standard PCR-based protocol coupled with capillary electrophoresis that can identify transgene homozygous and hemizygous individuals in a segregating population without knowledge of transgene insertion site.

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Genetic analysis of MIC-3 transgene with RKN resistance QTLs provides insight into the resistance regulatory mechanism and provides a framework for testing additional hypotheses. Resistance to root-knot nematode (RKN) (Meloidogyne incognita) in Upland cotton (Gossypium hirsutum) is mediated by two major quantitative trait loci (QTL) located on chromosomes 11 and 14. The MIC-3 (Meloidogyne Induced Cotton3) protein accumulates specifically within the immature galls of RKN-resistant plants that possess these QTLs.

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The reniform nematode, Rotylenchulus reniformis, is a sedentary semi-endoparasitic species with a host range that encompasses more than 77 plant families. Nematode effector proteins containing plant-ligand motifs similar to CLAVATA3/ESR (CLE) peptides have been identified in the Heterodera, Globodera, and Meloidogyne genera of sedentary endoparasites. Here, we describe the isolation, sequence analysis, and spatiotemporal expression of three R.

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Transgene-based analysis of the MIC-3 gene provides the first report of a cotton gene having a direct role in mediating cotton resistance to root-knot nematode. Major quantitative trait loci have been mapped to Upland cotton (Gossypium hirsutum L.) chromosomes 11 and 14 that govern the highly resistant phenotype in response to infection by root-knot nematode (RKN; Meloidogyne incognita); however, nearly nothing is known regarding the underlying molecular determinants of this RKN-resistant phenotype.

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The reniform nematode, Rotylenchulus reniformis, is a damaging semi-endoparasitic pathogen of more than 300 plant species. Transcriptome sequencing of R. reniformis parasitic females revealed an enrichment for sequences homologous to C-type lectins (CTLs), an evolutionarily ancient family of Ca(+2)-dependent carbohydrate-binding proteins that are involved in the innate immune response.

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The sedentary semi-endoparasitic nematode Rotylenchulus reniformis, the reniform nematode, is a serious pest of cotton and soybean in the United States. In recent years, interest in the molecular biology of the interaction between R. reniformis and its plant hosts has increased; however, the unusual life cycle of R.

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Phytonematodes use a stylet and secreted effectors to modify host cells and ingest nutrients to support their growth and development. The molecular function of nematode effectors is currently the subject of intense investigation. In this review, we summarize our current understanding of nematode effectors, with a particular focus on proteinaceous stylet-secreted effectors of sedentary endoparasitic phytonematodes, for which a wealth of information has surfaced in the past 10 yr.

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The identification of molecular markers that are closely linked to gene(s) in Gossypium barbadense L. accession GB713 that confer a high level of resistance to reniform nematode (RN), Rotylenchulus reniformis Linford & Oliveira, would be very useful in cotton breeding programs. Our objectives were to determine the inheritance of RN resistance in the accession GB713, to identify SSR markers linked with RN resistance QTLs, and to map these linked markers to specific chromosomes.

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Molecular markers closely linked to genes that confer a high level of resistance to root-knot nematode (RKN) [Meloidogyne incognita (Kofoid & White) Chitwood] in cotton (Gossypium hirsutum L.) germplasm derived from Auburn 623 RNR would greatly facilitate cotton breeding programs. Our objectives were to identify simple sequence repeat (SSR) markers linked to RKN resistance quantitative trait loci (QTL) and map these markers to specific chromosomes.

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Rotylenchulus reniformis, the reniform nematode, is a sedentary semi-endoparasitic nematode capable of infecting >300 plant species, including a large number of crops such as cotton, soybean, and pineapple. In contrast to other economically important plant-parasitic nematodes, molecular genetic data regarding the R. reniformis transcriptome is virtually nonexistant.

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Agrobacterium rhizogenes-induced cotton (Gossypium hirsutum L.) hairy roots were evaluated as a model system for studying molecular cotton-nematode interactions. Hairy root cultures were developed from the root-knot nematode (RKN) (Meloidogyne incognita [Kofoid and White] Chitwood, race 3)-resistant breeding line M315 and from the reniform nematode (RN) (Rotylenchulus reniformis Linford & Oliveira)-resistant accession GB713 (G.

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The molecular events underlying the resistance of Upland cotton (Gossypium hirsutum L.) to the root-knot nematode (RKN) are largely unknown. In this report, we further characterize the previously identified MIC3 gene including the identification of 14 related MIC cDNAs in nematode-infected roots of allotetraploid cotton that show >85% identity with MIC3.

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Compatible plant-nematode interactions involve the formation of an elaborate feeding site within the host root that requires the evasion of plant defense mechanisms by the parasite. Little is known regarding plant defense signaling pathways that limit nematode parasitism during a compatible interaction. Therefore, we utilized Arabidopsis thaliana mutants perturbed in salicylic acid (SA) biosynthesis or signal transduction to investigate the role of SA in inhibiting parasitism by the beet cyst nematode Heterodera schachtii.

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In Arabidopsis, mutation of RHD1, a UDP-glucose-4-epimerase, causes root-specific phenotypes, including hypersusceptibility to the cyst nematode Heterodera schachtii, increased root hair elongation, decreased root length, and root epidermal bulging. Previous experiments suggested that increased ethylene sensitivity or production mediated the rhd1-4 phenotypes. In the present study, double mutant analyses revealed that only rhd1-4 hypersusceptibility to H.

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