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Valerie M Williamson

Publications and source records attributed to Valerie M Williamson.

11 recordsLinked to original sources
PubMed2026

N6-methyladenine DNA modification modulates pathogen virulence in nematodes.

Understanding the global regulatory mechanisms that control pathogen virulence gene expression is essential for elucidating the molecular basis of pathogenicity. N6-methyladenine (6 mA) plays a crucial role in regulating gene expression in response to various environmental stresses; however, its role in pathogen virulence remains largely unexplored. Here, we report the widespread occurrence of 6 mA across 17 nematode isolates and map its genomic landscape in six notorious agriculturally important pathogen root-knot nematodes (RKNs). We demonstrated that 6 mA is characterized by a conserved GAG motif across nematodes, but exhibits species-specific distribution patterns and distinct effects on gene expression. In particular, its enrichment in transposable elements (TEs) differs between polyploid and diploid nematodes, suggesting lineage-specific epigenetic regulation potentially associated with polyploidy. We further identified two functional 6 mA demethylases, MiNMAD-1 and MiNMAD-2, and confirmed their catalytic activity and active sites. Host-induced gene silencing (HIGS) of minmad-1 significantly increased plant resistance to three polyploid RKN species. A detailed functional analysis revealed that minmad-1 knockdown broadly affected gene expression during the parasitic stage, including genes involved in virulence, thereby reducing nematode infectivity. Together, our findings suggest 6 mA demethylase as a key epigenetic regulator of RKNs' virulence, providing new insights into nematode biology and offering promising targets for the development of sustainable control strategies.

Animals↗
PubMed2006

Nematode resistance in plants: the battle underground.

Parasitic nematodes infect thousands of plant species, but some plants harbor specific resistance genes that defend against these pests. Several nematode resistance genes have been cloned in plants, and most resemble other plant resistance genes. Nematode resistance is generally characterized by host plant cell death near or at the feeding site of the endoparasitic worm. The timing and localization of the resistance response varies with the particular resistance gene and nematode interaction. Although there is genetic evidence that single genes in the nematode can determine whether a plant mounts a resistance response, cognate nematode effectors corresponding to a plant resistance gene have not been identified. However, recent progress in genetics and genomics of both plants and nematodes, and developments in RNA silencing strategies are improving our understanding of the molecular players in this complex interaction. In this article, we review the nature and mechanisms of plant-nematode interactions with respect to resistance in plants.

Animals↗
PubMed2006

Heterologous expression of the Mi-1.2 gene from tomato confers resistance against nematodes but not aphids in eggplant.

The Mi-1.2 gene in tomato (Solanum lycopersicum) is a member of the nucleotide-binding leucine-rich repeat (NBLRR) class of plant resistance genes, and confers resistance against root-knot nematodes (Meloidogyne spp.), the potato aphid (Macrosiphum euphorbiae), and the sweet potato whitefly (Bemisia tabaci). Mi-1.2 mediates a rapid local defensive response at the site of infection, although the signaling and defensive pathways required for resistance are largely unknown. In this study, eggplant (S. melongena) was transformed with Mi-1.2 to determine whether this gene can function in a genetic background other than tomato. Eggplants that carried Mi-1.2 displayed resistance to the root-knot nematode Meloidogyne javanica but were fully susceptible to the potato aphid, whereas a susceptible tomato line transformed with the same transgene was resistant to nematodes and aphids. This study shows that Mi-1.2 can confer nematode resistance in another Solanaceous species. It also indicates that the requirements for Mi-mediated aphid and nematode resistance differ. Potentially, aphid resistance requires additional genes that are not conserved between tomato and eggplant.

Animals↗
PubMed2005

EDS1 in tomato is required for resistance mediated by TIR-class R genes and the receptor-like R gene Ve.

In tobacco and other Solanaceae species, the tobacco N gene confers resistance to tobacco mosaic virus (TMV), and leads to induction of standard defense and resistance responses. Here, we report the use of N-transgenic tomato to identify a fast-neutron mutant, sun1-1 (suppressor of N), that is defective in N-mediated resistance. Induction of salicylic acid (SA) and expression of pathogenesis-related (PR) genes, each signatures of systemic acquired resistance, are both dramatically suppressed in sun1-1 plants after TMV treatment compared to wild-type plants. Application of exogenous SA restores PR gene expression, indicating that SUN1 acts upstream of SA. Upon challenge with additional pathogens, we found that the sun1-1 mutation impairs resistance mediated by certain resistance (R) genes, (Bs4, I, and Ve), but not others (Mi-1). In addition, sun1-1 plants exhibit enhanced susceptibility to TMV, as well as to virulent pathogens. sun1-1 has been identified as an EDS1 homolog present on chromosome 6 of tomato. The discovery of enhanced susceptibility in the sun1-1 (Le_eds1-1) mutant plant, which contrasts to reports in Nicotiana benthamiana using virus-induced gene silencing, provides evidence that the intersection of R gene-mediated pathways with general resistance pathways is conserved in a Solanaceous species. In tomato, EDS1 is important for mediating resistance to a broad range of pathogens (viral, bacterial, and fungal pathogens), yet shows specificity in the class of R genes that it affects (TIR-NBS-LRR as opposed to CC-NBS-LRR). In addition, a requirement for EDS1 for Ve-mediated resistance in tomato exposes that the receptor-like R gene class may also require EDS1.

Amino Acid Sequence↗
PubMed2004

Rme1 is necessary for Mi-1-mediated resistance and acts early in the resistance pathway.

The tomato gene Mi-1 confers resistance to root-knot nematodes (Meloidogyne spp.), potato aphid, and whitefly. Using genetic screens, we have isolated a mutant, rme1 (resistance to Meloidogyne spp.), compromised in resistance to M. javanica and potato aphid. Here, we show that the rme1 mutant is also compromised in resistance to M. incognita, M. arenaria, and whitefly. In addition, using an Agrobacterium-mediated transient assay in leaves to express constitutive gain-of-function mutant Pto(L205D), we demonstrated that the rme1 mutation is not compromised in Pto-mediated hypersensitive response. Moreover, the mutation in rme1 does not result in increased virulence of pathogenic Pseudomonas syringae or Mi-1-virulent M. incognita. Using a chimeric Mi-1 construct, Mi-DS4, which confers constitutive cell death phenotype and A. rhizogenes root transformation, we showed that the Mi-1-mediated cell death pathway is intact in this mutant. Our results indicate that Rme1 is required for Mi-1-mediated resistance and acts either at the same step in the signal transduction pathway as Mi-1 or upstream of Mi-1.

Animals↗
PubMed2004

Salicylic acid is part of the Mi-1-mediated defense response to root-knot nematode in tomato.

The Mi-1 gene of tomato confers resistance against three species of root-knot nematode in tomato (Lycopersicon esculentum). Transformation of tomato carrying Mi-1 with a construct expressing NahG, which encodes salicylate hydroxylase, a bacterial enzyme that degrades salicylic acid (SA) to catechol, results in partial loss of resistance to root-knot nematodes. Exogenous SA was toxic to roots expressing NahG but not to control roots. This toxicity is most likely due to the production of catechol from SA, and we report here that 100 microM catechol is toxic to tomato roots. Benzothiadiazole, a SA analog, completely restores nematode resistance in Mi-1 roots transformed with NahG but does not confer resistance to susceptible tomato roots. The localized cell death produced by transient expression in Nicotiana benthamiana of Mi-DS4, a constitutively lethal chimera of Mi-1 with one of its homologs, was prevented by coexpression of NahG. These results indicate that SA is an important component of the signaling that leads to nematode resistance and the associated hypersensitive response.

Animals↗
PubMed2004

Developmental regulation of Mi-mediated aphid resistance is independent of Mi-1.2 transcript levels.

Mi-1.2, a member of the intracellular, nucleotide-binding site-leucine-rich repeat family of resistance genes, confers resistance in tomato (Lycopersicon esculentum) against both root-feeding nematodes and leaf-feeding aphids. Nematode resistance is effective in all life stages of the plant; in contrast, Mi-mediated aphid resistance is developmentally regulated, and protects mature plants but not seedlings against aphid infestation. To determine if the onset of aphid resistance is regulated by Mi-1.2 transcript abundance, we compared aphid resistance and Mi-1.2 transcript levels in seedlings and flowering plants. Paired bioassays and RNase protection assays revealed that Mi-1.2 is transcribed in the leaves prior to the onset of aphid resistance, and that transcript levels are comparable in seedlings and flowering life stages. Furthermore, constitutive overexpression of Mi-1.2 in transgenic plants did not hasten the onset of aphid resistance in seedlings, or boost the level of resistance observed in flowering plants. These data demonstrate that Mi-1.2 transcript levels do not modulate the degree of aphid resistance in tomato leaves, or control the differences in regulation between aphid and nematode resistance.

Animals↗
PubMed2003

Plant-nematode interactions.

Root-knot nematodes and cyst nematodes are obligate, biotrophic pathogens of numerous plant species. These organisms cause dramatic changes in the morphology and physiology of their hosts. The molecular characterization of induced plant genes has provided insight into the plant processes that are usurped by nematodes as they establish their specialized feeding cells. Recently, several gene products have been identified that are secreted by the nematode during parasitism. The corresponding genes have strong similarity to microbial genes or to genes that are found in nematodes that parasitize animals. New information on host resistance genes and nematode virulence genes provides additional insight into this complex interaction.

Animals↗
PubMed2003

Leucine-rich repeat-mediated intramolecular interactions in nematode recognition and cell death signaling by the tomato resistance protein Mi.

The root-knot nematode resistance gene Mi from tomato encodes a nucleotide-binding/leucine-rich repeat (NB/LRR) protein with a novel amino-terminal domain compared to related disease-resistance genes. The closely linked paralog Mi-1.1, which does not confer nematode resistance, encodes a protein 91% identical to the functional copy, Mi-1.2. The chimeric construct Mi-DS3, which encodes the 161 amino-terminal residues from Mi-1.1 fused to the remainder of Mi-1.2, induces localized necrosis when transiently expressed in Nicotiana benthamiana leaves. We produced mutant constructs that exchanged sequences encoding each of the 40 amino acid differences from the Mi-1.1 LRR region into Mi-DS3 and into Mi-1.2. For 23 of the substitutions, necrosis was lost upon transient expression of the mutated Mi-DS3 in N. benthamiana, and nematode resistance was lost when the altered Mi-1.2 was expressed in the tomato roots. One substitution, R961D, failed to give Mi-DS3-induced necrosis, but produced a dominant lethal phenotype when introduced into Mi-1.2. This gain-of-function phenotype was suppressed by co-expression with the amino-terminal region of Mi-1.1, suggesting that residue 961 is critical for negative regulation by the corresponding N-terminal region. Substitutions of Mi-1.1 residues 984-986 retained the ability to cause necrosis in Mi-DS3, but resulted in loss-of-nematode resistance in Mi-1.2, suggesting that these residues are essential for nematode recognition. None of the loss-of-function mutations in Mi-1.2 had a dominant negative phenotype. These results indicate that the Mi-1.2 LRR is involved in regulation of the transmission of the resistance response as well as in recognition of the nematode.

Amino Acid Motifs↗
PubMed2003

The root-knot nematode resistance gene Mi-1.2 of tomato is responsible for resistance against the whitefly Bemisia tabaci.

The tomato gene Mi-1.2 confers resistance against root-knot nematodes and some isolates of potato aphid. Resistance to the whitefly Bemisia tabaci previously has been observed in Mi-bearing commercial tomato cultivars, suggesting that Mi, or a closely linked gene, is responsible for the resistance. The response of two biotypes of B. tabaci to tomato carrying the cloned Mi was compared with that of the isogenic untransformed tomato line Moneymaker. Our results indicate that Mi-1.2 is responsible for the resistance in tomato plants to both B- and Q- biotypes. Mi-1.2 is unique among characterized resistance genes in its activity against three very different organisms (root-knot nematodes, aphids, and whiteflies). These pests are among the most important on tomato crops worldwide, making Mi a valuable resource in integrated pest management programs.

Animals↗