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Results for “Tylenchoidea”

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PubMed2025

Candidate genes at the Rmi1 locus for resistance to Meloidogyne incognita in soybean.

The RKN resistance locus Rmi1 was fine-mapped to two genes on chromosome 10, a glycosyl hydrolase family 9 β-1,4-endoglucanase gene and a type I pectin methylesterase gene. Root-knot nematodes (Meloidogyne spp.) are a serious threat to soybean production in the southeast USA, with yield losses of more than $165 million in 2023. Development and deployment of resistant soybean cultivars is the most effective strategy for managing these nematode pests; however, the identity of the resistance genes and underlying mechanism of resistance remains obscure. An additive resistance gene, Resistance to M. incognita-1 (Rmi1), to the predominant species, was first identified in soybean cultivar Forrest but never mapped to a genomic region. Multiple mapping studies have identified a major quantitative trait locus (QTL) with additive action on chromosome 10. In this study, a population consisting of 170 F2:3 families derived from a cross of Bossier (susceptible) × Forrest (resistant) was initially used to confirm that Rmi1 is in the chromosome 10 QTL. Subsequently, 884 F5:6 recombinant inbred lines (RILs) derived from the same cross were used to fine-map the Rmi1 causal gene(s) to two genes - a β-1,4-endoglucanase (Glyma.10G017000, EG) and a pectin methylesterase/methylesterase inhibitor (Glyma.10G017100, PME1). Both gene candidates have the potential to play a role in the resistance response to M. incognita. Both gene promoters harbor SNPs and indels and the encoded proteins exhibit amino acid polymorphisms, including a premature stop in PME1 of resistant soybeans. Additionally, both genes show a higher expression level in susceptible roots compared to resistant roots in the absence of infection. This suggests that Rmi1 may confer one or more pre-existing differences related to cell wall modification in soybean roots, ultimately leading to a decrease in susceptibility.

Tylenchoidea↗

PubMed2026

Transgenic overexpression of GmAPC7-CT improves seed yield and reduces susceptibility to soybean mosaic virus and Meloidogyne incognita in soybean.

Stable transgenic soybean lines overexpressing the GmAPC7-CT gene have demonstrated increased seed yield and reduced susceptibility to the soybean mosaic virus and Meloidogyne incognita. The Anaphase-Promoting Complex subunit 7 (APC7) is a core structural component of the anaphase-promoting complex or cyclosome (APC/C). The terminal region of this AtAPC7 gene has been shown in Arabidopsis thaliana to accumulate more transcripts than the full-length gene. The AtAPC7-CT gene (terminal region of the AtAPC7) encodes a protein with significant homology to a tobacco viral replication inhibitor (IVR). Its stable overexpression in transgenic A. thaliana lines resulted in notable improvements in biomass, seed yield, earliness of vegetative-reproductive transitions, and reduced susceptibility to viruses. In this study, we generated stable transgenic soybean lines overexpressing the GmAPC7-CT gene (terminal region or 3' portion of Glyma.15G096000, corresponding to the AtAPC7-CT) and evaluated seed yield and susceptibility of these lines to soybean mosaic virus and Meloidogyne incognita. The GmAPC7-CT gene is 624 nucleotides long and encodes a 207-amino acid protein with two tetratricopeptide repeat (TPR) domains. GmAPC7-CT showed 100% amino acid identity with full-length GmAPC7, 81.16% identity with AtAPC7-CT, and 87.94% identity with tobacco IVR. Stable transgenic lines demonstrated significant advancements in plant development and seed yield, with the top three lines producing up to 43% more pods, 44% more seeds, and a 16% increase in seed weight. Furthermore, these soybean lines showed up to a 70% reduction in susceptibility to soybean mosaic virus and M. incognita, reflected by decreased viral RNA load and nematode reproduction factor. Collectively, these results support a conserved role of GmAPC7-CT in soybean and AtAPC7-CT in A. thaliana, acting similarly to the tobacco IVR. Thus, our findings underscore the strong biotechnological potential of the GmAPC7-CT gene to improve key agronomic traits in soybean through genetic engineering approaches, including conventional breeding, transgenesis, and genome editing.

Glycine max↗

PubMed2025

Quantitative trait loci for Globodera pallida resistance derived from wild potato species Solanum gourlayi.

Globodera pallida is a major pest that is responsible for huge losses in potato yields worldwide. Expanding the gene pool of cultivated potatoes with clones resistant to this pest is made possible by searching for resistance genes in wild Solanum species. The aim of this study was to identify quantitative trait loci (QTLs) for potato resistance to Globodera pallida derived from Solanum gourlayi. A resistant diploid potato clone, Sg 2/7 (Solanum gourlayi, accession CGN17592), was crossed with a susceptible potato hybrid clone, DW 94-4235, to generate an F1 mapping population. All clones were tested for nematode resistance using G. pallida, pathotypes Pa2 and Pa3, in 2 or 3 years (2017-2019), respectively. Diversity Array Technology (DArTseq) was used for genotyping and genetic map construction. QTLs for nematode resistance were identified on potato chromosomes II, IV, V, VI, VII, X, XI, and XII, explaining from 10.1 to 21.5% of phenotypic variance. The most significant QTL for resistance to G. pallida pathotype Pa2 was identified on chromosome XII, explaining 20.9% of the phenotypic variance in the dataset from 2017. The most significant QTL for resistance to the G. pallida Pa3 pathotype was identified on chromosome VI, with a CAPS marker Exp928 in its peak, explaining 21.5% of the phenotypic variance in the dataset from 2017. The novel QTLs for resistance to S. gourlayi may be useful for breeding resistant potato cultivars, further studies of candidate genes, and host responses of potato to G. pallida infection.

Quantitative Trait Loci↗

PubMed2026

Biological characterization and genome analysis of Bacillus thuringiensis GX0003935 with biocontrol activity against Meloidogyne enterolobii.

Meloidogyne enterolobii is a highly aggressive root-knot nematode, and reduced availability of chemical nematicides increases the need for effective biocontrol alternatives. We characterized Bacillus thuringiensis GX0003935 in terms of nematicidal activity, stability, biocontrol efficacy, and genome features. The culture broth and filtrate caused more than 97% corrected mortality of second-stage juveniles within 48 h, whereas bacterial suspension showed limited activity, suggesting that extracellular factors substantially contribute to nematicidal activity. The culture filtrate retained high nematicidal activity after exposure to UV irradiation, heat treatment, broad pH range, and prolonged storage, and the strain maintained stable activity during serial passaging. Furthermore, protease sensitivity assays, ammonium sulfate precipitation, and polarity characterization collectively suggested a composite active system involving proteinaceous and non-proteinaceous components. In pot trials, culture broth and filtrate reduced galling by approximately 74%. Genome sequencing combined with ANI/dDDH analyses confirmed GX0003935 as B. thuringiensis. Multiple candidates (proteases, chitinases, and toxin proteins) and secondary metabolite biosynthetic gene clusters were revealed, while known nematicidal Cry toxins were not detected. RT-qPCR results confirmed that the expression of these candidate genes at different growth stages. B. thuringiensis GX0003935 exhibits stable, extracellular-factor-associated nematicidal activity and effectively suppresses M. enterolobii in water spinach, indicating its potential as a biocontrol candidate.

Bacillus thuringiensis↗

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↗

PubMed2025

Adaptation of the Cyst Nematode Globodera pallida to the Colinear Potato Resistant QTLs GpaVvrn and GpaVspl Involved Distinct Genomic Regions and Absence of Cross-Virulence.

The use of alternative methods to control cyst nematode populations has accelerated since the ban of chemical nematicides in Europe. The resistant QTL GpaVvrn, derived from the wild species Solanum vernei, is widely present in resistant European potato cultivars and provides strong protection against Globodera pallida populations although a risk of resistance breakdown has already been demonstrated in both experimental evolution studies and field populations. The wild relative S. sparsipilum, harbouring the resistant QTL GpaVspl, would be an interesting alternative source of resistance to control virulent G. pallida. The goal of the present study was to understand the genomics of adaptation of the nematode to these two colinear resistant QTLs. Starting with two natural populations, an experimental evolution approach allowed, after 10 generations on resistant potato genotypes, selecting independent nematode lineages adapted to each QTL. These virulent lineages were analysed through a combination of phenotyping and genome scans approaches. Phenotyping enabled the quantification of virulence levels and confirmed resistance breakdowns. Pool-Seq whole genome sequencing followed by genome scan analyses identified genomic regions under selection, potentially involved in the adaptive mechanisms to each resistance factor. Candidate genes within these regions provided insights into the genetic basis of adaptation, revealing effectors known to suppress plant immunity. As genome scans highlighted distinct genomic regions for the adaptation to both resistant factors, we were able to predict and phenotypically confirm the absence of cross-virulence between nematode lineages evolving on GpaVvrn and GpaVspl. These findings have significant implications for the design of effective and sustainable resistance management strategies.

Animals↗

PubMed2026

Domestication-associated reduction of methyl salicylate in tomato root and its significance for resistance to root-knot nematode.

Methyl salicylate (MeSA) plays diverse roles in the aerial parts of plants. By contrast, its biosynthesis and function in roots remain poorly understood. Here, we investigated root MeSA biosynthesis and function in tomato. Genome-wide association studies (GWAS) were performed using root MeSA levels as the phenotype in a diversity panel of 167 accessions to identify associated loci. Candidate genes were biochemically characterized, and the role of MeSA in defense against root-knot nematode (RKN, Meloidogyne incognita) was evaluated using transgenic plants. MeSA was identified as a major root volatile in tomato and showed a domestication-associated reduction. GWAS revealed multiple loci associated with natural variation in root MeSA, including a major locus on Chromosome 9 encoding the salicylic acid methyltransferase (SlSAMT). SlSAMT-overexpressing plants showed reduced resistance to RKNs, whereas SlSAMT-knockdown plants exhibited enhanced resistance. Our results suggest complex roles of MeSA and the salicylic acid (SA) signaling pathway in belowground plant defense. The SA signaling pathway likely plays critical roles in protecting roots against diverse natural enemies, including RKNs. Nevertheless, RKNs appear to have co-opted MeSA as a host-location signal, and the domestication-associated reduction of root MeSA in tomato has likely contributed to enhanced resistance against RKNs.

Solanum lycopersicum↗

PubMed2026

A cooperative regulatory module between TAGL2 and JMJC1 activates specific defense genes against root-knot nematodes in tomato.

Plant-parasitic nematodes (PPNs) threaten global food security. Although epigenetic modifications are crucial for plant immunity, how histone modifiers contribute to root-knot nematodes (RKNs, Meloidogyne incognita) resistance remains unclear. Here, using genetic, molecular and biochemical approaches, we investigated the epigenetic and transcriptional mechanisms underlying RKN resistance mediated by the histone demethylase (HDM) JMJC1 and the MADS-box transcription factor TAGL2 in tomato (Solanum lycopersicum). We identified JMJC1 as an RKN-induced positive defense regulator targeting H3K9me3 and H3K27me3 histone marks. JMJC1 physically interacts with TAGL2, which also positively regulates RKN resistance. Transcriptomic analysis indicated that TAGL2 regulates multiple layers of the plant defense network, transcriptionally activating representative genes from distinct pathways (including PUB10, bHLH98, CCaMK, and SAUR3), which we validated as positive regulators of RKN resistance via virus-induced gene silencing (VIGS). At the chromatin level, TAGL2 and JMJC1 co-regulate these loci, associating with localized H3K9me3 and H3K27me3 reduction. Furthermore, TAGL2 directly activates JMJC1 transcription, establishing a positive feedback loop that amplifies immune signaling. Our findings reveal a cooperative model wherein a HDM and a transcription factor coordinate at specific loci to fine-tune multiple defense layers at both epigenetic and transcriptional levels, providing insights for breeding durable nematode-resistant plants.

Solanum lycopersicum↗

PubMed2026

Diversity at the HYP1 locus in potato cyst nematodes does not result from developmentally-programmed somatic mutations.

Most genetic diversity stems from spontaneous mutations, that is, errors in DNA repair or replication. But for dozens of organisms across the tree of life, mutations at specific loci are not spontaneous but developmentally programmed: effectively, some organisms edit their own DNA sequences. This is perhaps most common among pathogens and parasites, many of which use editing to diversify genes that produce important antigens. Plant-parasitic potato cyst nematodes are damaging agricultural pests that establish a lifelong feeding site inside the root of their host plant. We previously observed extensive diversity of rare alleles at HYP1, the most highly expressed gene that encodes a protein secreted by potato cyst nematodes during parasitism. Importantly, HYP1 alleles differ from each other by complex, in-frame rearrangements of short repeated sequence motifs within a single exon. Combining several lines of evidence, we previously hypothesized that potato cyst nematodes use developmentally-programmed mutations, or editing, to diversify HYP1 alleles in the soma. In the current work, we now test this hypothesis. We employ highly accurate long-read DNA sequencing of a simplified genetic system to identify potential rare edited alleles, we use a transgenic yeast system to describe large de novo mutations at HYP1, and we interpret our findings in light of key population genetic parameters as well as the genetic diversity surrounding HYP1 and across the genome.

Animals↗