{"title":"Exploring the Root Response to Multiple Stressors: Mechanisms Underlying Kiwifruit Vine Decline Syndrome (KVDS) Development.","authors":"Micol Guaschino, Heidi Hargarten, Christopher Cook, Huiting Zhang, Loren Honaas, Tracey Somera, Davide Spadaro","doi":"10.1094/MPMI-02-26-0017-R","DOIUrl":"https://doi.org/10.1094/MPMI-02-26-0017-R","url":null,"abstract":"<p><p>First reported in Italy in 2012, Kiwifruit Vine Decline Syndrome (KVDS) has emerged as a major threat to <i>Actinidia deliciosa</i> vines in the Mediterranean region, significantly impacting kiwifruit production. Infection with biotic agents alone (e.g., <i>Phytopythium vexans</i>) has proven insufficient to reproduce KVDS symptoms, with studies suggesting root flooding as a key factor in KVDS development. To date, research has provided insights into the response of <i>A. deliciosa</i> to individual stress factors; however, little is known about how these plants cope with stress combinations. We characterized the transcriptome response of <i>Actinidia deliciosa</i> cv. Hayward over time under biotic stress (inoculation with <i>P. vexans</i>), abiotic stress (root flooding), and their combination, mimicking KVDS development. This study reveals that although typical flooding responses (e.g., anaerobic metabolism shift, ethylene signaling) were present under combined stress, the overall transcriptomic profile was distinct and not predictable from individual stress responses. Notably, in the presence of flooding key biotic defense mechanisms were suppressed, including phenylpropanoid biosynthesis and auxin signaling, despite their upregulation during infection with <i>P. vexans</i> alone. These results suggest that KVDS may involve an interaction between stressors, in which abiotic stress responses could come at the cost of plant defense mechanisms.</p>","PeriodicalId":19009,"journal":{"name":"Molecular Plant-microbe Interactions","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ryan Gourlie, Megan C McDonald, Mohamed Hafez, Reem Aboukhaddour
{"title":"The Virulence Gene <i>ToxB</i> Is Both Amplified and Disrupted by Transposons in the Wheat Pathogen <i>Pyrenophora tritici-repentis</i>.","authors":"Ryan Gourlie, Megan C McDonald, Mohamed Hafez, Reem Aboukhaddour","doi":"10.1094/MPMI-01-26-0003-R","DOIUrl":"https://doi.org/10.1094/MPMI-01-26-0003-R","url":null,"abstract":"<p><p>Mechanisms that drive virulence gene duplication in plant pathogenic fungi remain poorly understood. In <i>Pyrenophora tritici-repentis</i> (<i>Ptr</i>), responsible for tan spot of wheat, <i>ToxB</i> is a multicopy virulence gene encoding a proteinaceous necrotrophic effector. <i>ToxB</i> exhibits a virulence dosage effect, where higher copy numbers are associated with increased disease severity. In this work, we sought to resolve a 25-year old question as to what drove the proliferation of <i>ToxB</i> within <i>Ptr</i>. To investigate this, 23 long-read assemblies were generated and analyzed from a collection of globally distributed isolates with various <i>ToxB</i> copy numbers, with a specific focus on regions containing <i>ToxB</i>. Extensive comparative alignments identified a Helitron-like element, <i>ToxB-HLE</i>, that appears to be driving the duplication of <i>ToxB</i> in an accessory region of chromosome 4. This region is entirely absent in isolates lacking <i>ToxB</i> or its nonfunctional homolog <i>toxb</i>. In addition to gene amplification by transposons, multiple independent transposon insertion events were identified in several isolates that disrupted the <i>ToxB</i> open reading frame creating inactive <i>toxb</i> haplotypes. This study provides strong evidence supporting the hypothesis that transposons play dual roles in the rapid evolution of fungal pathogenicity by both amplifying and disrupting a key virulence gene in a globally distributed plant pathogen.</p>","PeriodicalId":19009,"journal":{"name":"Molecular Plant-microbe Interactions","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katerina L Holan, Nicole C Thunes, Lori M Lincoln, Amy Wright, Brian Diers, Ricardo V Abdelnoor, Jamie A O'Rourke, Steven A Whitham, Kerry F Pedley, Michelle A Graham
{"title":"<i>Rpp2</i> Encodes a TIR-NBS-WH-LRR Protein That Confers Resistance to <i>Phakopsora pachyrhizi</i> in Soybean.","authors":"Katerina L Holan, Nicole C Thunes, Lori M Lincoln, Amy Wright, Brian Diers, Ricardo V Abdelnoor, Jamie A O'Rourke, Steven A Whitham, Kerry F Pedley, Michelle A Graham","doi":"10.1094/MPMI-02-26-0013-R","DOIUrl":"https://doi.org/10.1094/MPMI-02-26-0013-R","url":null,"abstract":"<p><p>The obligate biotrophic fungus <i>Phakopsora pachyrhizi</i> Syd. & P. Syd., the causal agent of soybean rust, is among the most formidable pathogens of soybean (<i>Glycine max</i> [L.] Merr.). The pathogen is now established in all major soybean growing areas of the world and presents a significant impediment to global soybean production. Most soybean germplasm is susceptible, enabling the fungus to penetrate and colonize the leaf tissue, causing tan-colored necrotic lesions to form at the site of infection. Severe infection reduces photosynthesis and causes premature defoliation, which ultimately decreases crop yield and seed quality. Eight genetic loci, <i>Rpp1/Rpp1b</i> to <i>Rpp7</i> and <i>Rpp6907</i>, that confer race-specific resistance to <i>P. pachyrhizi</i> (<i>Rpp</i>) have been identified. <i>Rpp2</i> was identified and characterized in the soybean accession PI 230970 and fine-mapped to a 188.1 kb interval on chromosome 16, a region predicted to contain several toll/interleukin-1 receptor nucleotide-binding leucine-rich repeat (TIR-NLR) genes. To identify <i>Rpp2</i>, we constructed a bacterial artificial chromosome (BAC) library from the resistant soybean accession PI 230970. Sequencing BACs that span the <i>Rpp2</i> locus identified fourteen candidate genes with homology to the TIR-NLR family of resistance genes with integrated winged-helix (WH) domains. Of these, seven are predicted to encode full-length R proteins. Co-silencing the <i>Rpp2</i> candidate genes compromised resistance in soybean accession PI 230970. Gene expression analysis suggests that a single gene, <i>Rpp2C7_PI</i>, which shares greatest homology to <i>Rpp2C6_Wms82</i> (Glyma.16G136600) in the Williams 82 reference genome, is responsible for <i>Rpp2</i>-mediated resistance.</p>","PeriodicalId":19009,"journal":{"name":"Molecular Plant-microbe Interactions","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}