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Powdery mildew, caused by Podosphaera macularis, is one of the most important diseases of hop in the Pacific Northwest of the United States. Resistant cultivars exist; however, recently, the pathogen has overcome two sources of resistance in popular cultivars. Breeding for new, emerging races of the pathogen is thus a continuing priority. We used RNA-seq to understand gene expression trends in a resistant (cv. USDA Nugget) and a susceptible (cv. Symphony) hop cultivar along a time series following inoculation. We found stronger transcriptional reprogramming in the resistant cultivar than the susceptible cultivar. Transcripts that increased in expression within 12 h post-inoculation in the resistant cultivar included genes in the jasmonic acid biosynthesis pathway, as well as phenylpropanoid biosynthesis. Transcripts that had a positive correlation with time post-inoculation in the resistant cultivar included genes involved in phosphorylation, cell-surface signaling pathways, and response to jasmonic acid. We used untargeted HPLC–HR-MS/MS analysis and confirmed an increase in jasmonic acid and several phenolic compounds. We hypothesize that resistance to powdery mildew in cv. Nugget may be at least partially due to perception of the pathogen outside of the cell, and transcriptional and metabolic reprogramming is mediated by jasmonic acid signaling. At least part of that transcriptional and metabolic reprogramming involves changes to lignin production, which might reinforce the cell wall. The multi-omics approach to describe the contrasting responses of a resistant and a susceptible hop cultivar following inoculation with this important pathogen may indicate new strategies for developing resistant germplasm and control methods. [Figure: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Verticillium wilt is one of the most devastating soilborne diseases in lettuce, and the use of host resistance is the most optimal choice for its management. This study focused on identifying and mapping the genetic loci for resistance against Verticillium dahliae race 3 in a mapping population of 200 F2:3 families developed from a cross between moderately resistant red-leaf lettuce ‘Sentry’ and susceptible green-leaf lettuce ‘La Brillante’. The population was genotyped using the tunable genotyping-by-sequencing (tGBS) approach. An ultra-high-density genetic linkage map containing 34,838 single nucleotide polymorphism markers grouped into 1,734 bins was constructed using F2 progeny and a sliding window approach. Three quantitative trait loci (QTLs) for resistance to V. dahliae race 3 were located on linkage groups (LGs) LG 2 (qVR3-2.1) and LG 4 (qVR3-4.1 and qVR3-4.2). Each of these QTLs explained up to ∼10% of the total phenotypic variation for the trait. At each locus, the resistance alleles were derived from cultivar Sentry that is partially resistant to the pathogen. Additional loci resistant to the disease are expected in this population, and transgressive segregation indicates that some of those loci could originate from the susceptible cultivar La Brillante. In addition, two QTLs for plant development were identified on LG 2 (qIPD-2.1) and LG 7 (qIPD-7.1), although no relationship was detected between resistance in these genotypes and the rate of plant growth. A major effect of QTL for red leaf color was detected on LG 9 (qRLC-9.1). Candidate genes linked to some of the QTLs for V. dahliae race 3 resistance, plant development, and leaf color were identified. The QTLs for resistance identified in Sentry could diversify the resistance gene pool and provide an alternative tool to manage a newly emerged V. dahliae race 3. [Figure: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Verticillium wilt (VW) is a destructive disease in cotton caused by Verticillium dahliae and has a significant impact on yield and quality. In the absence of safe and effective chemical control, VW is difficult to manage. Thus, at present, developing resistant varieties is the most economical and effective method of controlling Verticillium wilt of cotton. The CC-NBS-LRR (CNL) gene family is an important class of plant genes involved in disease resistance. This study identified 141 GbCNLs in Gossypium barbadense genome, with 37.5% (53 genes) GbCNLs enriched in 12 gene clusters (GC01–GC12) based on gene distribution in the chromosomes. Especially, seven GbCNLs from two largest clusters (GC11 and GC12) were significantly upregulated in the resistant cultivar (Hai No. 7124) and the susceptible (Giza No. 57). Virus-induced gene silencing of GbCNL130 in G. barbadense, one typical gene in the gene cluster 12 (GC12), significantly altered the response to VW, compromising plant resistance to V. dahliae. In contrast, GbCNL130 overexpression significantly increased the resistance to VW in the wild-type Arabidopsis thaliana. Based on our research findings presented here, we conclude that GbCNL130 promotes resistance to VW by activating the salicylic acid (SA)-dependent defense response pathway resulting in strong accumulation of reactive oxygen species and upregulation of pathogenesis-related (PR) genes. In conclusion, our study resulted in the discovery of a new CNL resistance gene in cotton, GbCNL130, that confers resistance to VW across different hosts.

Soilborne plant pathogenic species in the fungal genus Verticillium cause destructive Verticillium wilt disease on economically important crops worldwide. Since R gene-mediated resistance is only effective against race 1 of V. dahliae, fortification of plant basal resistance along with cultural practices are essential to combat Verticillium wilts. Plant hormones involved in cell signaling impact defense responses and development, an understanding of which may provide useful solutions incorporating aspects of basal defense. In this review, we examine the current knowledge of the interplay between plant hormones, salicylic acid, jasmonic acid, ethylene, brassinosteroids, cytokinin, gibberellic acid, auxin, and nitric oxide, and the defense responses and signaling pathways that contribute to resistance and susceptibility in Verticillium-host interactions. Though we make connections where possible to non-model systems, the emphasis is placed on Arabidopsis-V. dahliae and V. longisporum interactions since much of the research on this interplay is focused on these systems. An understanding of hormone signaling in Verticillium-host interactions will help to determine the molecular basis of Verticillium wilt progression in the host and potentially provide insight on alternative approaches for disease management.

Abstract microRNAs are powerful regulators of growth, development, and stress responses in plants. The Arabidopsis thaliana microRNA miR167 was previously found to regulate diverse processes including flower development, root development, and response to osmotic stress by controlling the patterns of expression of its target genes AUXIN RESPONSE FACTOR 6 (ARF6), ARF8, and IAA‐Ala RESISTANT 3. Here, we report that miR167 also modulates defense against pathogens through ARF6 and ARF8. miR167 is differentially expressed in response to the bacterial pathogen Pseudomonas syringae, and overexpression of miR167 confers very high levels of resistance. This resistance appears to be due to suppression of auxin responses and is partially dependent upon salicylic acid signaling, and also depends upon altered stomatal behavior in these plants. Closure of stomata upon the detection of P. syringae is an important aspect of the basal defense response, as it prevents bacterial cells from entering the leaf interior and causing infection. Plants overexpressing miR167 constitutively maintain small stomatal apertures, resulting in very high resistance when the pathogen is inoculated onto the leaf surface. Additionally, the systemic acquired resistance (SAR) response is severely compromised in plants overexpressing miR167, in agreement with previous work showing that the activation of SAR requires intact auxin signaling responses. This work highlights a new role for miR167, and also emphasizes the importance of hormonal balance in short‐ and long‐term defense and of stomata as an initial barrier to pathogen entry.

Cotton is an important economic crop worldwide. Verticillium wilt (VW) caused by Verticillium dahliae (V. dahliae) is a serious disease in cotton, resulting in massive yield losses and decline of fiber quality. Breeding resistant cotton cultivars is an efficient but elaborate method to improve the resistance of cotton against V. dahliae infection. However, the functional mechanism of several excellent VW resistant cotton cultivars is poorly understood at present. In our current study, we carried out RNA-seq to discover the differentially expressed genes (DEGs) in the roots of susceptible cotton Gossypium hirsutum cultivar Junmian 1 (J1) and resistant cotton G.hirsutum cultivar Liaomian 38 (L38) upon Vd991 inoculation at two time points compared with the mock inoculated control plants. The potential function of DEGs uniquely expressed in J1 and L38 was also analyzed by GO enrichment and KEGG pathway associations. Most DEGs were assigned to resistance-related functions. In addition, resistance gene analogues (RGAs) were identified and analyzed for their role in the heightened resistance of the L38 cultivar against the devastating Vd991. In summary, we analyzed the regulatory network of genes in the resistant cotton cultivar L38 during V. dahliae infection, providing a novel and comprehensive insight into VW resistance in cotton.

The proteins with lysin motif (LysM) are carbohydrate-binding protein modules that play a critical role in the host-pathogen interactions. The plant LysM proteins mostly function as pattern recognition receptors (PRRs) that sense chitin to induce the plant’s immunity. In contrast, fungal LysM blocks chitin sensing or signaling to inhibit chitin-induced host immunity. In this review, we provide historical perspectives on plant and fungal LysMs to demonstrate how these proteins are involved in the regulation of plant’s immune response by microbes. Plants employ LysM proteins to recognize fungal chitins that are then degraded by plant chitinases to induce immunity. In contrast, fungal pathogens recruit LysM proteins to protect their cell wall from hydrolysis by plant chitinase to prevent activation of chitin-induced immunity. Uncovering this coevolutionary arms race in which LysM plays a pivotal role in manipulating facilitates a greater understanding of the mechanisms governing plant-fungus interactions.

Cysteine-rich receptor-like kinases (CRKs) are a large subfamily of plant receptor-like kinases that play a critical role in disease resistance in plants. However, knowledge about the CRK gene family in cotton and its function against Verticillium wilt (VW), a destructive disease caused by Verticillium dahliae that significantly reduces cotton yields is lacking. In this study, we identified a total of 30 typical CRKs in a Gossypium barbadense genome (GbCRKs). Eleven of these (>30%) are located on the A06 and D06 chromosomes, and 18 consisted of 9 paralogous pairs encoded in the A and D subgenomes. Phylogenetic analysis showed that the GbCRKs could be classified into four broad groups, the expansion of which has probably been driven by tandem duplication. Gene expression profiling of the GbCRKs in resistant and susceptible cotton cultivars revealed that a phylogenetic cluster of nine of the GbCRK genes were up-regulated in response to V. dahliae infection. Virus-induced gene silencing of each of these nine GbCRKs independently revealed that the silencing of GbCRK18 was sufficient to compromise VW resistance in G. barbadense. GbCRK18 expression could be induced by V. dahliae infection or jasmonic acid, and displayed plasma membrane localization. Therefore, our expression analyses indicated that the CRK gene family is differentially regulated in response to Verticillium infection, while gene silencing experiments revealed that GbCRK18 in particular confers VW resistance in G. barbadense.