Phytopathology最新文献

Cercospora leaf spot, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugarbeet worldwide. Resistance to the sterol demethylation inhibitor (DMI) fungicide tetraconazole has been previously correlated with synonymous and nonsynonymous mutations in CbCyp51. Here, we extend these analyses to the DMI fungicides prothioconazole, difenoconazole, and mefentrifluconazole in addition to tetraconazole to confirm whether the synonymous and nonsynonymous mutations at amino acid positions 144 and 170 are associated with resistance to these fungicides. Nearly half of the 593 isolates of C. beticola collected in the Red River Valley of North Dakota and Minnesota in 2021 were resistant to all four DMIs. Another 20% were resistant to tetraconazole and prothioconazole but sensitive to difenoconazole and mefentrifluconazole. A total of 13% of isolates were sensitive to all DMIs tested. We found five CbCyp51 haplotypes and associated them with phenotypes to the four DMIs. The most predominant haplotype (E170_A/L144F_C) correlated with resistance to all four DMIs with up to 97.6% accuracy. The second most common haplotype (E170_A/L144) consisted of isolates associated with resistance phenotypes to tetraconazole and prothioconazole while also exhibiting sensitive phenotypes to difenoconazole and mefentrifluconazole with up to 98.4% accuracy. Quantitative PCR did not identify differences in CbCyp51 expression between haplotypes. This study offers an understanding of the importance of codon usage in fungicide resistance and provides crop management acuity for fungicide application decision-making.

Methods for causal inference from observational data are common in human disease epidemiology and social sciences but are used relatively little in plant pathology. We draw upon an extensive data set of the incidence of hop plants with powdery mildew (caused by Podosphaera macularis) collected from yards in Oregon from 2014 to 2017 and associated metadata on grower cultural practices, cultivar susceptibility to powdery mildew, and pesticide application records to understand variation in and causes of growers' fungicide use and associated costs. An instrumental causal forest model identified growers' spring pruning thoroughness, cultivar susceptibility to two of the dominant pathogenic races of P. macularis, network centrality of yards during May-June and June-July time transitions, and the initial strain of the fungus detected as important variables determining the number of pesticide active constituents applied by growers and the associated costs they incurred in response to powdery mildew. Exposure-response function models fit after covariate weighting indicated that both the number of pesticide active constituents applied and their associated costs scaled linearly with the seasonal mean incidence of plants with powdery mildew. Although the causes of pesticide use intensity are multifaceted, biological and production factors collectively influence the incidence of powdery mildew, which has a direct exposure-response relationship with the number of pesticide active constituents that growers apply and their costs. Our analyses point to several potential strategies for reducing pesticide use and costs for management of powdery mildew on hop. We also highlight the utility of these methods for causal inference in observational studies.

Soybean cyst nematode (SCN, Heterodera glycines) is most effectively managed through planting resistant soybean cultivars, but the repeated use of the same resistance sources has led to a widespread emergence of virulent SCN populations that can overcome soybean resistance. Resistance to SCN HG type 0 (Race 3) in soybean cultivar Forrest is mediated by an epistatic interaction between the soybean resistance genes rhg1-a and Rhg4. We previously developed two SCN inbred populations by mass-selecting SCN HG type 0 (Race 3) on susceptible and resistant recombinant inbred lines, derived from a cross between Forrest and the SCN-susceptible cultivar Essex, which differ for Rhg4. To identify SCN genes potentially involved in overcoming rhg1-a/Rhg4-mediated resistance, we conducted RNA sequencing on early parasitic juveniles of these two SCN inbred populations infecting their respective hosts, only to discover a handful of differentially expressed genes (DEGs). However, in a comparison with early parasitic juveniles of an avirulent SCN inbred population infecting a resistant host, we discovered 59 and 171 DEGs uniquely up- or downregulated in virulent parasitic juveniles adapted on the resistant host. Interestingly, the proteins coded by these 59 DEGs included vitamin B-associated proteins (reduced folate carrier, biotin synthase, and thiamine transporter) and nematode effectors known to play roles in plant defense suppression, suggesting that virulent SCN may exert a heightened transcriptional response to cope with enhanced plant defenses and an altered nutritional status of a resistant soybean host. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

California is the primary processing tomato (Solanum lycopersicum) producer in the United States. Fusarium oxysporum f. sp. lycopercisi race 3 (Fol3), the cause of Fusarium wilt, is a major driver of yield losses. Fol3 has recently been observed causing disease in resistant cultivars (I-3 R-gene), often reported in association with high soil salinity. This study was undertaken to better understand the role of salinity in compromising resistance-based management of Fol3. Surveys established opportunity for salinity-Fol3-tomato interactions in 44% of commercial fields examined, with harmful soil salt levels up to 3.6 dS/m (P < 0.001), high sodium (P < 0.001), and high sodicity (sodium adsorption ratio > 13; P < 0.001). In controlled field studies of Fol3 in NaCl/CaCl₂-treated soil, Fol3-resistant cultivars either only developed wilt under salt or only developed wilt above the industry non-hybrid threshold (2%) under salt across two trial years. The absence of yield differences indicates low to no economic impact of disease enhancement (P > 0.05). NaCl, CaCl₂, and Na₂SO₄ had no effect on Fol3 propagule production in liquid agar versus water agar controls (P > 0.05), although CaCl₂ increased propagule loads sevenfold versus ionic controls (polyethylene glycol) (P = 0.036). NaCl/CaCl₂ (2:1) reduced propagule loads up to 65% versus no salt (P = 0.029) in soil with pathogen-infested tomato tissue. These results together establish the opportunity for salinity-Fol3-tomato interactions and potential for salt to influence the efficacy of resistant cultivar-based management-this does not appear to be primarily due to salt enhancement of pathogen populations, pointing to a yet-unexplored direct influence of salt on host resistance.

Bursaphelenchus xylophilus (pine wood nematode, PWN), a migratory plant-parasitic nematode, acts as an etiological agent, inflicting considerable damage to pine forests worldwide. Plant immunity constitutes a crucial factor in resisting various pathogenic invasions. The primary defensive responses of host pines against PWN infection encompass terpene accumulation, defense response-related gene expression, and programmed cell death. Venom allergen-like proteins (VAPs), as potential effectors, are instrumental in facilitating the successful colonization of PWNs. In this study, we investigated the inhibition of B. xylophilus VAP (BxVAP1) expression by RNA interference in vitro. Following BxVAP1 silencing, the reproduction rate and migration rate of the PWN population in Pinus massoniana decreased, the expression of the α-pinene synthase gene was induced, other terpene synthase and pathogenesis-related genes were inhibited and delayed, the peak times and levels of terpene-related substances were changed, and the degree of cavitation in P. massoniana was diminished. Transient expression of BxVAP1 in Nicotiana benthamiana revealed that BxVAP1 was expressed in both the cell membrane and nucleus, inducing programmed cell death and the expression of pathogen-associated molecular pattern-triggered immunity marker genes (NbAcre31 and NbPTI5). This study is the first to demonstrate that silencing the BxVAP1 gene affects host defense responses, including terpenoid metabolism in P. massoniana, and that BxVAP1 can be recognized by N. benthamiana as an effector to trigger its innate immunity, expanding our understanding of the parasitic mechanism of B. xylophilus.

Epidemiological studies to better understand wheat blast (WB) spatial and temporal patterns were conducted in three field environments in Bolivia between 2019 and 2020. The temporal dynamics of wheat leaf blast (W_LB) and spike blast (W_SB) were best described by the logistic model compared with the Gompertz and exponential models. The nonlinear logistic infection rates were higher under defined inoculation in experiments two and three than under undefined inoculation in experiment one, and they were also higher for W_SB than for W_LB. The onset of W_LB began with a spatial clustering pattern according to autocorrelation analysis and Moran's index values, with higher severity and earlier onset for defined than for undefined inoculation until the last sampling time. The W_SB onset did not start with a spatial clustering pattern; instead, it was detected later until the last sampling date across experiments, with higher severity and earlier onset for defined than for undefined inoculation. Maximum severity (K_max) was 1.0 for W_SB and less than 1.0 for W_LB. Aggregation of W_LB and W_SB was higher for defined than for undefined inoculation. The directionality of hotspot development was similar for both W_LB and W_SB, mainly occurring concentrically for defined inoculation. Our results show no evidence of synchronized development but suggest a temporal and spatial progression of disease symptoms on wheat leaves and spikes. Thus, we recommend that monitoring and management of WB should be considered during early growth stages of wheat planted in areas of high risk.

The bacterial canker of kiwifruit caused by Pseudomonas syringae pv. actinidiae (Psa) is the most devastating disease threatening the global kiwifruit production. This pathogen delivers multiple effector proteins into plant cells to resist plant immune responses and facilitate their survival. Here, we focused on the unique effector HopZ5 in Psa, which previously has been reported to have virulence functions. In this study, our results showed that HopZ5 could cause macroscopic cell death and trigger a serious immune response by agroinfiltration in Nicotiana benthamiana, along with upregulated expression of immunity-related genes and significant accumulation of reactive oxygen species and callose. Subsequently, we confirmed that HopZ5 interacted with the phosphoserine-binding protein GF14C in both the nonhost plant N. benthamiana (NbGF14C) and the host plant kiwifruit (AcGF14C), and silencing of NbGF14C compromised HopZ5-mediated cell death, suggesting that GF14C plays a crucial role in the detection of HopZ5. Further studies showed that overexpression of NbGF14C both markedly reduced the infection of Sclerotinia sclerotiorum and Phytophthora capsica in N. benthamiana, and overexpression of AcGF14C significantly enhanced the resistance of kiwifruit against Psa, indicating that GF14C positively regulates plant immunity. Collectively, our results revealed that the virulence effector HopZ5 could be recognized by plants and interact with GF14C to activate plant immunity.

Wheat powdery mildew (WPM) is one of the most devasting diseases that affects wheat yield worldwide. Few efforts have been made to control such a serious disease. An effective way to control WPM is urgently needed. Biological control is an effective way to control plant diseases worldwide. In this study, the efficiency of three different Trichoderma spp. in controlling WPM at the seedling growth stage was tested using 35 highly diverse wheat genotypes. Highly significant differences were found in WPM resistance among the four treatments, confirming the efficiency of Trichoderma in controlling WPM. Of the three species, T. asperellum T34 (T34) was the most effective species in controlling WPM, as it reduced the symptoms by 50.56%. A set of 196 wheat genotypes was used to identify the genetic control of the WPM resistance induced by T34. A total of 39, 27, and 18 gene models were identified to contain the significant markers under Pm, T34, and the improvement in powdery mildew resistance due to T34 (T34_improvement) conditions. Furthermore, no gene model was common between T34 and Pm, suggesting the presence of completely different genetic systems controlling the resistance under T34 and Pm. The functional annotation and biological process pathways of the detected gene models confirm their association with the normal and induced resistance. This study, for the first time, confirms the efficiency of T34 in controlling WPM and provides a deep understanding of the genetic control of induced and normal resistance to WPM.

Although resistant cultivars are valuable in safeguarding crops against diseases, they can be rapidly overcome by pathogens. Numerous strategies have been proposed to delay pathogen adaptation (evolutionary control) while still ensuring effective protection (epidemiological control). For perennial crops, multiple resistance genes can be deployed (i) in the same cultivar (pyramiding strategy); in single-gene-resistant cultivars grown (ii) in the same field (mixture strategy) or (iii) in different fields (mosaic strategy); or (iv) in hybrid strategies that combine the three previous options. In addition, the spatial scale at which resistant cultivars are deployed can affect the plant-pathogen interaction: Small fields are thought to reduce pest density and disease transmission. Here, we used the spatially explicit stochastic model landsepi to compare the evolutionary and epidemiological control across spatial scales and deployment strategies relying on two major resistance genes. Our results, broadly focused on resistance to downy mildew of grapevine, show that the evolutionary control provided by the pyramiding strategy is at risk when single-gene-resistant cultivars are concurrently planted in the landscape (hybrid strategies), especially at low mutation probability. Moreover, the effectiveness of pyramiding compared with hybrid strategies is influenced by whether the adapted pathogen pays a fitness cost across all hosts or only for unnecessary virulence, particularly when the fitness cost is high rather than intermediate. Finally, field size did not affect model outputs for a wide range of mutation probabilities and associated fitness costs. The socioeconomic policies favoring the adoption of optimal resistant management strategies are discussed.

Exserohilum turcicum is a devastating fungal pathogen that infects both maize and sorghum, leading to severe leaf diseases of the two crops. According to host specificity, pathogenic isolates of E. turcicum are divided into two formae speciales, namely E. turcicum f. sp. zeae and E. turcicum f. sp. sorghi. To date, the molecular mechanism underlying the host specificity of E. turcicum is marginally known. In this study, the whole genomes of 60 E. turcicum isolates collected from both maize and sorghum were resequenced, which enabled identification of 233,022 single-nucleotide polymorphisms (SNPs) in total. Phylogenetic analysis indicated that all isolates are clustered into four genetic groups that have a close relationship with host source. This observation is validated by the result of principal component analysis. Analysis of population structure revealed that there is obvious genetic differentiation between two populations from maize and sorghum. Further analysis showed that 5,431 SNPs, including 612 nonsynonymous SNPs, are completely co-segregated with the host source. These nonsynonymous SNPs are located in 539 genes, among which 18 genes are predicted to encode secretory proteins, including six putative effector genes named SIX13-like, Ecp6, GH12, GH28-1, GH28-2, and CHP1. Sequence polymorphism analysis revealed various numbers of SNPs in the coding regions of these genes. These findings provide new insights into the molecular basis of host specificity in E. turcicum.