Wenxin Xue

Myzus persicae (Sulzer) is a globally important agricultural pest and a vector of numerous plant viruses. However, its potential global distribution under future climate change remains insufficiently quantified. In this study, we used 5531 occurrence records, six key bioclimatic variables, and an ENMeval-optimized maximum entropy (MaxEnt) model to predict the global habitat suitability of M. persicae. Predictions were made under current climatic conditions and two future Shared Socioeconomic Pathway (SSP) scenarios, SSP1-2.6 (SSP126) and SSP5-8.5 (SSP585), for the 2030s and 2050s. The model showed acceptable discriminatory performance, with a mean training AUC of 0.853, while four-fold spatial block validation produced a mean validation AUC of 0.874 ± 0.044. The mean temperature of the coldest quarter (Bio11) was the most influential predictor, showing a strong association between winter temperature and the predicted suitability of M. persicae. Under current climatic conditions, highly suitable habitats were concentrated mainly in temperate and subtropical agricultural regions. Future projections indicated an overall expansion of suitable habitats and a general tendency toward higher latitudes, with the greatest expansion of highly suitable habitat occurring under SSP126 in the 2050s. Conversely, suitability declined in some tropical and subtropical regions, suggesting that stronger warming may partly offset suitability gains at lower latitudes. These findings suggest that the projected changes in the climatic suitability of M. persicae may not be proportional to warming intensity and may inform global potential climatic risk assessment and climate-adaptive pest management.

Under global warming, the frequency and severity of agricultural pest outbreaks have intensified, posing serious threats to agriculture. The green peach aphid ( Myzus persicae (Hemiptera: Aphididae)), an important agricultural pest, exhibits green and red color morphs and differentiated thermal tolerance, yet the underlying molecular mechanisms remain unclear. In this study, based on transcriptome and 16S rDNA amplicon sequencing, we analyzed the gene expression patterns and microbial community dynamics of green and red morphs of M. persicae under high-temperature stresses (30 °C and 35 °C) and across different exposure durations, comparing their similarities and differences in heat-response processes. Principal component analysis of transcriptomic data indicated that temperature had a greater influence on the physiological responses of M. persicae than body color, with a more pronounced effect observed at 35 °C. Differential gene expression analysis revealed overlap in temperature-responsive genes but different response patterns between the two morphs, suggesting activation of divergent molecular response mechanisms. Genes encoding heat shock proteins, detoxification-related enzymes, ribosomal protein family and so on were significantly up-regulated under high temperature, with a more pronounced induction in the green morph, indicating morph-specific regulatory strategies in response to thermal stress. Moreover, 16S rDNA sequencing revealed that the primary symbiont Buchnera displayed different relative abundance trends in the green and red morphs, remaining relatively stable in the red morph but declining markedly in the green morph under heat stress, potentially associated with their variation in thermal tolerance. Collectively, this study elucidates the molecular responses and microbe-mediated regulatory mechanisms underlying thermal tolerance in green and red morphs of M. persicae , providing novel insights into the thermal adaptation of aphids and a theoretical basis for developing pest management strategies under global warming.

Tobacco Mosaic Virus (TMV) and Potato Virus Y (PVY) pose significant threats to crop production. Non-destructive and accurate surveillance is crucial to effective disease control. In this study, we propose the adoption of hyperspectral and machine learning technologies to discern the type and severity of tobacco leaves affected by PVY and TMV infection. Initially, we applied three preprocessing methods – Multivariate Scattering Correction (MSC), Standard Normal Variate (SNV), and Savitzky-Golay smoothing filter (SavGol) – to corrected the leaf full-length spectral sheet data (350-2500nm). Subsequently, we employed two classifiers, support vector machine (SVM) and random forest (RF), to establish supervised classification models, including binary classification models (healthy/diseased leaves or PVY/TMV infected leaves) and six-class classification models (healthy and various severity levels of diseased leaves). Based on the core evaluation index, our models achieved accuracies in the range of 91–100% in the binary classification. In general, SVM demonstrated superior performance compared to RF in distinguishing leaves infected with PVY and TMV. Different combinations of preprocessing methods and classifiers have distinct capabilities in the six-class classification. Notably, SavGol united with SVM gave an excellent performance in the identification of different PVY severity levels with 98.1% average precision, and also achieved a high recognition rate (96.2%) in the different TMV severity level classifications. The results further highlighted that the effective wavelengths captured by SVM, 700nm and 1800nm, would be valuable for estimating disease severity levels. Our study underscores the efficacy of integrating hyperspectral technology and machine learning, showcasing their potential for accurate and non-destructive monitoring of plant viral diseases.

The devastating impact of chemical pesticides has prompted a shift towards sustainable agricultural pest management, such as biological control with natural enemies. In recent years, commercialization advancements have enabled the suppression of pest populations through augmentative releases of biological control agents, with natural enemies being a major tactic. China has successfully implemented natural-enemy-based biocontrol strategies, particularly for controlling aphids and lepidopterans. This article provides a comprehensive overview of the state-of-the-art natural-enemy-based biocontrol against arthropod pests in tobacco in China, including practical achievements in mass-rearing methods, augmentative release strategies, and the wide-scale use of natural enemies. Current and potential future challenges for natural-enemy-based biocontrol in China are also discussed.

Pesticide resistance relies on a myriad of mechanisms, ranging from single mutations to a complex and polygenic architecture, and it involves mechanisms such as target-site insensitivity, metabolic detoxification, or a combination of these, with either additive or synergistic effects. Several resistance mechanisms against abamectin, a macrocyclic lactone widely used in crop protection, have been reported in the cosmopolitan pest Tetranychus urticae . However, it has been shown that a single mechanism cannot account for the high levels of abamectin resistance found across different mite populations. Here, we used experimental evolution combined with bulked segregant analyses to map quantitative trait loci (QTL) associated with abamectin resistance in two genetically unrelated strains of T. urticae . In these two independent QTL mapping experiments, three and four QTLs were identified, of which three were shared between experiments. Shared QTLs contained genes encoding subunits of the glutamate-gated chloride channel (GluCl) and harboured previously reported mutations, including G314D in GluCl1 and G326E in GluCl3 , but also novel resistance candidate loci, including DNA helicases and chemosensory receptors. Surprisingly, the fourth QTL, present only in only one of the experiments and thus unique for one parental resistant strain, revealed a non-functional variant of GluCl2 , suggesting gene knock-out as resistance mechanism. Our study uncovers the complex basis of abamectin resistance, and it highlights the intraspecific diversity of genetic mechanisms underlying resistance in a cosmopolitan pest.

BACKGROUND: Mitochondrial Electron Transport Inhibitors of complex I (METI‐I), such as tebufenpyrad and fenpyroximate, are acaricides that have been used extensively to control Tetranychus urticae Koch (Acari: Tetranychidae) for more than 20 years. Because of the ability of this spider mite to rapidly develop acaricide resistance, field (cross‐) resistance monitoring and elucidation of resistance mechanisms are extremely important for resistance management (RM). In the present study, 42 European T. urticae field populations were screened for tebufenpyrad and fenpyroximate resistance, and the correlation between resistance and the H92R substitution in PSST was investigated.RESULTS: According to the calculated lethal concentration values that kill 90% of the population (LC₉₀), tebufenpyrad and fenpyroximate would fail to control many of the collected populations at recommended field rates. Six populations exhibited high to very high resistance levels (200‐ to over 1950‐fold) to both METI‐Is. Analysis based on the LC₅₀ values displayed a clear correlation between tebufenpyrad and fenpyroximate resistance, further supporting cross‐resistance, which is of great operational importance in acaricide RM. The previously uncovered METI‐I target‐site mutation H92R in the PSST homologue of complex I (NADH:ubiquinone oxidoreductase) was found with high allele frequencies in populations resistant to tebufenpyrad and fenpyroximate. Synergist assays showed this mutation is not the only factor involved in METI‐I resistance and additive or synergistic effects of multiple mechanisms most likely determine the phenotypic strength.CONCLUSIONS: The predictive value of resistance by H92R is very high in European populations and offers great potential to be used as a molecular diagnostic marker for METI‐I resistance. © 2022 Society of Chemical Industry.

Several genetic variants of the cd1- and ef-helices of the Q_o site of mitochondrial cytochrome b have been associated with bifenazate resistance in the spider mite Tetranychus urticae, an important crop pest around the world. Maternal inheritance of bifenazate resistance has provided strong evidence for the involvement of many of these mutations alone or in combination. A number of populations highly resistant to bifenazate were uncovered that carried the G126S substitution in combination with other target-site mutations. This G126S mutation has therefore been investigated in several studies in the context of resistance evolution and the development of diagnostic markers. However, experimental data that link bifenazate resistance with the presence of the G126S mutation without additional cd1- and ef-helices mutations, remain very limited. Here, we genotyped 38 T. urticae field populations for cytochrome b and uncovered nine field populations with a fixed or segregating G126S substitution without other target-site mutations in the conserved cd1- and ef-helices of the cytochrome b Q_o pocket. Toxicity bioassays showed that all nine field populations were very susceptible to bifenazate, providing strong evidence that G126S alone does not confer bifenazate resistance. These findings also implicate that previous T. urticae populations with G126S found to be low to moderately resistant to bifenazate, evolved alternative mechanisms of resistance, and more importantly, that this mutation cannot be used as a molecular diagnostic for bifenazate resistance.

BACKGROUND: The cys‐loop ligand‐gated ion channels, including the glutamate‐gated chloride channel (GluCl) and GABA‐gated chloride channel (Rdl) are important targets for drugs and pesticides. The macrocyclic lactone abamectin primarily targets GluCl and is commonly used to control the spider mite Tetranychus urticae, an economically important crop pest. However, abamectin resistance has been reported for multiple T. urticae populations worldwide, and in several cases was associated with the mutations G314D in GluCl1 and G326E in GluCl3. Recently, an additional I321T mutation in GluCl3 was identified in several abamectin resistant T. urticae field populations. Here, we aim to functionally validate this mutation and determine its phenotypic strength.RESULTS: The GluCl3 I321T mutation was introgressed into a T. urticae susceptible background by marker‐assisted backcrossing, revealing contrasting results in phenotypic strength, ranging from almost none to 50‐fold. Next, we used CRISPR‐Cas9 to introduce I321T, G314D and G326E in the orthologous Drosophila GluCl. Genome modified flies expressing GluCl I321T were threefold less susceptible to abamectin, while CRISPRed GluCl G314D and G326E flies were lethal. Last, functional analysis in Xenopus oocytes revealed that the I321T mutation might reduce GluCl3 sensitivity to abamectin, but also suggested that all three T. urticae Rdls are affected by abamectin.CONCLUSION: Three different techniques were used to characterize the role of I321T in GluCl3 in abamectin resistance and, combining all results, our analysis suggests that the I321T mutation has a complex role in abamectin resistance. Given the reported subtle effect, additional synergistic factors in resistance warrant more investigation. © 2020 Society of Chemical Industry

BACKGROUND: Milbemectin and abamectin are frequently used to control the spider mite Tetranychus urticae. The development of abamectin resistance in this major pest has become an increasing problem worldwide, potentially compromising the use of milbemectin. In this study, a large collection of European field populations was screened for milbemectin and abamectin resistance, and both target‐site and metabolic (cross‐)resistance mechanisms were investigated.RESULTS: High to very high levels of abamectin resistance were found in one third of all populations, while milbemectin resistance levels were low for most populations. The occurrence of well‐known target‐site resistance mutations in glutamate‐gated chloride channels (G314D in GluCl1 and G326E in GluCl3) was documented in the most resistant populations. However, a new mutation, I321T in GluCl3, was also uncovered in three resistant populations, while a V327G and L329F mutation was found in GluCl3 of one resistant population. A differential gene‐expression analysis revealed the overexpression of detoxification genes, more specifically cytochrome P450 monooxygenase (P450) and UDP‐glycosyltransferase (UGT) genes. Multiple UGTs were functionally expressed, and their capability to glycosylate abamectin and milbemectin, was tested and confirmed.CONCLUSIONS: We found a clear correlation between abamectin and milbemectin resistance in European T. urticae populations, but as milbemectin resistance levels were low, the observed cross‐resistance is probably not of operational importance. The presence of target‐site resistance mutations in GluCl genes was confirmed in most but not all resistant populations. Gene‐expression analysis and functional characterization of P450s and UGTs suggests that also metabolic abamectin resistance mechanisms are common in European T. urticae populations. © 2020 Society of Chemical Industry