Transcriptional Responses of Resistant and Susceptible Wheat Exposed to Wheat Curl Mite.

(1) Background: The wheat curl mite (Aceria tosichella Keifer) is a key pest of wheat (Triticum aestivum L.) worldwide. While a number of wheat cultivars resistant to the mites have been employed to minimize the impact on the yield and quality of grain, little is known regarding the mechanisms underlying host plant resistance. Therefore, the goal of this study was to explore changes in transcriptome of resistant and susceptible wheat in order to quantify the molecular changes that drive host plant resistance. (2) Methods: Two varieties, wheat curl mite-susceptible (Karl 92) and wheat curl mite-resistant (TAM112) wheat, both at 2-week postemergence, were used in this study. Half of the plants were exposed to wheat curl mite herbivory and half remained mite-free and served as controls. Transcriptome changes were quantified using RNA-seq and compared among treatments to identify genes and pathways affected by herbivores. (3) Results: We identified a number of genes and pathways involved in plant defenses against pathogens, herbivores, and abiotic stress that were differentially expressed in the resistant wheat exposed to wheat curl mite herbivory but were unaffected in the susceptible wheat. (4) Conclusions: Our outcomes indicated that resistant wheat counteracts wheat curl mite exposure through effective induction of genes and pathways that enhance its defense responses.

Neonicotinoid Insecticides Alter the Transcriptome of Soybean and Decrease Plant Resistance.

Neonicotinoids are widely used systemic insecticides that have been associated with spider mite outbreaks on diverse plants. These insecticides have complex effects on plant physiology, which have been speculated to drive enhanced performance of spider mites. We used RNA-Seq to explore how neonicotinoids modify gene expression in soybean thereby lowering plant resistance. We exposed soybean (Glycine max L.) to two neonicotinoid insecticides, thiamethoxam applied to seeds and imidacloprid applied as a soil drench, and we exposed a subset of these plants to spider mites (Tetranychus cinnabarinus). Applications of both insecticides downregulated genes involved in plant-pathogen interactions, phytohormone pathways, phenylpropanoid pathway, and cell wall biosynthesis. These effects were especially pronounced in plants exposed to thiamethoxam. Introduction of spider mites restored induction of genes in these pathways in plants treated with imidacloprid, while expression of genes involved in phenylpropanoid synthesis, in particular, remained downregulated in thiamethoxam-treated plants. Our outcomes indicate that both insecticides suppress genes in pathways relevant to plant⁻arthropod interactions, and suppression of genes involved in cell wall synthesis may explain lower plant resistance to spider mites, cell-content feeders. These effects appear to be particularly significant when plants are exposed to neonicotinoids applied to soybean seeds.

Effects of sugarcane aphid herbivory on transcriptional responses of resistant and susceptible sorghum.

BACKGROUND: Sugarcane aphid (Melanaphis sacchari) outbreaks in sorghum that were first reported in 2013 are now the most significant threat to this crop in all major sorghum production areas in the U.S. The outcomes of interactions between sugarcane aphid and sorghum and thus the severity of the outbreaks depend on sorghum genotype and potentially also on the phenology of sorghum. Mechanisms underlying these interactions are not known, however. Thus, the goal of this research was to characterize transcriptional changes in a commercially available resistant and a susceptible genotype of sorghum at 2- and 6-wk post-emergence exposed to M. sacchari herbivory. The effects of sorghum age and genotype on the daily change in aphid densities were also evaluated in separate greenhouse experiments. RESULTS: A higher number of diffentially expressed genes (DEGs) was recovered from the 2-wk plants exposed to aphid herbivory compared to the 6-wk plants across genotypes. Further, gene ontology and pathway analysis indicated a suite of transcriptional changes in the resistant genotype that were weak or absent in the susceptible sorghum. Specifically, the aphid-resistant genotype exposed to M. sacchari up-regulated several genes involved in defense, which was particularly evident in the 2-wk plants that showed the most robust transcriptional responses. These transcriptional changes in the younger resistant sorghum were characterized by induction of hormone-signaling pathways, pathways coding for secondary metabolites, glutathion metabolism, and plant-pathogen interaction. Furthermore, the 2-wk resistant plants appeared to compensate for the effects of oxidative stress induced by sugarcane aphid herbivory with elevated expression of genes involved in detoxification. These transcriptional responses were reflected in the aphid population growth, which was significantly faster in the susceptible and older sorghum than in the resistant and younger plants. CONCLUSION: This experiment provided the first insights into molecular mechanisms underlying lower population growth of M. sacchari on the resistant sorghum genotype. Further, it appears that the younger resistant sorghum was able to mount a robust defense response following aphid herbivory, which was much weaker in the older sorghum. Several pathways and specific genes provide specific clues into the mechanisms underlying host plant resistance to this invasive insect.

ddRAD Sequencing Identifies Pesticide Resistance-Related Loci and Reveals New Insights into Genetic Structure of Bactericera cockerelli as a Plant Pathogen Vector.

(1) Background: Many hemipteran insects transmit plant pathogens that cause devastating crop diseases, while pest management frequently relies primarily on insecticide applications. These intense insecticide applications lead to the development of insecticide resistance, as was the case for potato psyllid, Bactericera cockerelli (Hemiptera: Triozidae), a vector of Candidatus Liberibacter solanacearum, which causes zebra chip disease in potato. (2) Methods: Here, we use double-digest restriction site-associated DNA (ddRAD) to genotype eight psyllid populations (one susceptible and seven resistant to neonicotinoid insecticides). (3) Results: Association tests identified over 400 loci that were strongly segregated between susceptible and resistant populations. Several loci were located within genes involved in insecticide resistance, gene regulation, fertility, and development. Moreover, we explored the genetic structure of these eight populations and discovered that routinely utilized haplotyping was not an accurate predictor of population structure. Pairwise comparisons of the fixation index (FST) of populations of the same haplotype were not different from pairwise FST of populations that belonged to different haplotypes. (4) Conclusions: Our findings suggest that neonicotinoid insecticide resistance has a genetic basis, most likely as a result of similar selection pressure. Furthermore, our results imply that using a single maternally inherited gene marker to designate genetic lineages for potato psyllids should be re-evaluated.