Background/Objectives: The utilization of methyl-thiophanate (MT) in vegetables and fruits is widespread due to its broad efficiency, yet its potential impact on silkworm growth remains uncertain. This study aims to examine the effects of MT on the growth of silkworms. Specifically, we assessed the weights of fifth-instar larvae that were fed mulberry leaves saturated with three concentrations (2.5, 5, and 10 mg/mL) of MT, as well as the weights of a control group. Methods: TEM was used to show the status of the silkworm midgut after MT supplementation. Oxidative stress was evaluated in the presence of MT. Furthermore, a transcriptomic sequencing experiment was conducted to investigate the mechanism through which the development of silkworms is induced by MT. Results: Our findings indicate that the supplementation of MT hindered larval growth compared to the control group, suggesting a toxic effect of MT on silkworms. The transmission electron microscopy (TEM) results show that MT supplementation induced autophagy in the silkworm midgut. MT was also found to induce oxidative stress in silkworms through the activation of reactive oxygen (ROS), superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) activities. Subsequent transcriptomic analysis revealed 1265 significantly differentially expressed genes (DEGs) in response to MT. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that these DEGs were associated with antioxidant defense, detoxification processes, lysosome biogenesis, and metabolic pathways. Conclusions: These findings suggest that MT toxicity in silkworm larvae is mediated through the induction of oxidative stress and alterations in metabolism. This study contributes to our understanding of the impacts of MT exposure on silkworms and provides insights into potential pesticides for use in mulberry gardens.

Grafting profoundly influences fruit tree performance, yet the molecular mechanisms underlying rootstock–scion interactions in mulberry (Morus multicaulis) remain poorly understood. To investigate the regulatory networks linking grafting to scion physiology, we performed an integrated analysis combining small RNA sequencing, transcriptome-based KEGG pathway assessment, and qRT-PCR validation of key target genes across five rootstock–scion combinations. High-throughput miRNA profiling of phloem tissues identified 71 conserved and 156 novel miRNAs, which exhibited distinct, genotype-dependent expression patterns. Recurrent activation of nutrient- and stress-responsive families (e.g., miR399, miR397, and miR395) was observed. Target prediction and functional enrichment analyses revealed that these miRNAs likely regulate pathways related to metabolic processes, hormone signaling, cell wall modification, and stress responses. The expression trends of their predicted target genes—including TCP4, Laccase-3, and ATP sulfurylase 1—were subsequently confirmed by qRT-PCR, revealing significant rootstock-specific regulation. Collectively, this study establishes a reference framework for elucidating the molecular mechanisms underlying scion biological processes in Morus species, which is of great significance for improving fruit quality, enhancing abiotic and biotic stress resistance, and boosting long-term planting productivity.

The silkworm, Bombyx mori, a key economic insect, has been employed as a model organism to investigate the toxicological effects and underlying mechanisms of zinc iron oxide nanoparticle exposure on its growth and development, midgut tissue structure, and physiological functions. Exposure to zinc iron oxide inhibited larval growth and development, which was accompanied by pathological alterations in the midgut, including a reduction in columnar cells, vacuolation, chromatin condensation, microvilli shedding, and disrupted tight junctions, which directly impaired the intestinal barrier integrity and nutrient absorption. Furthermore, zinc iron oxide exposure resulted in elevated reactive oxygen species levels, decreased superoxide dismutase and glutathione contents, and increased catalase activity, indicating the activation of oxidative stress. This stress-induced mitochondrial response, characterized by the observation of autophagic vesicles, suggests the potential mitophagy of activation in action to zinc iron oxide exposure, thereby preserving cellular homeostasis. This was also associated with the downregulation of most genes involved in purine metabolism, the peroxisome, the biosynthesis of amino acids, the ribosome pathway, and carbon metabolism pathways, leading to reduced protein synthesis and energy supply, ultimately resulting in larval developmental retardation. This study elucidates the intestinal-targeted toxicity of zinc iron oxide nanoparticles in lepidopteran insects, providing direct in vivo experimental evidence for evaluating the ecological risk of zinc iron oxide in sericulture environments. Furthermore, it offers a novel research avenue for developing intestinal intervention strategies aimed at mitigating the toxic effects of nanomaterials and ensuring the stability of economically important traits in silkworms.