Honeybees (Apis mellifera) are indispensable pollinators vital to global biodiversity, ecosystem stability, and agricultural productivity, and they promote over 35% of food crops and 75% of flowering plants. Yet, they are in unprecedented decline, partly as a result of neonicotinoid pesticide use elsewhere. These effects on honey bee health are synthesized in this paper through molecular, physiological, and behavioral data showing that sublethal effects of neonicotinoids impair honey bee health. As neurotoxic insecticides that target nicotinic acetylcholine receptors (nAChRs), these insecticides interfere with neurotransmission and underlie cognitive impairment, immune suppression, and oxidative stress. Developmental toxicity is manifested in larvae as retarded growth, reduced feeding, and increased death; queen and drone reproduction are impaired, lowering colony viability. As a result, adult bees have shortened lives and erratic foraging, are further disoriented, and experience impaired navigation, communication, and resource collection. Together, these effects cascade to reduced brood care, thermoregulatory failure, and heretofore unrecognized increased susceptibility to pathogens, increasing the probability of colony collapse at the colony level. Contaminants such as pesticides may cause pollinator exposure and, in turn, may cause their population to be undermined if they are not mitigated; therefore, urgent mitigation strategies, including integrated pest management (IPM), regulatory reforms, and adoption of biopesticides, are needed to mitigate pollinator exposure. The focus of this review lies in the ecological necessity of restructuring how agriculture is managed to simultaneously meet food security and the conservation of honeybee health, the linchpin of global ecosystems.

Epigenetics, as an important scientific field that bridges genomic function and phenotypic plasticity, increasingly demonstrates its value in bee research. In recent years, with the rapid development of omics technologies, there have been significant advancements in the study of epigenetics in honeybees. This article reviews the role of epigenetic regulation in the development, behavioral regulation, and immune response of honeybee larvae from the perspectives of DNA methylation, histone modification, and non-coding RNA. With the continuous deepening of related research, honeybee epigenetics not only opens new paths for understanding the formation mechanisms of complex traits in social insects but also provides solid theoretical support and innovative perspectives for the study of social insects and beekeeping practices. These insights also inform sustainable beekeeping practices.

Honey bees (Apis mellifera) are essential pollinators, responsible for the pollination of over 80% of crops and flowering plants globally. However, there is concern that the extensive use of pesticides, particularly atrazine, can harm pollinators. Despite the widespread use of atrazine, the sublethal effects on honey bees remain unclear. This study investigated the effects of atrazine on honey bee sucrose sensitivity and clarified the underlying molecular mechanisms using transcriptomic analyses. Atrazine exposure reduced the sucrose sensitivity of honey bees substantially, likely through the inhibition of functional genes associated with cognition in the brain. Genes related to neurodegenerative diseases and behavior were differentially expressed in response to atrazine. These findings provide novel insights into the neurophysiological and behavioral effects of atrazine on honey bees, contributing to a better understanding of pesticide risks and informing future environmental regulations.

Heat stress has caused significant impacts on the poultry industry globally. Tianjin-monkey Chicken (TM) is a local naked neck chicken genetic resource in China, characterized by its heat stress resistance due to a low feather coverage. We conducted heat stress stimulation tests on TM and a normal feathered chicken (Jingfen No. 6 Layer, JF), and the breast muscle tissues were collected for transcriptome sequencing. A total of 157 differentially expressed genes (DEGs) and 1435 DEGs were respectively obtained from the comparisons of JFN-vs-JFT and TMN-vs-TMT. GO enrichment analysis found that biological process (BP) terms including phospholipid homeostasis, regulation of aggrephagy, positive regulation of aggrephagy, and negative regulation of lipase activity may be closely related to heat stress resistance in JF chickens. While catabolism-related BP terms were mainly enriched for DEGs of TM, such as catabolic process, protein catabolic process and cellular catabolic process. KEGG pathway analysis showed that the MAPK signaling pathway was enriched both in TM and JF with high connectivity. In addition, some pathways with higher connectivity (Metabolic pathways, FoxO signaling pathway, TGF-beta signaling pathway and AMPK signaling pathway) may be closely associated with resistance to heat stress in JF. In Tianjin-monkey Chicken, we also identified several pathways potentially involved in heat stress regulation, including Ubiquitin mediated proteolysis, Autophagy-animal and Regulation of actin cytoskeleton. Protein-Protein Interaction Networks (PPI) for the 24 co-differentially expressed genes revealed four key genes (Klf9, Asb2, Tmem164 and Arrdc2) associated with heat stress both in JF and TM. Our findings will enrich the research on heat stress resistance in chicken skeletal muscle, while also providing a theoretical basis for the genetic improvement of heat stress resistance in chickens.

The gut microbiota of social bees is vital for host health, yet pesticide exposure can disrupt these communities. Because most active ingredients are poorly soluble, toxicological tests often use cosolvents, but their effects remain unclear. We assessed four common cosolvents (DMSO, DMF, acetone, and Tween 80) at laboratory-relevant concentrations on honeybee survival, pollen consumption, body weight, and gut microbiota. In parallel, in vitro assays tested their impact on five dominant gut symbionts. The results showed no significant changes in survival, feeding, body weight, bacterial load, community composition, or core taxa abundance. Similarly, cosolvents did not inhibit bacterial growth in vitro. These findings demonstrate that commonly used cosolvents exert no detectable influence on honeybee physiology or gut microbiota. Although negative, this evidence is critical: it rules out cosolvents as hidden confounders, improving confidence in pesticide toxicology studies and providing essential reference data for pollinator risk assessment.

The mandibular gland in worker bees synthesizes and secretes the organic acids present in royal jelly, and its development directly affects yield and quality. Therefore, we aimed to analyze the differences in morphology and gene expression in the mandibular glands of Apis mellifera carnica worker bees of different ages (3, 6, 9, 12, and 16 d). We dissected their mandibular glands and performed morphological and transcriptomic analyses to investigate the development of the mandibular gland and the molecular regulatory mechanisms involved in royal jelly secretion. Microscopy revealed that mandibular gland development is likely completed in the early stages. There were no significant differences in the structural morphology or organelles involved in the secretion of royal jelly at different ages. Transcriptomics revealed a total of 1554 differentially expressed genes, which were mainly involved in fat metabolism, lipid transport, and energy metabolism. The extracellular matrix–receptor interaction pathway was significantly enriched and contributed to the royal jelly secretion process. These results elucidate the genetic basis of the role of the mandibular gland in royal jelly secretion in A. mellifera and provide a reference for the genetic improvement of bees with high royal jelly production in the future.