Division of labor in social insects is enabled by coordinated changes in physiology, neural signaling, and gene regulation, yet it remains unclear to what extent behavioral maturation reflects incremental changes in individual genes and/or a reorganization of transcriptomic regulation at the system level. Here, we analyze the nurse-to-forager transition in worker honeybees ( Apis mellifera ) from a network perspective, treating the transcriptome as a gene–gene correlation system whose global organization reflects collective regulatory states. Using fat body gene expression data across five developmental time points that span an interval of behavioral transition, we construct signed gene–gene correlation networks and quantify their macro- and mesostate properties. We then descend to the level of the gene and construct microstate gene lists of interacting genes. Behavioral maturation of worker honeybees is accompanied by coordinated, nonmonotonic changes in global network structure rather than simple global shifts in interaction strength across the network. Early stages exhibit broadly positive, globally synchronized correlations, whereas later stages show increased modular segregation and the emergence of antagonistic gene–gene relationships. Despite this differentiation, networks remain fully connected with high global efficiency, consistent with a flexible small-world–like organization. Positive correlations primarily support global integration, while negative correlations act as localized, boundary-enforcing constraints. Negative correlations form a structured pattern of antagonism that is sparse and module-specific, occurring primarily between functional gene modules rather than within them. Network layouts and module analyses reveal two polarized, attractor-like regulatory states, a structure recapitulated in a vitellogenin-centered subnetwork and consistent with prior experimental perturbation studies.
Pathogen adaptations to new hosts are central to the disease ecology of cross-species transmission and host switching of viruses. The rabies virus is a model for adaptations to different hosts as it induces behavioral changes that facilitate transmission, while being maintained in distinct species-specific cycles of infection. Here, we demonstrate that the rabies virus requires distinct transmission dynamics in two hosts with different ecologies to establish maintenance, using agent-based modeling, analyses of virus glycoprotein-mediated manipulation of neuroreceptor function, and phylogenetic analysis. Epidemiological models suggest that rabies virus variants adapted to arctic foxes, which sustain rabies virus at very low host densities, require a higher probability of transmission than viruses adapted to raccoons. Using in vitro electrophysiology, we demonstrate that the rabies glycoprotein-derived peptides from arctic fox rabies variants are more potent antagonists of alpha7 nicotinic acetylcholine receptors. These findings suggest a possible functional basis for the behavioral modifications that drive enzootic rabies transmission in the context of host ecology. In addition, a large proportion of residues that may drive rabies virus adaptation to raccoons and arctic foxes are found within this neurotoxin-like region. Furthermore, a residue in the neurotoxin-like region of the mature rabies virus glycoprotein (residue 183) has been associated with pathogenicity, host switching, and disease ecology in previous studies. We propose the hypothesis that rabies virus transmission dynamics adapt to the ecology and physiology of novel hosts through the selection of glycoproteins that elicit specific degrees of behavioral modification and transmission probability.
Aflatoxins produced by some species of Aspergillus pose a significant threat to global food safety, because they contaminate a variety of crops including maize. In this study, we used host-induced gene silencing (HIGS) to reduce aflatoxin accumulation in maize upon infection with Aspergillus flavus and Aspergillus parasiticus . Two RNAi constructs were designed and introduced into maize, one targeting two essential fungal genes involved in ergosterol biosynthesis ( CYP51A and CYP51B ) and the other targeting three aflatoxin biosynthesis genes ( AflC , AflD , and AflR ). The presence of RNAi transgenes was confirmed in 17 and 14 independent lines possessing the CYP51A/CYP51B RNAi construct and the AflC/AflD/AflR RNAi construct, respectively. Most transgenic lines had single-locus integrations and one or two copies of the transgene. Transgene expression varied considerably among the lines. Small RNA sequencing confirmed the production of siRNAs from the HIGS trigger sequences. Levels of CYP51A , AflC , AflD, and AflR transcripts in Aspergillus spp. were successfully decreased upon infection of transgenic maize. However, significant reduction in the level of CYP51B transcripts was not achieved and the CYP51A/CYP51B RNAi transgene had no discernible effect on fungal growth in infected maize. In contrast, we observed significant reductions in aflatoxin accumulation in four AflC/AflD/AflR RNAi transgenic lines infected with A. flavus and in two transgenic lines infected with A. parasiticus . Notably, one AflC/AflD/AflR transgenic line exhibited minimal aflatoxin contamination upon kernel infection with A. parasiticus . These results demonstrate the potential of HIGS to reduce aflatoxin production in mature corn kernels.
The search for high-performance lubricants is of broad relevance to biomedical applications, including artificial joints, regenerative scaffolds, and osteoarthritis therapies. Here we introduce glycerosomes—phosphatidylcholine (PC)-based vesicles containing glycerol—as a promising boundary lubricant. Using a surface force balance, we show that glycerosomes achieve a friction coefficient as low as 10 − 5 under a high compression pressure of 15.6 MPa, representing a 20-fold reduction compared to conventional PC liposomes. This level of lubrication surpasses any previously reported boundary lubricant system at such pressures in aqueous media. Mechanistically, glycerosomes exhibit substantially lower adhesion energy than PC liposomes, and theoretical simulations reveal enhanced vesicle stability and flexibility. Our findings establish glycerosomes as a superior hydration lubrication platform, with promising implications for both biomedical implants and industrial applications requiring robust lubricity.
