Ouch! The stinger of a honey bee is revealed as a tiny autonomous double-piston venom pump
Peer-Reviewed Publication
This October, things are getting a little creepy and crawly. We're shining a light on the fascinating world of arthropods, from insects and spiders to scorpions, centipedes and more, and exploring the latest research on the creatures that crawl, creep and fly all around us.
Updates every hour. Last Updated: 19-Oct-2026 21:16 ET (20-Oct-2026 01:16 GMT/UTC)
Australian scientists have used high speed video to uncover the unique mechanism that allows a honey bee’s stinger to continue to pump venom into its target even after it has separated from the bee’s body.
Skin is an entry point for tick-borne pathogens, but the responses of its different cell types remain incompletely understood. Researchers reporting in hLife mapped skin-cell responses to Rickettsia heilongjiangensis in wild-type mice, mice lacking type I or both type I and type II interferon receptors. They also examined patient samples and clinical data. Macrophage gene expression varied across interferon receptor backgrounds, whereas neutrophils retained signatures related to oxidative phosphorylation and protein degradation across all three mouse models. Fibroblast responses also differed in timing. In evaluable human tick-bite skin samples, the lipid peroxidation marker MDA appeared only in lesions from rickettsial PCR-positive patients, while MPO and OGG1 staining occurred in both PCR-positive and PCR-negative patients. Among patients with confirmed spotted fever group rickettsial infection and clear lesion and fever information, fever was less frequent in those with local skin lesions. The findings identify distinct cellular responses and a clinical association, while leaving open whether these local responses influence infection outcomes.
Background: Scabies, caused by the mite Sarcoptes scabiei, affects more than 200 million people at any one time and can be complicated by severe secondary bacterial disease. The same mite causes sarcoptic mange in companion animals, livestock and wildlife. Population-scale nuclear genomic data spanning diverse hosts and geographical regions remain limited.
Methods: We generated whole-genome sequence data for 106 S. scabiei samples and incorporated 19 publicly available datasets from humans, companion animals, livestock and wildlife. After quality filtering, 83 of 125 sample-level datasets were retained. We assessed ancestry, phylogenetic relationships, nucleotide diversity, genetic differentiation, gene-level variation and candidate selection signals.
Results: We identified 1,568,031 filter-passing nuclear variants, including 698,136 single-nucleotide polymorphisms; sample-level heterozygosity estimates ranged from 0.27% to 11%. ADMIXTURE, principal component and phylogenetic analyses supported seven ancestry clusters broadly corresponding to host-associated groups, with pairwise fixation-index estimates ranging from 0.22 to 0.92. Multi-metric analysis identified 1,600 candidate selection blocks – eight hard-sweep, 486 soft-sweep and 1,106 ancient-adaptation blocks – and six conserved low-diversity blocks. Variable genes showed nominal enrichment for DNA repair, cell adhesion and signalling, whereas invariable genes showed nominal enrichment for ribosomal function, oxidative phosphorylation and mitochondrial processes.
Conclusions: This expanded multi-host analysis reinforces and extends evidence that host association is a prominent correlate of genome-wide population structure in S. scabiei. The findings provide a population-genomic resource for future host-stratified One Health surveillance and investigations of transmission, adaptation and acaricide resistance in scabies and sarcoptic mange.