Han Yang

Aggressive behavior is a critical issue affecting health and survival in aquaculture animals, however, the molecular mechanism of aggression in reptiles has not been fully understood. Using the Chinese softshell turtle (Pelodiscus sinensis) as a model, we modified the resident-intruder model to compare aggressive and non-aggressive individuals. Integrated brain transcriptomic and metabolomic analysis revealed enrichment in glutamatergic and GABAergic pathways between aggressive and non-aggressive individuals. Aggressive individuals showed upregulated glutamate receptor genes (GRIA2, GRIA3, GRIK3) and altered GABAergic system. Correlation networks confirmed coordinated gene-metabolite covariation in these pathways. Drug injection tests demonstrated that NMDA receptor antagonist MK-801 significantly reduced attacks, indicating that glutamatergic signaling is a primary driver of aggressive behavior. These findings highlight conserved excitatory mechanisms in vertebrate aggression with reptile-specific characteristics and offer targets for low aggressiveness breeding in aquaculture.

Aggressive behavior has attracted the attention of evolutionary geneticists, however, the molecular mechanism of aggression in reptiles has not been fully understood. Using the Chinese softshell turtle (Pelodiscus sinensis) as a model, we modified the resident-intruder model to compare aggressive and non-aggressive individuals. Integrated brain transcriptomic and metabolomic analysis revealed enrichment in glutamatergic and GABAergic pathways: aggressive turtles showed upregulated glutamate receptor genes (GRIA2, GRIA3, GRIK3) and elevated glutamate levels, with altered GABAergic system suggesting compensatory responses. Correlation networks confirmed coordinated gene-metabolite covariation in these pathways. Drug injection tests demonstrated that NMDA receptor antagonist MK-801 significantly reduced attacks, indicating that glutamatergic signaling is a primary driver of aggressive behavior. Changes of Monoaminergic and acetylcholinergic systems suggest multi-system support. These findings highlight conserved excitatory mechanisms in vertebrate aggression with reptile-specific characteristics and offer targets for low aggressiveness breeding in aquaculture.

Key appendage innovations have driven the origin and expansion of arthropods, such as spinnerets enabling spiders to occupy three-dimensional space and diversify into more than 53,000 species. Here, we investigate the genetic basis of spinneret emergence in spiders by examining the complex history and functional importance of arachnid genome evolution. Using chromosome-scale genomes from newly sequenced spiders and the whip scorpion, we integrate evidence from macrosynteny and phylogenetic analyses to provide further strong support for a whole-genome duplication (WGD) event that occurred during early Arachnopulmonata evolution. Following this event, the abdominal-A gene pair not only exhibits functional divergence but also jointly facilitates the emergence of spinnerets. Furthermore, we integrated single-cell transcriptomic analyses and functional validation to confirm that the dachshund-1 gene also regulates spinneret development. The network of duplicated gene pairs may form a cornerstone in the origin and evolution of key morphological traits, revealing that the long-term effects of ancient WGDs on innovation and diversification also occurred in arthropods.

Marine-terrestrial transition represents an important aspect of organismal evolution that requires numerous morphological and genetic innovations and has been hypothesized to be caused by geological changes. We used talitrid crustaceans with marine-coastal-montane extant species at a global scale to investigate the marine origination and terrestrial adaptation. Using genomic data, we demonstrated that marine ancestors repeatedly colonized montane terrestrial habitats during the Oligocene to Miocene. Biological transitions were well correlated with plate collisions or volcanic island formation, and top-down cladogenesis was observed on the basis of a positive relationship between ancestral habitat elevation and divergence time for montane lineages. We detected convergent variations of convoluted gills and convergent evolution of SMC3 associated with montane transitions. Moreover, using CRISPR-Cas9 mutagenesis, we proposed that SMC3 potentially regulates the development of exites, such as talitrid gills. Our results provide a living model for understanding biological innovations and related genetic regulatory mechanisms associated with marine-terrestrial transitions.

SARS-coronavirus-2–induced immune dysregulation and inflammatory responses are involved in the pathogenesis of coronavirus disease-2019 (COVID-19). However, very little is known about immune cell and cytokine alterations in specific organs of COVID-19 patients. Here, we evaluated immune cells and cytokines in postmortem tissues, i.e., lungs, intestine, liver, kidneys, and spleen of three patients with COVID-19. Imaging mass cytometry revealed monocyte, macrophage, and dendritic cell (DC) infiltration in the lung, intestine, kidney, and liver tissues. Moreover, in patients with COVID-19, natural killer T cells infiltrated the liver, lungs, and intestine, whereas B cells infiltrated the kidneys, lungs, and intestine. CD11b⁺ macrophages and CD11c⁺ DCs also infiltrated the lungs and intestine, a phenomenon that was accompanied by overproduction of the immunosuppressive cytokine interleukin (IL)-10. However, CD11b⁺ macrophages and CD11c⁺ DCs in the lungs or intestine of COVID-19 patients did not express human leukocyte antigen DR isotype. In contrast, tumor necrosis factor (TNF)-α expression was higher in the lungs, intestine, liver, and kidneys, but not in the spleen, of all COVID-19 patients (compared to levels in controls). Collectively, these findings suggested that IL-10 and TNF-α as immunosuppressive and pro-inflammatory agents, respectively,—might be prognostic and could serve as therapeutic targets for COVID-19.