Biology subjects

Mannino, G.

Publications and source records attributed to Mannino, G..

3 recordsLinked to original sources

bioRxiv2026

Isolation and introductions disrupt the homogeneity of Argentine ants in Europe.

The introduction of alien species into new habitats stands as a pressing economic and ecological challenge but it is also essential for unveiling evolutionary processes. The introduction of the Argentine ant (Linepithema humile) led to the spread of a single supercolony through different continents and thousands of kilometres like in Europe, from Northwest Spain to Greece. It was assumed that the high invasiveness of the species mainly relied on the lack of agonism among colonies, an effect derived from its introduction. However, recent studies suggest that local adaptations and evolutionary divergence could involve the disruption of the Argentine ant "empire" into a mosaic of competitive colonies. We investigated how isolation affects population divergence by comparing mainland and island populations in two distant regions colonized in Spain and in Greece with morphology, agonism, cuticular hydrocarbons, and genetic diversity of ant workers. Our results showed that all colonies sampled belonged to the most spread supercolony in Europe (main supercolony) except one sampled in Crete (Heraklion; Greece), which resulted to be a supercolony not registered in Europe. The Heraklian supercolony showed a different chemical and genetic profile and hostile agonism towards the other Greek colonies. Differences between islands and mainland colonies belonging to the main supercolony were higher in Galiza than in Greece. Surprisingly, the chemical profile of the Cretan colony belonging to the main supercolony showed more similarity with the Galizan colonies than with the Greek mainland, suggesting that L. humile may have been introduced into Greece through this island instead of the mainland. Our study suggests that local adaptations in Argentine ant colonies can trigger competition between colonies. Our data strongly support the existence of a candidate supercolony which highlights either ongoing introductions of L. humile in Europe or gaps in our understanding of its metapopulation dynamics.

evolutionary biology↗

bioRxiv2025

Somatic TYK2 activating mutations in tumor-infiltrating T cells promote anti-cancer immunity

Cancer cells evolve to increase fitness and evade the immune system, but it is not clear if tumor infiltrating lymphocytes (TILs) undergo selection for somatic mutations that augment anti-cancer immunity. Using single molecule whole exome sequencing in TILs, we identified somatic mutations in Tyrosine-protein kinase 2 (TYK2), several of which increased TYK2 phosphorylation, JAK-STAT signaling, and interferon gamma signaling. Among these mutations, TYK2D810V was recurrently observed in patients with diverse cancer types. In vitro, TYK2D810V enhanced T cells effector functions and cytokine production. We generated mice with a germline Tyk2D807V mutation that recapitulated the human TYK2D810Vmutation. These mice were healthy and did not develop autoimmune disorders. However, they possessed enhanced anti-tumor effects in the context of syngeneic and autochthonous cancer models. Adoptive therapy with Tyk2D807V CD8 T cells also decreased cancer growth. Thus, naturally occurring mutations in non-malignant lymphocytes can antagonize cancer and inspire new immunotherapies strategies.

cancer biology↗

bioRxiv2025

Mechanistic basis for protection against fatty liver disease by CIDEB loss-of-function mutations

Background & AimsSomatic and germline CIDEB mutations are associated with protection from chronic liver diseases. The mechanistic basis and whether CIDEB suppression would be an effective therapy against fatty liver disease remain unclear. Methods21 CIDEB somatic mutations were introduced into cells to assess functionality. In vivo screening was used to trace Cideb mutant clones in mice fed normal chow, western (WD), and choline-deficient, L-amino acid-defined, high-fat (CDA-HFD) diets. Constitutive and conditional Cideb knockout mice were generated to study Cideb in liver disease. Isotope tracing was used to evaluate fatty acid oxidation and de novo lipogenesis. Transcriptomics, lipidomics, and metabolic analyses were utilized to explore molecular mechanisms. Double knockout models (Cideb/Atgl and Cideb/Ppara) tested mechanisms underlying Cideb loss. ResultsMost CIDEB mutations showed that they impair function, and lineage-tracing showed that loss-of-function clones were positively selected with some, but not all fatty liver inducing diets. Cideb KO mice were protected from WD, CDA-HFD, and alcohol diets, but had the greatest impact on CDA-HFD induced liver disease. Hepatocyte-specific Cideb deletion could ameliorate disease after MASLD establishment, modeling the impact of therapeutic siRNAs. Cideb loss protected livers via increased {beta}-oxidation, specifically through ATGL and PPARa activation. ConclusionsCideb deletion is more protective in some types of fatty liver disease. {beta}-oxidation is an important component of the Cideb protective mechanism. CIDEB inhibition represents a promising approach, and somatic mutations in CIDEB might predict the patient populations that might benefit the most.

physiology↗