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Cote, G.

Publications and source records attributed to Cote, G..

3 recordsLinked to original sources

Status of Round Goby Invasion Fronts in New York and Quebec: Implications for Lake Champlain

Invasive round goby Neogobius melanostomus have advanced eastward through the state of New York and provinces of Ontario and Quebec over the past two decades and are approaching Lake Champlain, one of the largest lakes in North America. This manuscript describes international efforts to monitor round goby populations during 2021-2025 on (a) the southern approach to Lake Champlain via the Hudson River and Champlain Canal, and (b) the northern approach to Lake Champlain via the Saint Lawrence River and Richelieu River. Monitoring utilized environmental DNA (eDNA), backpack electrofishing, beach seining, benthic trawling, and viral hemorrhagic septicemia virus (VHSV) testing. In the Champlain Canal, round goby were captured as far north as the downstream side of the C1 dam (97 kilometers [km] from Lake Champlain) while eDNA detections occurred as far north as the upstream side of the C2 dam (90 km from Lake Champlain). In the Richelieu River, round goby were captured as far south as Saint-Marc-sur-Richelieu (82 km from Lake Champlain) while the southern-most eDNA detections occurred near the Canadian side of the international border (4 km from Lake Champlain). Water temperature influenced habitat usage of round goby in the Champlain Canal, with catch rates in near-shore areas declining at < 10 {degrees}C. All VHSV test results were non-detections at the mouth of the Richelieu River, while one positive and two inconclusive results occurred along the Champlain Canal. Together, these data have informed multiple mitigation measures and have implications for management of aquatic invasive species across North America.

ecology↗

Captive rearing effects on the methylome of Atlantic salmon after oceanic migration: sex-specificity and intergenerational stability

Captive rearing in salmon hatcheries can have considerable impacts on both fish phenotype and fitness within a single generation, even in the absence of genetic change. Evidence for hatchery-induced changes in DNA methylation is becoming abundant, though questions remain on the sex-specificity of these effects, their persistence until spawning, and potential for transmission to future generations. Here we performed whole genome methylation sequencing of fin tissue for 16 hatchery and 16 wild Atlantic salmon (Salmo salar) returning to spawn in the Rimouski River, Quebec. We identified two cohorts of hatchery-reared salmon through methylation analysis, one of which was epigenetically similar to wild fish, suggesting that supplementation efforts may be able to minimize the epigenetic effects of hatchery rearing. We found considerable sex-specific effects of hatchery rearing, with few genomic regions being affected in both males and females. We also analysed the methylome of 32 F1 offspring from four groups (pure wild, pure hatchery origin, and reciprocal hybrids). We found that few epigenetic changes due to parental hatchery rearing persisted in the F1 offspring though the patterns of inheritance appear to be complex, involving nonadditive effects. Our results suggest that the epigenetic effects of hatchery rearing can be minimal in F0. There may also be minimal epigenetic inheritance and rapid loss of epigenetic changes associated with hatchery rearing. However, due to sex-specificity and nonadditive patterns of inheritance, methylation changes due to captive rearing are rather complex and the field would benefit from further research on minimizing the epigenetic effects of captive rearing in conservation efforts.

evolutionary biology↗

Opposing immune and genetic forces shape oncogenic programs in synovial sarcoma

Synovial sarcoma is an aggressive mesenchymal neoplasm, driven by the SS18-SSX fusion, and characterized by immunogenic antigens expression and exceptionally low T cell infiltration levels. To study the cancer-immune interplay in this disease, we profiled 16,872 cells from 12 human synovial sarcoma tumors using single-cell RNA-sequencing (scRNA-Seq). Synovial sarcoma manifests antitumor immunity, high cellular plasticity and a core oncogenic program, which is predictive of low immune levels and poor clinical outcomes. Using genetic and pharmacological perturbations, we demonstrate that the program is controlled by the SS18-SSX driver and repressed by cytokines secreted by macrophages and T cells in the tumor microenvironment. Network modeling predicted that SS18-SSX promotes the program through HDAC1 and CDK6. Indeed, the combination of HDAC and CDK4/6 inhibitors represses the program, induces immunogenic cell states, and selectively targets synovial sarcoma cells. Our study demonstrates that immune evasion, cellular plasticity, and cell cycle are co-regulated and can be co-targeted in synovial sarcoma and potentially in other malignancies.

cancer biology↗