Seager, M. | Search bioRxiv

bioRxiv2026

Operationalizing site-level conservation for migratory birds across the Americas flyways

Conserving migratory birds effectively requires full annual cycle strategies that identify where on-the-ground efforts can have the greatest impact. Here, we present a hemispheric spatial framework to identify priority areas for 112 migratory bird species across the Americas. Building on full annual cycle prioritizations, we defined finer-scale spatial planning units that reflect differences in migratory and congregational behaviors between shorebirds and landbirds. We compiled population data for each planning unit and focal species and applied conservation planning tools to design area-efficient portfolios of sites and landscapes that secure 10% of each species population within the Americas flyways. The resulting minimum area portfolios include 175 shorebird sites and 80 landbird landscapes optimized to meet the species-specific 10% representation targets across breeding, non-breeding, and passage seasons. We also identified a broader set of complementary solutions, ranked by an importance score, to provide decision-makers with flexible options for strategic resource allocation. This framework provides the scientific foundation for the Americas Flyways Initiative (AFI), which aims to catalyze investment in nature-based solutions and bird-friendly infrastructure to enhance the conservation of migratory birds and strengthen the resilience of the Americas flyways by 2050.

ecology↗

bioRxiv2025

Functional classification of GNAI1 disorder variants in C. elegans uncovers conserved and cell-specific mechanisms of dysfunction

Heterotrimeric G proteins transduce signals from G protein coupled receptors, which mediate key aspects of neuronal development and function. Mutations in the GNAI1 gene, which encodes Gi1, cause a disorder characterized by developmental delay, intellectual disability, hypotonia, and epilepsy. However, the mechanistic basis for this disorder remains unknown. Here, we show that GNAI1 is required for ciliogenesis in human cells and use C. elegans as a whole-organism model to determine the functional impact of seven GNAI1-disorder patient variants. Using CRISPR-Cas9 editing in combination with robust cellular (cilia morphology) and behavioral (chemotaxis) assays, we find that T48I, K272R, A328P, and V334E orthologous variants impact both cilia assembly and function in AWC neurons, M88V and I321T have no impact on either phenotype, and D175V exerts neuron-specific effects on cilia-dependent sensory behaviors. Finally, we validate in human ciliated cell lines that D173V, K270R, and A326P GNAI1 variants disrupt ciliary localization of the encoded human Gi1 proteins similarly to their corresponding orthologous substitutions in the C. elegans ODR-3 (D175V, K272R, and A328P). Overall, our findings determine the in vivo effects of orthologous GNAI1 variants and contribute to mechanistic understanding of GNAI1 disorder pathogenesis as well as neuron-specific roles of ODR-3 in sensory biology. ARTICLE SUMMARYG subunits of heterotrimeric G proteins transduce signaling from G protein coupled receptors and play important roles in cell communication and complex behaviors. Mutations in the GNAI1 gene, which encodes Gi1 protein, have been recently linked to a neurodevelopmental disorder; however, it remains unknown how GNAI1 patient mutations disrupt neuronal development or function to manifest in disease. We demonstrate that GNAI1 is required for ciliogenesis and use C. elegans as a whole-animal model in combination with human cells to identify cell-specific and conserved mechanisms of G dysfunction.

developmental biology↗