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Ward, S. G.

Publications and source records attributed to Ward, S. G..

2 recordsLinked to original sources

Drivers of individual plant species contributions to β-diversity are scale-dependent

Species introductions and native extirpations are driving biotic homogenisation in plant communities by reducing {beta}-diversity. Individual species vary in their contributions to {beta}-diversity (Species Contribution to {beta}-Diversity; species-{beta}), yet our understanding of how species characteristics shape these contributions remains limited. Additionally, although the ecological processes influencing {beta}-diversity are known to vary with spatial scale, we lack understanding of how species contributions, or their underlying determinants, change across scales. Here, we modelled how plant functional traits, phylogenetic relatedness, and introduction status influence their contributions to {beta}-diversity using plant community data from 429 plots surveyed from 2017-2023 across three nested spatial scales (up to 1 km2) in nine sites spanning four countries. We extended the analysis to broader spatial extents (100 km2 to the entire UK) using GBIF occurrence data. We found that functional traits associated with competitive ability influenced species-{beta}, but the direction and strength of their effects varied with scale. Likewise, phylogenetic novelty increased species-{beta} at small scales but reduced it at larger ones. After accounting for traits and phylogeny, introduced species consistently contributed less to {beta}-diversity than native species--especially at broader spatial extents. These results demonstrate that species ecological and evolutionary characteristics shape their contributions to {beta}-diversity, but that these effects are scale-dependent. Our findings highlight the importance of scale-explicit approaches in understanding both the determinants of {beta}-diversity, and how we can combat its loss to mitigate biotic homogenisation.

ecology↗

AXL-GAS6/PROS1 Interaction: A Critical Switch Between Aberrant- and Healthy Repair Following Alveolar Lung Injury

RationaleIdiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by aberrant alveolar repair and excessive fibrosis. The TAM-family receptor tyrosine kinase AXL, activated by GAS6 and PROS1, is implicated in tissue remodeling, but ligand-specific AXL signaling during alveolar repair remains poorly defined. ObjectivesTo investigate ligand specific AXL signaling in IPF and how it impacts epithelial proliferation and repair after alveolar injury in-vivo and in-vitro. MethodsSingle cell RNA sequencing was utilized to understand cell specific expression patterns in IPF patients, followed by functional studies in primary human cell culture and functional spatial digital profiling (FuncOmap) analysis in patient tissue. Longitudinal assessment of repair process after alveolar-specific injury in-vivo was used to complement the in-vitro approach. ResultsAXL expression showed enrichment in basal and aberrant basaloid cells of IPF patients. In-vitro GAS6 increased proliferation of basal cells, while PROS1 counteracted this effect. FuncOmap analysis demonstrates direct in-situ interactions between AXL and both ligands, providing evidence for biological relevance. Investigating longitudinal repair processes in-vivo revealed dynamic regulation of AXL ligands as well as AXL. ConclusionsThese findings highlight the importance of ligand-specific AXL signaling in lung repair and suggest that it dysregulation may contribute to IPF pathogenesis, offering potential therapeutic targets for restoring normal repair processes.

molecular biology↗