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Mackay, G.

Publications and source records attributed to Mackay, G..

2 recordsLinked to original sources

Sweet signals: Using floral traits to predict nectar sugar availability

Floral nectar is a key energy resource for many animals, yet its availability remains poorly quantified across plant communities. We tested whether floral traits can predict nectar rewards across diverse floras. We analysed relationships between floral morphology and nectar traits in 156 flowering plant species from temperate and tropical regions. Nectar volume, sugar concentration, and total sugar content were measured, and linear mixed-effects models were used to assess floral trait-nectar relationships in tubular and non-tubular flowers. Phylogenetic signal was evaluated using Blombergs K and Pagels {lambda}. Nectar volume increased strongly with corolla size in both floral types. Total sugar content scaled approximately 1:1 with nectar volume despite variation in sugar concentration, indicating that sugar reward is driven primarily by nectar volume. Floral morphology consistently predicted nectar rewards across floras, whereas phylogenetic relatedness explained relatively little variation. These findings provide a scalable framework for estimating floral sugar resources across landscapes.

plant biology↗

LPP3 mediates self-generation of chemotactic LPA gradients by melanoma cells

Melanoma cells steer out of tumours using self-generated lysophosphatidic acid (LPA) gradients. The cells break down LPA, which is present at high levels around the tumours, creating a dynamic gradient that is low in the tumour and high outside. They then also migrate up this gradient, creating a complex and evolving outward chemotactic stimulus. Here we introduce a new assay for self-generated chemotaxis, and show that raising LPA levels causes a delay in migration rather than loss of chemotactic efficiency. Knockdown of the lipid phosphatase LPP3 - but not its homologues LPP1 or LPP2 - diminishes the cells ability to break down LPA. This is specific for chemotactically active LPAs, such as the 18:1 and 20:4 species. Inhibition of autotaxin-mediated LPA production does not diminish outward chemotaxis, but loss of LPP3-mediated LPA breakdown blocks it. Similarly, in both 2D and 3D invasion assays, knockdown of LPP3 diminishes melanoma cells ability to invade. Our results demonstrate that LPP3 is the key enzyme in melanoma cells breakdown of LPA, and confirm the importance of attractant breakdown in LPAmediated cell steering.

cancer biology↗