Donor perspectives on strengthening capacity development for conservation

Global perspectives on the pathways for developing capacity for conservation remain limited. Hindering the robustness of solutions is a dearth of opportunities to foster discussion and dialogue among capacity development practitioners, academics, partners, beneficiaries and donors. Additionally, little is known about donor perspectives on capacity development, and about pathways to developing a more sustainable investment in capacity development for conservation. The 2019 Capacity Building for Conservation Conference in London, UK, provided a unique opportunity to convene more than 150 capacity development practitioners from the global conservation community. The Conference included structured opportunities to hear donor perspectives on strengthening capacity development. Session leaders took detailed notes to document donor perspectives and the discussions around them. A thematic analysis of this empirical evidence resulted in the identification of four key themes with corresponding recommendations, consisting of (1) collaborative design of capacity development initiatives, (2) monitoring and evaluation, (3) longer-term and flexible investments, and (4) building strong relationships between donors and grantees. Given the Convention on Biological Diversity is currently drafting the long-term strategic framework for capacity development post-2020, and global calls to protect significant portions of our land- and seascapes, our recommendations are timely and may inform a way forward

Diacylglycerol Kinase-α Mediates Hepatocyte Growth Factor-induced Epithelial Cell Scatter by Regulating Rac Activation and Membrane Ruffling

Diacylglycerol kinases (Dgk) phosphorylate diacylglycerol (DG) to phosphatidic acid (PA), thus turning off and on, respectively, DG-mediated and PA-mediated signaling pathways. We previously showed that hepatocyte growth factor (HGF), vascular endothelial growth factor, and anaplastic lymphoma kinase activate Dgkα in endothelial and leukemia cells through a Src-mediated mechanism and that activation of Dgkα is required for chemotactic, proliferative, and angiogenic signaling in vitro. Here, we investigate the downstream events and signaling pathways regulated by Dgkα, leading to cell scatter and migration upon HGF treatment and v-Src expression in epithelial cells. We report that specific inhibition of Dgkα, obtained either pharmacologically by R59949 treatment, or by expression of Dgkα dominant-negative mutant, or by small interfering RNA-mediated down-regulation of endogenous Dgkα, impairs 1) HGF- and v-Src-induced cell scatter and migration, without affecting the loss of intercellular adhesions; 2) HGF-induced cell spreading, lamellipodia formation, membrane ruffling, and focal adhesions remodeling; and 3) HGF-induced Rac activation and membrane targeting. In summary, we provide evidence that Dgkα, activated downstream of tyrosine kinase receptors and Src, regulates crucial steps directing Rac activation and Rac-dependent remodeling of actin cytoskeleton and focal contacts in migrating epithelial cells