Biology subjects

Vogel, S. M.

Publications and source records attributed to Vogel, S. M..

4 recordsLinked to original sources

bioRxiv2022

Identifying the potential for sustainable human wildlife coexistence by integrating willingness to coexist with habitat suitability models

Persistence of large mammals in the Anthropocene depends on human willingness to coexist with them, but this is rarely incorporated into habitat suitability or conservation priority assessments. We propose a framework that integrates human willingness-to-coexist with habitat suitability assessments to identify areas of high potential for sustainable coexistence. We demonstrate its applicability for elephants and rhinos in the socio-ecological system of Maasai Mara, Kenya, by integrating spatial distributions of peoples willingness-to-coexist based on Bayesian hierarchical models using 556 household interviews, with socio-ecological habitat suitability mapping validated with long-term elephant observations from aerial surveys. Willingness-to-coexist was higher if people had little personal experience with a species, and strongly reduced by experiencing a species as a threat to humans. The sustainable coexistence potential framework highlights areas of low socio-ecological suitability, and areas that require more effort to increase positive stakeholder engagement to achieve long-term persistence of large herbivores in human-dominated landscapes.

ecology↗

bioRxiv2019

TAK1 Regulates Endothelial Integrity Through Stabilization of Junctions via GSK3β and FoxO1

TLR4 signaling in endothelial cells (ECs) induces vascular injury by disrupting the endothelial junctional barrier. However, it is not known whether TLR4 signaling can also promote endothelial barrier repair after vascular injury. Here we addressed the role of TAK1 activation downstream of TLR4 in the mechanism of vascular integrity. In inducible EC-restricted TAK1 knockout (TAK1i{Delta}EC) mice, the endothelial barrier was compromised. Blocking TAK1 activity caused spontaneous loss of the endothelial barrier. Importantly, TAK1 inactivated GSK3{beta} via AKT to prevent {beta}-catenin downregulation. We observed in ECs of GSK3{beta}i{Delta}EC mice an increase in {beta}-catenin transfer to the nucleus to form a complex with transcription factor FoxO1, thus repressing the expression of the tight junction protein claudin-5 and causing vascular leak. Strikingly, in TAK1i{Delta}EC mice, FoxO1 expression was dramatically increased while expression of AKT was suppressed, and in vivo inhibition of FoxO1 prevented sepsis-induced lung vascular leak in GSK3{beta}i{Delta}EC and TAK1i{Delta}EC mice. Further, EC-restricted deletion of FoxO1 in mice suppressed sepsis-induced lung vascular leak and mortality. Our findings point to the potential of targeting the TAK1-AKT-GSK3{beta}-FoxO1 axis as a therapeutic approach to treat uncontrolled lung vascular leak in sepsis.

cell biology↗

bioRxiv2019

Do African savanna elephants (Loxodonta africana) eat crops because they crave micronutrients?

O_LIElephants can cause negative consequences for both themselves and for humans by consuming agricultural crops. It is unclear whether savanna elephant crop consumption is merely opportunistic behaviour or related to insufficient quality of natural forage. We analysed the role of vegetation quality on elephant crop consumption. We focused on the role of micronutrients, as natural elephant diets are thought to be insufficient in elements such as sodium and phosporus, which can influence their foraging decisions.\nC_LIO_LIFor 12 months across four seasons we collected elephant feeding trail data along with tree, grass and crop samples. We investigated how the quality and availability of these items influenced elephant dietary choices across months and seasons. Subsequently, we compared levels of fibre, digestible energy, dry matter intake, and micronutrients, together with secondary compounds (tannins) across the three vegetation groups. As elephants do not make dietary choices based on one component, we also analysed the nutrient balance of food items with right-angle mixture models.\nC_LIO_LIThe levels of phosphorus, magnesium and dry matter intake corresponded to foraging preference. Compared to trees and grasses, crops contained significantly higher amounts of digestible energy content, dry matter intake, nitrogen, phosphorus, calcium and magnesium. PCA results showed that crops differed in phosphorus and magnesium levels. The right-angle mixture models indicated that except for one tree species, all food items elephants consumed were relatively deficient in phosphorus.\nC_LIO_LIThe combined results of these analyses suggest a phosphorus deficiency in elephant diet in northern Botswana. Crops, with their high absolute phosphorus levels and dry matter intake, provide an alternative source of phosphorus to reduce the deficiency. This may explain the high intensity of crop consumption in the wet season in our study area. A potential mitigation measure against elephant crop consumption might be to provide supplementary phosphorus sources.\nC_LI

ecology↗

bioRxiv2019

EphB1 in Endothelial Cells Regulates Caveolae Formation and Endocytosis

Caveolae, the cave-like structures abundant in endothelial cells (ECs), are important in regulating key functions such as caveolae-mediated endocytosis and generation of nitric oxide. Here we show that deletion of the receptor tyrosine kinase EphB1 (EphB1-/-) in mice markedly reduced the caveolae number in ECs of heart and lung vessels and prevented caveolae-mediated endocytosis. EphB1 expressed in adult ECs was shown to bind the caveolin-1 (Cav-1) scaffold domain (CSD) via the CSD binding motif (CSDBM) on EphB1. We demonstrated that activation of EphB1 by the native ligand Ephrin B1 uncoupled EphB1 from Cav-1, and licensed Src-dependent Y-14 Cav-1 phosphorylation. Deletion of CSDBM on EphB1 prevented EphB1/Cav-1 interaction and the activation of Src and Src mediated Y-14 Cav-1 phosphorylation. These studies identify the central role of endothelium expressed EphB1 in regulating caveolae biogenesis and caveolae-mediated endocytosis.

cell biology↗