Taxa specific responses to flooding shape patterns of abundance in a river rock pool metacommunity

Connectivity and habitat area are important landscape characteristics that drive patterns of abundance and diversity across scales. However, responses to connectivity and patch size are dependent on species traits. Riverine landscapes are highly dynamic both spatially and temporally with hydrologic connectivity being a major driver of abundance and diversity. Here we modeled densities of the Virginia river snail and skimmer dragonfly nymphys, two taxa with differences in their dispersal abilities and life histories, as a function of flooding, patch area, and season in over 300 riverine rock pools. We found key differences in how each taxon responded to these predictors with increasing pool flood height having a strong negative effect on snail densities and dragonfly nymph densities increasing as pools became more isolated from the river channel. Our study highlights how differences in response to landscape characteristics are dependent on organism traits. These findings give insight into patterns of abundance and diversity across scales

Data from: warming and top-down control of stage-structured prey: linking theory to patterns in natural systems

<p>Warming has broad and often nonlinear impacts on organismal physiology and traits, allowing it to impact species interactions like predation through a variety of pathways that may be difficult to predict. Predictions are commonly based on short-term experiments and models, and these studies often yield conflicting results depending on the environmental context, spatiotemporal scale, and the predator and prey species considered. Thus, the accuracy of predicted changes in interaction strength, and their importance to the broader ecosystems they take place in, remain unclear. Here, we attempted to link one such set of predictions generated using theory, modeling, and controlled experiments to patterns in the natural abundance of prey across a broad thermal gradient. To do so, we first predicted how warming will impact a stage-structured predator-prey interaction in riverine rock pools between Pantala spp. dragonfly nymph predators and Aedes atropalpus mosquito larval prey. We then described temperature variation across a set of hundreds of riverine rock pools (n = 775) and leveraged this natural gradient to look for evidence for or against our model's predictions. Our model's predictions suggested that warming should weaken predator control of mosquito larval prey by accelerating their development and shrinking the window of time that aquatic dragonfly nymphs could consume them in. This was consistent with data collected in rock pool ecosystems, where the negative effects of dragonfly nymph predators on mosquito larval abundance were weaker in warmer pools. Our findings provide additional evidence to substantiate our model-derived predictions, while emphasizing the importance of assessing similar predictions using natural gradients of temperature whenever possible.</p><p>Funding provided by: National Science Foundation<br>Crossref Funder Registry ID: https://ror.org/021nxhr62<br>Award Number: 1556686</p><p>Funding provided by: National Science Foundation<br>Crossref Funder Registry ID: https://ror.org/021nxhr62<br>Award Number: 1556743</p&gt

Insulin regulates multiple signaling pathways leading to monocyte/macrophage chemotaxis into the wound tissue

Wound healing is a complex process that involves sequential phases that overlap in time and space and affect each other dynamically at the gene and protein levels. We previously showed that insulin accelerates wound healing by stimulating faster and regenerative healing. One of the processes that insulin stimulates is an increase in monocyte/macrophage chemotaxis. In this study, we performed experiments in vivo and in vitro to elucidate the signaling transduction pathways that are involved in insulin-induced monocyte/macrophage chemotaxis. We found that insulin stimulates THP-1 cell chemotaxis in a dose-dependent and insulin receptor-dependent manner. We also show that the kinases PI3K-Akt, SPAK/JNK, and p38 MAPK are key molecules in the insulin-induced signaling pathways that lead to chemoattraction of the THP-1 cell. Furthermore, both PI3K-Akt and SPAK/JNK signaling involve Rac1 activation, an important molecule in regulating cell motility. Indeed, topical application of Rac1 inhibitor at an early stage during the healing process caused delayed and impaired healing even in the presence of insulin. These results delineate cell and molecular mechanisms involved in insulin-induced chemotaxis of monocyte/macrophage, cells that are critical for proper healing