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Biology subjects

Woods, J. P.

Publications and source records attributed to Woods, J. P..

2 recordsLinked to original sources

Mating display plasticity predicts the biogeography of complex communication and population persistence in changing climates

Animals often produce complex combinations of signals to enhance display detection, interpretation, and the information conveyed during communication. Combined signals can serve many functions in communication systems, but we know little about how signal combinations initially evolve and why they often vary in complexity across broad geographic gradients. Here, we show that environmentally driven changes in the coordinated production of multiple signals determine whether the signals can interact in functional ways, and thereby shape the capacity for selection to favor increased display complexity. Our behavioral experiment in a focal species of Schizocosa wolf spider reveal that shifts to hotter and wetter environments can enable males with exaggerated morphological ornaments to also produce exaggerated courtship behaviors, allowing these signals to interactively affect mating success. Congruently, phylogenetic analyses show that species in hotter and wetter regions of North America have repeatedly evolved more complex courtship displays alongside exaggerated morphological ornaments. Biogeographic analyses further suggest that geographic gradients in display complexity may arise not only from in situ evolution, but also from more frequent establishment of species with complex displays in hotter and wetter regions. Finally, we found that species with complex displays were more likely to persist in areas that have faced more severe climate warming and intensified precipitation in the last 50 years--conditions that should enhance the functioning of complex mating displays for reproductive success. Altogether, our findings reveal a novel association between plasticity in inter-signal interactions and variation in the complexity of communication systems across scales of biological organization.

evolutionary biology↗

An activating mutation in Pdgfrb causes skeletal stem cell defects with osteopenia andovergrowth in mice

Autosomal dominant PDGFR{beta} gain-of-function mutations in mice and humans cause a spectrum of wasting and overgrowth disorders afflicting the skeleton and other connective tissues, but the cellular origin of these disorders remains unknown. We demonstrate that skeletal stem cells (SSCs) isolated from mice with a gain-of-function D849V point mutation in PDGFR{beta} exhibit SSC colony formation defects that parallel the wasting or overgrowth phenotypes of the mice. Single-cell RNA transcriptomics with the SSC colonies demonstrates alterations in osteoblast and chondrocyte precursors caused by PDGFR{beta}D849V. Mutant SSC colonies undergo poor osteogenesis in vitro and mice with PDGFR{beta}D849V exhibit osteopenia. Increased expression of Sox9 and other chondrogenic markers occurs in SSC colonies from mice with PDGFR{beta}D849V. Increased STAT5 phosphorylation and overexpression of Igf1 and Socs2 in PDGFR{beta}D849V SSCs suggests that overgrowth in mice involves PDGFR{beta}D849V activating the STAT5-IGF1 axis locally in the skeleton. Our study establishes that PDGFR{beta}D849V causes osteopenic skeletal phenotypes that are associated with intrinsic changes in SSCs, promoting chondrogenesis over osteogenesis.

developmental biology↗