bioRxiv Science⌕ Search

Biology subjects

Kidder, E. J.

Publications and source records attributed to Kidder, E. J..

2 recordsLinked to original sources

A field experiment assessing the roles of drought, herbivory, and local climate on cyanogenesis cline formation and local adaptation in Trifolium repens

Projecting how a population will adapt to environmental changes requires a mechanistic understanding of the specific biotic and abiotic factors that impose selection on that population. In white clover (Trifolium repens), clines in an antiherbivore defense mechanism, hydrogen cyanide (HCN), form via variation in selection imposed by the environment. However, the specific environmental factors that select for or against chemical defense phenotypes in white clover remain unresolved. We performed a field experiment in high and low latitude study sites, with a factorial manipulation of precipitation and herbivory at each site. These factors are hypothesized to be important in driving HCN cline formation, so we investigated their effects on fitness of a white clover F3 recombinant population, segregating for the alleles underlying the HCN chemical defense phenotype. Surprisingly, we found precipitation and herbivory either did not drive differential selection on HCN or its metabolic components, or did not impose selection in a manner consistent with the maintenance of observed HCN clines. Instead, we find that the production only one of the metabolic components of HCN, cyanogenic glycosides, resulted in a fitness advantage, even when lacking the ability to produce HCN. This was most prominent at the northern study site, which is again contrary to expectations. These results suggest additional physiological roles that cyanogenic glycosides may play in adaptation and the evolutionary ecology of white clover. This study highlights the importance of experimental manipulations of environmental factors to understand how selection acts on genes underlying important phenotypic traits, often in unexpected ways.

evolutionary biology↗

SMAD6 Integrates Endothelial Cell Homeostatic Flow Responses Downstream of Notch

ABSTRACTLaminar shear stress regulates blood vessel morphogenesis and subsequent quiescence, leading to vascular homeostasis. Although important for vessel function, how vascular homeostasis is set up and maintained is poorly understood. SMAD6, a scaffold for several signaling pathways, is expressed in developing arteries and its expression is flow-regulated. We found that SMAD6 is essential for endothelial cell flow-mediated responses downstream of the mechanosensor Notch1. Endothelial cells with reduced SMAD6 levels failed to align under homeostatic laminar shear flow, while forced SMAD6 expression rescued misalignment induced by reduced Notch1 signaling. SMAD6-dependent homeostatic laminar flow responses required the Notch ligand Dll4 and Notch transcriptional activity. Mechanistically, neither the N-terminal nor the C-terminal domain of SMAD6 alone rescued flow alignment upon loss of Notch signaling. Endothelial cells with reduced Smad6 levels had compromised barrier function, and RNA profiling revealed upregulation of proliferation-associated genes and down regulation of junction-associated genes. Among junction-related genes affected by SMAD6 levels, the proto-cadherin PCDH12 was upregulated by homeostatic flow and required for proper flow-mediated endothelial cell alignment. Thus, SMAD6 is a critical integrator of flow-mediated signaling inputs downstream of Notch1, as vessels transition from an angiogenic to a homeostatic phenotype.Competing Interest StatementThe authors have declared no competing interest.View Full Text

cell biology↗