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Britton, S. E.

Publications and source records attributed to Britton, S. E..

4 recordsLinked to original sources

Genotype-by-environment-by-environment (GxExE) interactions have the potential to shape adaptation in response to multiple stressors

Rapid adaptation in complex environments depends not only on the amount of genetic variation, but also on patterns of covariation among traits targeted by selection. Anthropogenic stressors create rapidly changing and multifaceted environments and provide powerful systems in which to investigate the potential for adaptation to multiple coinciding stressors. We investigate the combined effects of heat and chemical stress on survival in the black scavenger fly, Sepsis neocynipsea, and determine the genetic basis for resistance. In a fully factorial experiment, we expose isofemale lines to combinations of heat stress and ivermectin, a veterinary antiparasitic to which these flies are naturally exposed in agricultural landscapes. Using a Bayesian quantitative genetic approach, we estimate broad-sense genetic variation and cross-environmental genetic correlations. First, we show that these two stressors have synergistic effects on survival, with heat stress exacerbating the lethal effects of ivermectin. Second, we find that the largest component of genetic variation is the response to heat and ivermectin in combination (genotype-by-environment-by-environment; GxExE). Third, cross-environmental genetic correlations are weak, implying that relative genetic performance is dependent on the specific combination of stressors. Together, these results suggest that incorporating GxExE is essential for understanding adaptive potential in multi-stressor environments.

evolutionary biology↗

Spatial and temporal coordination of signaling pathways in tissue differentiation: developmental atlas of protein expression during zebra finch beak maturation

BackgroundMorphogenesis depends on spatial and temporal coordination of signaling pathways, yet the colocalization of proteins across pathways remains poorly understood. Here we examine cellular and histological localization of regulatory proteins forming core craniofacial developmental pathways during beak morphogenesis of the zebra finch (Taeniopygia guttata). ResultsWe present an atlas of spatiotemporal coexpression of {beta}-catenin, Bmp4, CaM, Dkk3, Fgf8, Ihh, Tgf{beta}2, and Wnt4 across embryonic stages HH29-42 revealing both established and novel patterns of expression. Overall, in the earliest stages (HH29-32), most proteins show broad and overlapping expression across epithelial and mesenchymal tissues. By stage HH36, expression becomes increasingly compartmentalized, with pronounced differentiation among tissue types. Notably, at later stages, proteins showed tissue-specific distributions in boundary versus core regions of chondrogenic and osteogenic domains indicating coordinated cross-pathway patterning during cartilage and bone formation. ConclusionsOsteogenesis in the zebra finch beak is organized by coordinated signaling between boundary-associated cells and differentiating cores, with cross-pathway feedback establishing bone and cartilage differentiation while maintaining boundaries. Our results corroborated core elements of craniofacial signaling dynamics, while revealing unexpected subcellular localization for several proteins that showed regulatory complexity not captured by prior transcript-level maps. This atlas provides a protein-level baseline for comparative and mechanistic studies of beak morphogenesis.

developmental biology↗

Ultimate paths of least resistance: Intrinsically disordered links as developmental resets in regulatory protein networks

Development and evolution require both stability and adaptability, yet how these opposite properties are reconciled is unclear. Here, we show that intrinsically disordered proteins (IDPs) act as reset mechanisms in conserved regulatory networks facilitating developmental transitions by integrating physical processes with genetic regulation. By tracing the ontogeny of mesenchymal cells in avian beak primordia, we demonstrate that mechanosensitive IDPs mediate shifts between physical cell states via dosage-dependent binding plasticity, converting stochastic protein variation into discreet regulatory networks. The disorder-enabled connectivity in these proteins resets their regulatory specialization and promotes population divergence. Comparative analyses across avian proteomes confirm that binding plasticity in transcriptional IDPs drives their diverse regulatory associations and accelerates their evolution. By resetting specialized states in conserved regulatory networks, IDPs flexibly regulate developmental pathways and reconcile precision with evolvability.

evolutionary biology↗

Cell jamming transitions shape regulatory protein gradients and prime evolutionary divergence

A long-standing goal of evolutionary developmental biology is to identify the mechanisms underlying criticality of developmental transitions that allow processes governing individual cells scale up to the organism-level patterning. The viscoelastic properties of embryonic tissues imply collective cell behaviors, leading to the expectation that signaling networks should capitalize on the material properties of tissues, structuring morphogenesis around the spatial and temporal transitions that they induce. Here, we show that this interaction is evident even prior to tissue differentiation and is traceable to behavior of individual cells. In avian beak primordia, we find that fields of mesenchymal cells undergo cycles of local jamming dynamically modulating coordination of cell shape and movement. These cycles progressively alter the spatial reach of regulatory proteins, strongly expanding or restricting their gradients based on tissue mechanical state. Tissue-level gradients of proteins most sensitive to local cell jamming transitions also diverge the most across populations, priming tissue compartmentalization. These findings suggest that the material state transition is an effective interface for integration of stochastic physical processes and genetic regulation and is well placed to underlie criticality of developmental systems allowing local rules governing cell-state transitions scale up to tissue-level patterning. More broadly, our findings reveal how transient material transitions reset developmental trajectories and promote diversification while preserving robustness.

evolutionary biology↗