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Renee Duckworth

Renee Duckworth

· ProfessorVerified

University of Arizona · Ecology and Evolutionary Biology

Active 2000–2026

h-index24
Citations3.0k
Papers4811 last 5y
Funding$1.2M
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About

Renee Duckworth is a Professor of Ecology and Evolutionary Biology at the University of Arizona, a position she has held since 2023. Her research integrates ecological and evolutionary concepts with the ultimate goal of understanding how complex traits evolve. The central aims of her work are to understand how behavior evolves and how evolutionary changes in behavior influence population dynamics that ultimately shape macroevolutionary processes. To achieve these goals, she employs large-scale field experiments, empirical measures of lifetime fitness, field endocrinology, and molecular multi-generational pedigree reconstruction to investigate the dynamics of trait evolution, particularly in the context of range expansion and species coexistence in passerine birds. Her current projects include studying eco-evolutionary feedbacks between behavioral change and population density, investigating the proximate epigenetic basis of maternal effects on dispersal strategies, exploring neuroendocrine mechanisms and developmental constraints on personality traits, and conducting comparative studies across vertebrates on the evolution of traits that affect range limits and species coexistence. Her work aims to elucidate the mechanisms underlying behavioral stability, dispersal strategies, and trait evolution, contributing significantly to the understanding of evolutionary ecology and behavioral evolution.

Research topics

  • Psychology
  • Neuroscience
  • Biology
  • Developmental psychology
  • Endocrinology
  • Physics
  • Ecology
  • Genetics

Selected publications

  • Ultimate paths of least resistance: intrinsically disordered proteins as developmental resets in regulatory networks

    Proceedings of the Royal Society B Biological Sciences · 2026-01-14 · 1 citations

    articleOpen accessSenior author

    Evolution requires flexibility, needed for exploration and adjustment, and stability, needed for function. In development, these conflicting requirements are met by regulatory complexes of factors that can transiently reassemble into functional groups at each successive context. Two hallmarks of these complexes-interchangeability and accessibility of binding partners-implicate intrinsically disordered proteins (IDPs) as likely key organizers. We test whether the binding plasticity of IDPs and their capacity to sustain phase-separated regulatory assemblies can reconcile developmental continuity with microevolutionary divergence in avian beak primordia. We found that the axes of the core regulatory network governing shifts between mechanical states of homogeneous cells in early development align with population divergence in this regulatory network, a pattern produced by IDPs' dosage-dependent binding plasticity. This disorder-enhanced connectivity converts the stochastic variation in protein concentration at each transition into discrete network configurations, resetting regulatory specializations and promoting plasticity and population divergence. Comparative analyses of avian proteomes confirm that binding promiscuity in regulatory IDPs broadens their interaction repertoires and accelerates their evolution. By enabling reversible transitions between specialized network states, IDPs can ensure developmental continuity and evolutionary persistence, reconciling precision with evolvability in avian beak diversification.

  • Stress-induced maternal effects on offspring: linking multivariate egg investment to environmental quality

    SSRN Electronic Journal · 2026-01-01

    preprintOpen accessSenior author
  • Cell jamming transitions can affect regulatory protein gradients and prime evolutionary divergence

    Journal of The Royal Society Interface · 2025-11-01 · 4 citations

    articleOpen accessSenior author

    A long-standing goal of evolutionary developmental biology is to identify the rules by which processes governing individual cells scale up to organism-level patterning. The viscoelastic properties of embryonic tissues imply collective cell behaviours, leading to the expectation that gene regulatory networks should capitalize on the material properties of tissues. Here, we show that large-scale variation in morphogenesis can be traced to cell-level dynamic. In avian beak primordia, we find that fields of mesenchymal cells undergo cycles of local jamming that predictably change coordination of cell shapes and movements. These cycles, in turn, alter the spatial reach of regulatory proteins, shaping their gradients in relation to tissue mechanical state. Long-range gradients of proteins most sensitive to local jamming differ the most across populations and, through their priming of tissue compartmentalization, can facilitate evolutionary divergence in beak morphology. Jamming transitions might thus allow these tissues to reconcile seemingly contradictory needs: robust maintenance, facilitated by jamming phase that resets or synchronizes cells, and adaptive flexibility, promoted by unjamming phase, that allow rearrangements, explorations or expansions. These transitions can also integrate stochastic physical processes and biological regulation allowing local rules governing cell behaviours to propagate to tissue-level patterning, ultimately promoting diversification and plasticity while preserving robustness.

  • Author response for "Ultimate paths of least resistance: Intrinsically disordered proteins as developmental resets in regulatory networks"

    2025-11-03

    peer-reviewSenior author
  • Author response for "Ultimate paths of least resistance: Intrinsically disordered proteins as developmental resets in regulatory networks"

    2025-11-11

    peer-reviewSenior author
  • Author response for "Ultimate paths of least resistance: Intrinsically disordered proteins as developmental resets in regulatory networks"

    2025-11-04

    peer-reviewSenior author
  • Cell jamming transitions shape regulatory protein gradients and prime evolutionary divergence

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-06 · 3 citations

    preprintOpen accessSenior author

    Abstract 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.

  • Author response for "Ultimate paths of least resistance: Intrinsically disordered proteins as developmental resets in regulatory networks"

    2025-09-17

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

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-17 · 1 citations

    articleOpen access1st authorCorresponding

    Abstract Background: Morphogenesis 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 ). Results: We present an atlas of spatiotemporal coexpression of β-catenin, Bmp4, CaM, Dkk3, Fgf8, Ihh, Tgfβ2, 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. Conclusions: Osteogenesis 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.

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

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-18 · 2 citations

    preprintOpen accessSenior author

    ABSTRACT 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.

Recent grants

Frequent coauthors

Awards & honors

  • NSF CAREER (2014-2021)
  • Fellow, American Ornithological Society (2017)
  • Young Investigator Prize, American Society of Naturalists (2…
  • Ned K. Johnson Young Investigator Award, American Ornitholog…
  • Early Career Scientist Award, Evolutionary Ecology, Universi…
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