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Woollard, A.

Publications and source records attributed to Woollard, A..

4 recordsLinked to original sources

Mechanical Stretch Counteracts Hypomagnetic Field-Induced Changes in YAP Nuclear Localization in C2C12 Myoblasts

The geomagnetic field (GMF) is a persistent environmental factor that influences biological processes. Reduced geomagnetic field exposure can alter cellular processes, but its effects on cellular mechanotransduction and responsiveness to mechanical stimulation remain poorly understood. Here, we developed an in vitro platform combining a programmable uniaxial stretching device with a mu-metal shielding chamber to independently manipulate mechanical stretch and magnetic field exposure. Using C2C12 myoblasts, we evaluated culture conditions and cyclic stretching parameters to identify a regimen that promoted nuclear localization of the mechanosensitive transcriptional coactivator yes-associated protein (YAP). We then compared cell and nuclear morphology and YAP nucleocytoplasmic localization under geomagnetic field (GMF) and hypomagnetic field (HMF; approximately 5 nT) conditions, with or without cyclic stretch. Under static conditions, HMF exposure increased cell and nuclear areas, promoted nuclear elongation, reduced nuclear circularity, and decreased the nuclear YAP level. Cyclic stretch induced nuclear alignment perpendicular to the stretching direction under both magnetic field conditions, without significantly altering cell or nuclear area or nuclear elongation. Importantly, cyclic stretch increased nuclear YAP localization under both GMF and HMF conditions, restoring it in HMF-exposed cells to levels comparable to those in stretched cells under GMF. These findings indicate that C2C12 myoblasts remain responsive to mechanical stimulation under HMF conditions and that cyclic stretch can counteract the HMF-associated reduction in nuclear YAP localization. Our platform provides a foundation for investigating how magnetic and mechanical cues jointly regulate myoblast behavior.

biophysics↗

Constraining pesticide resistance using evolution-informed selection regimes

The rapid evolution of pesticide resistance in sexually reproducing pests threatens global food security, yet the evolutionary principles needed to design durable resistance management strategies remain poorly tested experimentally. Theory predicts that deploying multiple pesticide compounds simultaneously should suppress resistance more effectively than sequential rotations, but empirical support in sexual pest populations has remained inconclusive. Here, we directly test how selection regime shapes resistance evolution using a genetically defined, obligately mating Caenorhabditis elegans system. We evolved large dioecious populations from a near-isogenic ancestor carrying two major-effect resistance alleles under contrasting pesticide deployment regimes. We show that compound mixtures combined with a substantial refuge consistently produced the strongest constraint on resistance evolution, markedly slowing the spread of resistance even when resistance alleles were neither recessive nor rare. Species-agnostic computational simulations reproduced the overall evolutionary dynamics, suggesting broad applicability. Overall, our results provide direct experimental evidence that pesticide resistance evolution can be predictably constrained by manipulating selection regimes.

evolutionary biology↗

Stable Cortical Body Maps Before and After Arm Amputation

The adult brains capacity for cortical reorganization remains debated. Using longitudinal neuroimaging in three adults, followed up to five years before and after arm amputation, we compared cortical activity elicited by movement of the hand (pre-amputation) versus phantom hand (post-amputation) and lips (pre/post-amputation). We observed stable representations of both hand and lips. By directly quantifying activity changes across amputation, we overturn decades of animal and human research, demonstrating amputation does not trigger large- scale cortical reorganization.

neuroscience↗

C. elegans Runx/CBFβ suppresses POP-1(TCF) to convert asymmetric to proliferative division of stem cell-like seam cells

A correct balance between proliferative and asymmetric cell divisions underlies normal development, stem cell maintenance and tissue homeostasis. What determines whether cells undergo symmetric or asymmetric cell division is poorly understood. To gain insight in the mechanisms involved, we studied the stem cell-like seam cells in the Caenorhabditis elegans epidermis. Seam cells go through a reproducible pattern of asymmetric divisions, instructed by non-canonical Wnt/{beta}-catenin asymmetry signaling, and symmetric divisions that increase the seam cell number. Using time-lapse fluorescence microscopy, we show that symmetric cell divisions maintain the asymmetric localization of Wnt/{beta}-catenin pathway components. Observations based on lineage-specific knockout and GFP-tagging of endogenous pop-1 support the model that POP-1TCF induces differentiation at a high nuclear level, while low nuclear POP-1 promotes seam cell self-renewal. Before symmetric division, the transcriptional regulator rnt-1Runx and cofactor bro-1CBF{beta} temporarily bypass Wnt/{beta}-catenin asymmetry by downregulating pop-1 expression. Thereby, RNT-1/BRO-1 appears to render POP-1 below the level required for its repressor function, which converts differentiation into self-renewal. Thus, opposition between the C. elegans Runx/CBF{beta} and TCF stem-cell regulators controls the switch between asymmetric and symmetric seam cell division.

developmental biology↗