Chrissy Hammond

Using transgenic reporters to visualize bone and cartilage signaling during development in vivo.

Expression of glycosaminoglycan epitopes during zebrafish skeletogenesis.

Spinal deformity in aged zebrafish is accompanied by degenerative changes to their vertebrae that resemble osteoarthritis.

Glucocerebrosidase deficiency in zebrafish affects primary bone ossification through increased oxidative stress and reduced Wnt/β-catenin signaling.

Finite element modelling predicts changes in joint shape and cell behaviour due to loss of muscle strain in jaw development.

Differential effects of altered patterns of movement and strain on joint cell behaviour and skeletal morphogenesis.

The Golgi matrix protein giantin is required for normal cilia function in zebrafish.

Wnt signalling controls the response to mechanical loading during zebrafish joint development.

Giantin-knockout models reveal a feedback loop between Golgi function and glycosyltransferase expression.

Regulator of calcineurin-2 is a centriolar protein with a role in cilia length control.

The mechanical impact of loss on joints; mutant zebrafish show changes to joint development and function, which leads to early-onset osteoarthritis.

Zebrafish as an Emerging Model for Osteoporosis: A Primary Testing Platform for Screening New Osteo-Active Compounds.

Scleraxis genes are required for normal musculoskeletal development and for rib growth and mineralization in zebrafish.

A Rare Mutation in SMAD9 Associated With High Bone Mass Identifies the SMAD-Dependent BMP Signaling Pathway as a Potential Anabolic Target for Osteoporosis.

Finite element and deformation analyses predict pattern of bone failure in loaded zebrafish spines.

Zebrafish as a model to study autophagy and its role in skeletal development and disease.

Potential of zebrafish as a model to characterise MicroRNA profiles in mechanically mediated joint degeneration.

Muscle defects due to perturbed somite segmentation contribute to late adult scoliosis.

NCOA3 identified as a new candidate to explain autosomal dominant progressive hearing loss.

Skeletal Biology and Disease Modeling in Zebrafish.

Exposure to hypergravity during zebrafish development alters cartilage material properties and strain distribution.

Transformed notochordal cells trigger chronic wounds in zebrafish, destabilizing the vertebral column and bone homeostasis.

Opportunities and Challenges in Functional Genomics Research in Osteoporosis: Report From a Workshop Held by the Causes Working Group of the Osteoporosis and Bone Research Academy of the Royal Osteoporosis Society on October 5th 2020.

Pharmacological Manipulation of Early Zebrafish Skeletal Development Shows an Important Role for Smad9 in Control of Skeletal Progenitor Populations.

Wnt16 Elicits a Protective Effect Against Fractures and Supports Bone Repair in Zebrafish.

Giantin is required for intracellular N-terminal processing of type I procollagen.

3D assessment of intervertebral disc degeneration in zebrafish identifies changes in bone density that prime disc disease.

Autophagy coordinates chondrocyte development and early joint formation in zebrafish.

Corrigendum to: NCOA3 identified as a new candidate to explain autosomal dominant progressive hearing loss.

Dominating lengthscales of zebrafish collective behaviour.

Regenerating zebrafish scales express a subset of evolutionary conserved genes involved in human skeletal disease.

Growth orientations, rather than heterogeneous growth rates, dominate jaw joint morphogenesis in the larval zebrafish.

Osteomodulin downregulation is associated with osteoarthritis development.

Compressive stress gradients direct mechanoregulation of anisotropic growth in the zebrafish jaw joint.