Chrissy L. Hammond

This study investigates the functional roles of TANGO1S domains in maintaining ER-Golgi architecture by analyzing domain-deletion mutants in knockout cells.

This study uses Prime Editors in zebrafish to achieve precise DNA insertion and substitution without exogenous donor DNA, showing higher efficiency for short modifications with nuclease-based PEn.

This study shows nanovibrational stimulation preferentially enhances osteogenic responses in zebrafish without significantly affecting other tissues.

This study shows that loss of lmx1ba in zebrafish causes premature osteoarthritis by disrupting skeletal homeostasis and joint maintenance in adult life.

This paper introduces coagulative granular hydrogels stabilized by enzyme-catalyzed fibrin networks to enhance mechanical integrity and support tissue regeneration.

This paper develops a deep learning framework for automated segmentation of 3D CT data and validates its biomechanical accuracy using zebrafish mandibles.

This study shows that telomerase deficiency in zebrafish accelerates brain ageing by promoting senescence, inflammation, and blood-brain barrier dysfunction.

The paper characterizes lmx1b paralogues in zebrafish, revealing distinct roles in skeletal, kidney, and muscle development, and identifies a new role in notochord cell inflation.

This study identifies TMEM263 as an ER-resident protein essential for lipid droplet formation and growth, showing its role in lipid condensation and organismal development.

This study genetically modifies zebrafish to demonstrate how altering individual traits can tune collective behavior, showing mutant fish exhibit more orderly motion than wildtype.

This study identifies cyclical compression loading as critical for normal joint morphogenesis in zebrafish, showing that dynamic mechanical stimuli, not static compression, regulate joint shape and growth.

This study uses computational modeling to show that growth orientation, not growth rate, primarily drives jaw joint morphogenesis in larval zebrafish.

The paper identifies genes involved in human bone disease by analyzing transcriptomic changes during zebrafish scale regeneration.

This study shows that autophagy is essential for proper chondrocyte maturation and joint formation in zebrafish, with its disruption causing premature hypertrophy and developmental defects.

The paper shows transformed notochordal cells in zebrafish cause skeletal damage, chronic wound-like responses, and bone homeostasis disruption, linking chordomas to inflammation and IVD degeneration.

The paper identifies NCOA3 as a candidate gene for autosomal dominant progressive hearing loss through linkage analysis and functional studies in zebrafish.

A rare SMAD9 mutation is linked to high bone mass, suggesting the BMP pathway as a potential osteoanabolic target.

This study examines the effects of col11a2 loss in zebrafish on joint development and function, showing increased stiffness and early onset osteoarthritis.

This study shows that zebrafish lacking sp7 can replace teeth without attachment bone, but with poor differentiation and abnormal tooth orientation.

This study shows that Wnt signaling mediates mechanical strain responses during zebrafish joint development, affecting cell proliferation and migration but not chondrocyte intercalation.

This paper develops a zebrafish model to study joint dysplasia by manipulating the mechanical environment, identifying cellular factors that predict recovery of joint shape and function.

This study shows that loss of giantin in zebrafish causes cilia function defects, with morphants showing fewer cilia and mutants having elongated cilia.