Matthew P. Harris

The paper identifies late embryonic developmental changes in penguin forelimbs that lead to flattened bone morphology and reduced musculature, driven by molecular programs associated with tendon-attachment sites.

The paper shows that the regulatory landscape controlling Hoxd gene expression in limbs was co-opted from an ancestral cloacal program in tetrapods.

The paper identifies ancestral dorsal-ventral patterning mechanisms in fish fins and shows evolutionary innovations in their regulation.

This study develops a zebrafish injury model to study heterotopic ossification, identifies differentially regulated genes, and shows that Kcnk5b and Il11ra influence bone formation after injury.

This study shows that graded Fibronectin (FN1) cues guide calvarial osteoblast migration and suture patency, with disruptions in FN1 or related pathways causing craniosynostosis in mice.

The paper develops genetic tools for the mangrove killifish, improving embryo yield and enabling targeted gene knockout studies.

The paper investigates how oncogenic clones drive controlled overgrowth in zebrafish, identifying a heterochronic shift during bone development as the mechanism.

This study characterizes macrodactyly, a localized overgrowth disorder, by linking it to somatic mosaic PIK3CA mutations and demonstrating nerve and vascular regulation of growth through a novel animal model.

TRACCER improves convergence analysis by incorporating topological relationships, identifying significant genetic signals in marine mammal transitions and mammalian longevity.

The paper identifies genetic regulators of fin proportion in flying fish through comparative genomics and zebrafish mutants, revealing a conserved signaling pathway involving amino acid transport and potassium channels.

This study identifies celsr1a as essential for tissue homeostasis and aging onset in zebrafish, showing its role in maintaining progenitor cells and that caloric restriction can mitigate its effects.

The paper identifies a zebrafish mutant with proportional overgrowth due to Kcc4a loss of function and shows its role in bioelectric signaling for growth regulation.

This study shows zebrafish mutants with type I collagen mutations closely mimic human collagenopathies, revealing phenotypic variability linked to disease severity and potential for identifying genetic modifiers.

The paper identifies kcnk5b as a key regulator of allometric growth in zebrafish fins by integrating calcineurin signaling.