Kurt C. Marsden

This study identifies Cyfip2's role in visual sensorimotor circuit development in zebrafish, showing it mediates actin remodeling via Rac1 to enable visually-driven behaviors.

This study shows that disrupting vitamin D receptor signaling in zebrafish during early development causes lasting behavioral deficits in sensory processing.

The paper identifies Chd7 target genes that mediate CHARGE syndrome phenotypes using transcriptomic and proteomic analysis of zebrafish brain tissue.

This study examines how testing arena size and embryo media affect sensorimotor behaviors in zebrafish larvae, showing significant impacts on startle sensitivity, locomotion, and other behaviors.

This study identifies Cyfip2's role in regulating the acoustic startle threshold through FMRP, actin polymerization, and GABAB receptor function in zebrafish.

The paper shows that mutation location in chd7 affects morphological and behavioral phenotypes in a zebrafish CHARGE syndrome model.

This study shows that 2,4-DAB is more toxic than BMAA and AEG in zebrafish larvae, causing neurodegeneration-like molecular changes and motor dysfunction.

This study identifies eight genes, including Dolk and Kv1.1, that regulate zebrafish startle behavior through a common genetic pathway, with Dolk affecting Kv1.1 protein localization.

The paper shows that ZO1, a scaffolding protein, is required for Connexin localization at electrical synapses, which is necessary for functional gap junctions and synaptic transmission.

The paper identifies a genetic basis for molecular asymmetry at vertebrate electrical synapses in zebrafish, showing that two Connexins function presynaptically and postsynaptically, respectively, and are required for escape responses.