Disrupting synapse formation between the retina and the brain in zebrafish larvae-by eliminating the molecular motor Kif5A-triggers a compensatory increase in the branching of retinal axons aimed at restoring synapse number.

Planarians provide evidence for a common evolutionary origin of vertebrate and invertebrate excretory systems and provide a novel experimental model to study human kidney diseases.

Large-scale developmental defects in mice occur with the ablation of the epithelial-specific splicing factors Esrp1 and Esrp2.

Many tumors are depleted of mitochondrial DNA; this depletion is associated with changes in gene expression and with the incidence of critical somatic mutations and alterations.

Building on previous work (Reznik et al., 2016), independent measurements of mitochondrial genome copy number and expression indicate that several solid tumor types suppress respiratory metabolism compared to normal tissue.

A zebrafish model for a particular form of human deafness (DFNB63) changes our view of this disease by revealing a defect in the localization of Transmembrane channel-like proteins that are essential for mechanotransduction in sensory cells.

Careful analysis of adverse drug reaction reports reveals noise and biases embedded in this data and allows for systematic mitigation of these effects to produce much more robust understanding of side effects of marketed drugs.

Neural and network activity within a pontine-cortical micturition circuit are finely coordinated with urodynamics to assure appropriate voiding behaviors.

Precisely-timed bursts of closed-loop vagus nerve stimulation during rehabilitation restore neural connectivity and substantially improve recovery of motor function after SCI.

Engagement of both host and parasite signaling pathways proves a novel approach for developing improved anti-parasitic therapies.