The lab investigates how early brain development shapes vulnerability to neuropsychiatric disorders, with a focus on the molecular and environmental factors that influence the formation and function of neural circuits. We frequently use zebrafish to visualize developing brain networks and to model genetic conditions.

Using zebrafish, we visualize developing brain networks and model genetic conditions such as tuberous sclerosis complex (TSC), where mutations in the TSC1 or TSC2 genes lead to chronic overactivation of the mTORC1 signaling pathway. This pathway acts as a central hub that helps the developing brain interpret and respond to internal and external cues, and when it becomes hyperactive – as is often seen in autism spectrum disorder (ASD) – sensory information can be processed in atypical ways. In our TSC zebrafish model, we discovered that the loss of normal light preference stems from disrupted processing of light signals in a brain region called the left dorsal habenula. Neurons in this region in Tsc2-deficient fish were overly active and failed to adapt to repeated light exposure, indicating a breakdown in normal sensory filtering. Importantly, these abnormalities were reversed with rapamycin, a drug that inhibits mTORC1. This work reveals how excessive mTORC1 activity can directly impair sensory processing, providing a mechanistic link between early developmental signaling defects and the atypical sensory responses often observed in ASD.