Depdc5 knockdown causes <scp>mTOR</scp>‐dependent motor hyperactivity in zebrafish

Abstract

This study demonstrates that Depdc5 knockdown leads to early-onset phenotypic features related to motor and neuronal hyperactivity. Restoration of phenotypic features by WT but not epilepsy-associated Depdc5 mutants, as well as by mTORC1 inhibition confirm the role of Depdc5 in the mTORC1-dependent molecular cascades, defining this pathway as a potential therapeutic target for <i>DEPDC5</i>-inherited forms of focal epilepsy.