The TAP/NXF1-Binding Region of HuD Is Required for Translation and Neuronal Differentiation

Abstract

The neuronal ELAV protein HuD is known to promote neuronal differentiation and stimulate cap-dependent translation, but the underlying mechanism remains incompletely understood. Here, we identify a functional domain within the HuD linker that governs interaction with the nuclear export factor TAP/NXF1 and stimulates translation. Using a series of deletion mutants, we show that TAP/NXF1 binding is functionally separable from cytoplasmic localization, and that loss of this interaction correlates with impaired translation and neurite outgrowth. These findings reveal a critical subdomain within HuD that recruits TAP/NXF1 to promote translation and neuronal differentiation, establishing a mechanistic link between RNA export factors and ELAV-mediated translational control.