An exon junction complex-independent function of Barentsz in neuromuscular synapse growth

EMBO Rep. 2022 Jan 5;23(1):e53231. doi: 10.15252/embr.202153231. Epub 2021 Nov 2.

Abstract

The exon junction complex controls the translation, degradation, and localization of spliced mRNAs, and three of its core subunits also play a role in splicing. Here, we show that a fourth subunit, Barentsz, has distinct functions within and separate from the exon junction complex in Drosophila neuromuscular development. The distribution of mitochondria in larval muscles requires Barentsz as well as other exon junction complex subunits and is not rescued by a Barentsz transgene in which residues required for binding to the core subunit eIF4AIII are mutated. In contrast, interactions with the exon junction complex are not required for Barentsz to promote the growth of neuromuscular synapses. We find that the Activin ligand Dawdle shows reduced expression in barentsz mutants and acts downstream of Barentsz to control synapse growth. Both barentsz and dawdle are required in motor neurons, muscles, and glia for normal synapse growth, and exogenous Dawdle can rescue synapse growth in the absence of barentsz. These results identify a biological function for Barentsz that is independent of the exon junction complex.

Keywords: Barentsz; Dawdle; exon junction complex; neuromuscular junction; synapse.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Drosophila / metabolism
  • Drosophila Proteins* / metabolism
  • Eukaryotic Initiation Factor-4A / genetics
  • Eukaryotic Initiation Factor-4A / metabolism
  • Exons / genetics
  • RNA-Binding Proteins* / metabolism
  • Synapses / metabolism

Substances

  • Drosophila Proteins
  • RNA-Binding Proteins
  • btz protein, Drosophila
  • Eukaryotic Initiation Factor-4A

Associated data

  • GEO/GSE165971