Premium
An exon junction complex‐independent function of Barentsz in neuromuscular synapse growth
Author(s) -
Ho Cheuk Hei,
Paolantoni Chiara,
Bawankar Praveen,
Tang Zuojian,
Brown Stuart,
Roignant JeanYves,
Treisman Jessica E
Publication year - 2021
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.202153231
Subject(s) - exon , biology , neuromuscular junction , microbiology and biotechnology , synapse , alternative splicing , protein subunit , rna splicing , mutant , translation (biology) , neuroscience , genetics , gene , messenger rna , rna
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.