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

Details

Serval ID
serval:BIB_CBC52F96717F
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
An exon junction complex-independent function of Barentsz in neuromuscular synapse growth.
Journal
EMBO reports
Author(s)
Ho C.H., Paolantoni C., Bawankar P., Tang Z., Brown S., Roignant J.Y., Treisman J.E.
ISSN
1469-3178 (Electronic)
ISSN-L
1469-221X
Publication state
In Press
Peer-reviewed
Oui
Pages
e53231
Language
english
Notes
Publication types: Journal Article
Publication Status: aheadofprint
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
Pubmed
Web of science
Create date
03/11/2021 15:47
Last modification date
20/11/2021 6:34
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