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Extramacrochaetae promotes branch and bouton number via the sequestration of daughterless in the cytoplasm of neurons
Journal article   Open access   Peer reviewed

Extramacrochaetae promotes branch and bouton number via the sequestration of daughterless in the cytoplasm of neurons

Edward A Waddell, Jennifer M Viveiros, Erin L Robinson, Michal A Sharoni, Nina K Latcheva and Daniel R Marenda
Developmental neurobiology (Hoboken, N.J.), v 79(8), pp 805-818
Aug 2019
PMID: 31581354
url
https://doi.org/10.1101/686014View
SubmittedCC BY V4.0 Open

Abstract

Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Cell Proliferation - physiology Cytoplasm - metabolism Drosophila melanogaster - genetics Drosophila melanogaster - metabolism Drosophila Proteins - genetics Drosophila Proteins - metabolism Gene Expression Regulation, Developmental - genetics Neurogenesis - physiology Neurons - metabolism Presynaptic Terminals - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism
The Class I basic helix-loop-helix (bHLH) proteins are highly conserved transcription factors that are ubiquitously expressed. A wealth of literature on Class I bHLH proteins has shown that these proteins must homodimerize or heterodimerize with tissue-specific HLH proteins in order to bind DNA at E-box consensus sequences to control tissue-specific transcription. Due to its ubiquitous expression, Class I bHLH proteins are also extensively regulated posttranslationally, mostly through dimerization. Previously, we reported that in addition to its role in promoting neurogenesis, the Class I bHLH protein daughterless also functions in mature neurons to restrict axon branching and synapse number. Here, we show that part of the molecular logic that specifies how daughterless functions in neurogenesis is also conserved in neurons. We show that the Type V HLH protein extramacrochaetae (Emc) binds to and represses daughterless function by sequestering daughterless to the cytoplasm. This work provides initial insights into the mechanisms underlying the function of daughterless and Emc in neurons while providing a novel understanding of how Emc functions to restrict daughterless activity within the cell.

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Web of Science research areas
Developmental Biology
Neurosciences
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