The Hunchback temporal transcription factor establishes, but is not required to maintain, early-born neuronal identity

Keiko Hirono,Chris Q Doe,Ellie S Heckscher,Minoree Kohwi,Matt Q Clark

doi:10.1186/s13064-017-0078-1

Abstract

BackgroundDrosophila and mammalian neural progenitors typically generate a diverse family of neurons in a stereotyped order. Neuronal diversity can be generated by the sequential expression of temporal transcription factors. In Drosophila, neural progenitors (neuroblasts) sequentially express the temporal transcription factors Hunchback (Hb), Kruppel, Pdm, and Castor. Hb is necessary and sufficient to specify early-born neuronal identity in multiple lineages, and is maintained in the post-mitotic neurons produced during each neuroblast expression window. Surprisingly, nothing is currently known about whether Hb acts in neuroblasts or post-mitotic neurons (or both) to specify first-born neuronal identity.MethodsHere we selectively remove Hb from post-mitotic neurons, and assay the well-characterized NB7-1 and NB1-1 lineages for defects in neuronal identity and function.ResultsWe find that loss of Hb from embryonic and larval post-mitotic neurons does not affect neuronal identity. Furthermore, removing Hb from post-mitotic neurons throughout the entire CNS has no effect on larval locomotor velocity, a sensitive assay for motor neuron and pre-motor neuron function.ConclusionsWe conclude that Hb functions in progenitors (neuroblasts/GMCs) to establish heritable neuronal identity that is maintained by a Hb-independent mechanism.We suggest that Hb acts in neuroblasts to establish an epigenetic state that is permanently maintained in early-born neurons.

Highlights

Drosophila and mammalian neural progenitors typically generate a diverse family of neurons in a stereotyped order
Loss of Hunchback from both neuroblast and neurons eliminates early-born neuronal identity We wanted to determine whether our hb RNAi transgene was strong enough to eliminate detectable Hb protein and replicate the hb null mutant phenotype
We conclude that hb RNAi is capable of removing some Hb protein from NB7-1 and all detectable Hb protein from the U1 neuron, resulting in abnormal U1 neuronal identity

Summary

Introduction

Drosophila and mammalian neural progenitors typically generate a diverse family of neurons in a stereotyped order. In both mammals and Drosophila, the earliest steps are spatial patterning to define a neuroectodermal territory, followed by more precise spatial patterning to generate distinct progenitor domains (reviewed in [23, 43]) Both mammals and Drosophila progenitors can sequentially express temporal transcription factors that specify neural identity based on birth-order (mouse: [2, 14, 32]) (fly: [3,4,5,6,7, 9, 18, 22, 24, 25, 34, 35, 37, 46]).

Results

Discussion

Conclusion