ArticleNeural development2017
The Hunchback temporal transcription factor establishes, but is not required to maintain, early-born neuronal identity.
Article in Neural development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Hunchback functions in the postmitotic larval MDN to restrict axon outgrowth, synapse formation, and backward locomotion.Genes & development · 2026Article
- Imp and Chinmo are required for embryonic motor neuron axon and dendrite targeting.Biology open · 2025Article
- Single-cell transcriptomic analysis reveals diversity within mammalian spinal motor neurons.Nature communications · 2023Article
- Hunchback activates Bicoid in Pair1 neurons to regulate synapse number and locomotor circuit function.Current biology : CB · 2022Article
- Hunchback prevents notch-induced apoptosis in the serotonergic lineage of Drosophila Melanogaster.Developmental biology · 2022Article
- Synthetic reconstruction of theeLife · 2022Article
- Enhancer of trithorax/polycomb, Corto, regulates timing of hunchback gene relocation and competence in Drosophila neuroblasts.Neural development · 2022Article
- A shared transcriptional code orchestrates temporal patterning of the central nervous system.PLoS biology · 2021Article
- FIMTrack: An open source tracking and locomotion analysis software for small animals.PLoS computational biology · 2017Article
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Authors and funding
5 authors.
Funding
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.
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