ArticleNeural development2012
The transcription factor Uncx4.1 acts in a short window of midbrain dopaminergic neuron differentiation.
Article in Neural development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
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- Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity.eLife · 2019Article
- Characterization of paralogousGene: X · 2019Article
- Whole-Body Single-Cell Sequencing Reveals Transcriptional Domains in the Annelid Larval Body.Molecular biology and evolution · 2018Article
- The effects of short-term high-fat feeding on exercise capacity: multi-tissue transcriptome changes by RNA sequencing analysis.Lipids in health and disease · 2017Article
- Differentiation renders susceptibility to excitotoxicity in HT22 neurons.Neural regeneration research · 2013Article
- Patterning, specification, and differentiation in the developing hypothalamus.Wiley interdisciplinary reviews. Developmental biologyReview
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Authors and funding
9 authors at 6 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe homeobox containing transcription factor Uncx4.1 is, amongst others, expressed in the mouse midbrain. The early expression of this transcription factor in the mouse, as well as in the chick midbrain, points to a conserved function of Uncx4.1, but so far a functional analysis in this brain territory is missing. The goal of the current study was to analyze in which midbrain neuronal subgroups Uncx4.1 is expressed and to examine whether this factor plays a role in the early development of these neuronal subgroups.
resultsWe have shown that Uncx4.1 is expressed in GABAergic, glutamatergic and dopaminergic neurons in the mouse midbrain. In midbrain dopaminergic (mDA) neurons Uncx4.1 expression is particularly high around E11.5 and strongly diminished already at E17.5. The analysis of knockout mice revealed that the loss of Uncx4.1 is accompanied with a 25% decrease in the population of mDA neurons, as marked by tyrosine hydroxylase (TH), dopamine transporter (DAT), Pitx3 and Ngn2. In contrast, the number of glutamatergic Pax6-positive cells was augmented, while the GABAergic neuron population appears not affected in Uncx4.1-deficient embryos.
conclusionWe conclude that Uncx4.1 is implicated in the development of mDA neurons where it displays a unique temporal expression profile in the early postmitotic stage. Our data indicate that the mechanism underlying the role of Uncx4.1 in mDA development is likely related to differentiation processes in postmitotic stages, and where Ngn2 is engaged. Moreover, Uncx4.1 might play an important role during glutamatergic neuronal differentiation in the mouse midbrain.
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