ArticleNeuroscience bulletin2021
Homeobox Gene Six3 is Required for the Differentiation of D2-Type Medium Spiny Neurons.
Article in Neuroscience bulletin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development.Nature neuroscience · 2024Article
- Context-dependent regulation of Notch signaling in glial development and tumorigenesis.Science advances · 2023Article
- Chd5 Regulates the Transcription Factor Six3 to Promote Neuronal Differentiation.Stem cells (Dayton, Ohio) · 2023Article
- DNA methylation and hydroxymethylation characterize the identity of D1 and D2 striatal projection neurons.Communications biology · 2022Article
- Transcription factor Sp9 is a negative regulator of D1-type MSN development.Cell death discovery · 2022Article
- Dlx1/2-dependent expression of Meis2 promotes neuronal fate determination in the mammalian striatum.Development (Cambridge, England) · 2022Article
- The transcription factorFrontiers in cell and developmental biology · 2022Article
- From Progenitors to Progeny: Shaping Striatal Circuit Development and Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Comprehensive Analysis of Hub Genes Associated With Competing Endogenous RNA Networks in Stroke Using Bioinformatics Analysis.Frontiers in genetics · 2021Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medium spiny neurons (MSNs) in the striatum, which can be divided into D1 and D2 MSNs, originate from the lateral ganglionic eminence (LGE). Previously, we reported that Six3 is a downstream target of Sp8/Sp9 in the transcriptional regulatory cascade of D2 MSN development and that conditionally knocking out Six3 leads to a severe loss of D2 MSNs. Here, we showed that Six3 mainly functions in D2 MSN precursor cells and gradually loses its function as D2 MSNs mature. Conditional deletion of Six3 had little effect on cell proliferation but blocked the differentiation of D2 MSN precursor cells. In addition, conditional overexpression of Six3 promoted the differentiation of precursor cells in the LGE. We measured an increase of apoptosis in the postnatal striatum of conditional Six3-knockout mice. This suggests that, in the absence of Six3, abnormally differentiated D2 MSNs are eliminated by programmed cell death. These results further identify Six3 as an important regulatory element during D2 MSN differentiation.
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