ArticleDevelopment (Cambridge, England)2013
Dynamic temporal requirement of Wnt1 in midbrain dopamine neuron development.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
- Exploring potential developmental origins of common neurodegenerative disorders.Biochemical Society transactions · 2024Review
- Using genome and transcriptome data from African-ancestry female participants to identify putative breast cancer susceptibility genes.Nature communications · 2024Article
- A loss-of-function mutation in human Oxidation Resistance 1 disrupts the spatial-temporal regulation of histone arginine methylation in neurodevelopment.Genome biology · 2023Article
- A novel mutation in intron 1 of Wnt1 causes developmental loss of dopaminergic neurons in midbrain and ASD-like behaviors in rats.Molecular psychiatry · 2023Article
- Differentiated Embryo-Chondrocyte Expressed Gene1 and Parkinson's Disease: New Insights and Therapeutic Perspectives.Current neuropharmacology · 2023Review
- Suppression of Wnt/β-Catenin Signaling Is Associated with Downregulation of Wnt1, PORCN, and Rspo2 in Alzheimer's Disease.Molecular neurobiology · 2023Article
- Roles of Transcription Factors in the Development and Reprogramming of the Dopaminergic Neurons.International journal of molecular sciences · 2022Review
- Human Brain-Based Models Provide a Powerful Tool for the Advancement of Parkinson's Disease Research and Therapeutic Development.Frontiers in neuroscience · 2022Review
- Pluripotent stem cell derived dopaminergic subpopulations model the selective neuron degeneration in Parkinson's disease.Stem cell reports · 2021Article
- The mouse dorsal raphe nucleus as understood by temporal Fgf8 lineage analysis.The Journal of comparative neurology · 2021Article
- Dysfunction of the proteoglycan Tsukushi causes hydrocephalus through altered neurogenesis in the subventricular zone in mice.Science translational medicine · 2021Article
- Neurodevelopmental defects and neurodegenerative phenotypes in human brain organoids carrying Parkinson's disease-linkedScience advances · 2021Article
- (D620N) VPS35 causes the impairment of Wnt/β-catenin signaling cascade and mitochondrial dysfunction in a PARK17 knockin mouse model.Cell death & disease · 2020Article
- Comprehensive bioinformatic analysis of Wnt1 and Wnt1-associated diseases.Intractable & rare diseases research · 2020Article
- Dose-Dependent and Subset-Specific Regulation of Midbrain Dopaminergic Neuron Differentiation by LEF1-Mediated WNT1/b-Catenin Signaling.Frontiers in cell and developmental biology · 2020Article
- Midbrain Dopaminergic Neuron Development at the Single Cell Level:Frontiers in cell and developmental biology · 2020Review
- Article
- Crosstalk of Intercellular Signaling Pathways in the Generation of Midbrain Dopaminergic Neurons In Vivo and from Stem Cells.Journal of developmental biology · 2019Review
- Using intracellular markers to identify a novel set of surface markers for live cell purification from a heterogeneous hIPSC culture.Scientific reports · 2018Article
- Temporal Expression ofFrontiers in neuroanatomy · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Wnt1-expressing progenitors generate midbrain dopamine (MbDA) and cerebellum (Cb) neurons in distinct temporal windows and from spatially discrete progenitor domains. It has been shown that Wnt1 and Lmx1a participate in a cross-regulatory loop that is utilized during MbDA neuron development. However, Wnt1 expression dynamically changes over time and precedes that of Lmx1a. The spatial and temporal requirements of Wnt1 in development and specifically its requirement for MbDA neurons remain to be determined. To address these issues, we generated a conditional Wnt1 allele and temporally deleted Wnt1 coupled with genetic lineage analysis. Using this approach, we show that patterning of the midbrain (Mb) and Cb by Wnt1 occurs between the one-somite and the six- to eight-somite stages and is solely dependent on Wnt1 function in the Mb, but not in the Cb. Interestingly, an En1-derived domain persists after the early deletion of Wnt1 and mutant cells express OTX2. However, the En1-derived Wnt1-mutant domain does not contain LMX1a-expressing progenitors, and MbDA neurons are depleted. Thus, we demonstrate an early requirement of Wnt1 for all MbDA neurons. Subsequently, we deleted Wnt1 in the ventral Mb and show a continued late requirement for Wnt1 in MbDA neuron development, but not in LMX1a-expressing progenitors. Specifically, Wnt1 deletion disrupts the birthdating of MbDA neurons and causes a depletion of MbDA neurons positioned medially and a concomitant expansion of MbDA neurons positioned laterally during embryogenesis. Collectively, our analyses resolve the spatial and temporal function of Wnt1 in Mb and Cb patterning and in MbDA neuron development in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.