HDAC1 and HDAC2 Regulate Intermediate Progenitor Positioning to Safeguard Neocortical Development

Tang, Ting; Zhang, Yandong; Cai, Zheping; Lu, Zhiheng; Li, Leiting; Huang, Ru; Hagelkrüys, Astrid; Matthias, Patrick; Zhang, Heng; Seiser, Christian; Xie, Yunyun

doi:10.1016/j.neuron.2019.01.007

Cited by 40 publications

(39 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HDAC1 activity is reduced when it is bound to β-catenin through LEF1, which regulates downstream target genes (Billin and others 2000). HDAC1 and HDAC2 precisely regulate the spatial positioning of progenitor cells for neocortical development through the proneural gene Neurogenin2 (Tang and others 2019). The genetic deletion of both HDAC1 and HDAC2 activates and stabilizes β-catenin and its effector TCF7L2, which changes the expression of a myelin gene (Olig2) and regulates pandrocyte differentiation (Ye and others 2009).…”

Section: Wnt/β-catenin Signaling In Neural Stem Cell Homeostasismentioning

confidence: 99%

Wnt/β-Catenin Signaling in Neural Stem Cell Homeostasis and Neurological Diseases

et al. 2020

View full text Add to dashboard Cite

Neural stem/progenitor cells (NSCs) maintain the ability of self-renewal and differentiation and compose the complex nervous system. Wnt signaling is thought to control the balance of NSC proliferation and differentiation via the transcriptional coactivator β-catenin during brain development and adult tissue homeostasis. Disruption of Wnt signaling may result in developmental defects and neurological diseases. Here, we summarize recent findings of the roles of Wnt/β-catenin signaling components in NSC homeostasis for the regulation of functional brain circuits. We also suggest that the potential role of Wnt/β-catenin signaling might lead to new therapeutic strategies for neurological diseases, including, but not limited to, spinal cord injury, Alzheimer’s disease, Parkinson’s disease, and depression.

show abstract

Section: Wnt/β-catenin Signaling In Neural Stem Cell Homeostasismentioning

confidence: 99%

Wnt/β-Catenin Signaling in Neural Stem Cell Homeostasis and Neurological Diseases

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Recent epigenetic studies offer some answers for this process (Figure 2), indeed some early life events really induce epigenetic changes for many neuromodulator receptors or transporters, such as methylation DNA of MAO. The normal development of the brain requires strict regulation of proliferation and differentiation of neural stem cells (NSCs), thereby ensuring specific number of neurons to be generated at a specific time and at a specific location (Tang et al, 2019). DNA demethylation of CpG dinucleotide sites play an important role in the cell fate characteristics of NSCs (He et al, 2020).…”

Section: Changes Caused By Early Life Stressmentioning

confidence: 99%

“…The normal development of the brain requires strict regulation of proliferation and differentiation of neural stem cells (NSCs), thereby ensuring specific number of neurons to be generated at a specific time and at a specific location ( Tang et al, 2019 ). DNA demethylation of CpG dinucleotide sites play an important role in the cell fate characteristics of NSCs ( He et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior

Jiang

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Major depressive disorder (MDD) is coming to be the regarded as one of the leading causes for human disabilities. Due to its complicated pathological process, the etiology is still unclear and the treatment is still targeting at the monoamine neurotransmitters. Early life stress has been known as a major cause for MDD, but how early life stress affects adult monoaminergic activity is not clear either. Recently, DNA methylation is considered to be the key mechanism of epigenetics and might play a role in early life stress induced mental illness. DNA methylation is an enzymatic covalent modification of DNA, has been one of the main epigenetic mechanisms investigated. The metabolic enzyme for the monoamine neurotransmitters, monoamine oxidases A/B (MAO A/MAO B) are the prime candidates for the investigation into the role of DNA methylation in mental disorders. In this review, we will review recent advances about the structure and physiological function of monoamine oxidases (MAO), brief narrative other factors include stress induced changes, early life stress, perinatal depression (PD) relationship with other epigenetic changes, such as DNA methylation, microRNA (miRNA). This review will shed light on the epigenetic changes involved in MDD, which may provide potential targets for future therapeutics in depression pathogenesis.

show abstract

“…Multiple mechanisms regulating progenitor cell proliferation have recently been uncovered. Regulation of gene transcription by epigenetic mechanisms has emerged as a key factor where histone deacetylases and methyltransferases regulate the generation and position of IPCs, neuron migration, and cortical lamination 49, 50 . Similarly, regulation of chromatin accessibility and other mechanisms related to non-coding genomic regions critically determines levels and patterns of gene expression in the developing cortex, defining neuron production, cortex size, and area identity 51, 52 .…”

Section: Neurogenesismentioning

confidence: 99%

Recent advances in understanding neocortical development

Borrell

2019

F1000Res

View full text Add to dashboard Cite

The neocortex is the largest part of the mammalian brain and is the seat of our higher cognitive functions. This outstanding neural structure increased massively in size and complexity during evolution in a process recapitulated today during the development of extant mammals. Accordingly, defects in neocortical development commonly result in severe intellectual and social deficits. Thus, understanding the development of the neocortex benefits from understanding its evolution and disease and also informs about their underlying mechanisms. Here, I briefly summarize the most recent and outstanding advances in our understanding of neocortical development and focus particularly on dorsal progenitors and excitatory neurons. I place special emphasis on the specification of neural stem cells in distinct classes and their proliferation and production of neurons and then discuss recent findings on neuronal migration. Recent discoveries on the genetic evolution of neocortical development are presented with a particular focus on primates. Progress on all these fronts is being accelerated by high-throughput gene expression analyses and particularly single-cell transcriptomics. I end with novel insights into the involvement of microglia in embryonic brain development and how improvements in cultured cerebral organoids are gradually consolidating them as faithful models of neocortex development in humans.

show abstract

HDAC1 and HDAC2 Regulate Intermediate Progenitor Positioning to Safeguard Neocortical Development

Abstract: Highlights d HDAC1 and HDAC2 control IP positioning in early cortical development d Mispositioned IPs differentiate into neurons at the ventricular surface d Ventricular zone integrity requires proper IP positioning d HDAC1 and HDAC2 control IP positioning through Neurog2

Cited by 40 publications

References 57 publications

Wnt/β-Catenin Signaling in Neural Stem Cell Homeostasis and Neurological Diseases

Wnt/β-Catenin Signaling in Neural Stem Cell Homeostasis and Neurological Diseases

Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior

Recent advances in understanding neocortical development

Contact Info

Product

Resources

About