Function of Proneural Genes Ascl1 and Asense in Neurogenesis: How Similar Are They?

Soares, Diogo S.; Homem, Catarina C.F.; Castro, Diogo S.

doi:10.3389/fcell.2022.838431

Cited by 12 publications

(4 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Syt8-belonging to the synaptotagmin family, which is important in exocytosis during neurotransmission 16 -had a high level of gene activity in the spine and DRG regions. Ascl1, which encodes a transcription factor that is involved in the commitment and differentiation of neuron and oligodendrocytes 17 , showed strong enrichment in the brain and also the dorsal spinal cord (Fig. 2c and Supplementary Fig.…”

Section: Spatial Mapping Of the E13 Mouse Embryomentioning

confidence: 99%

Spatial profiling of chromatin accessibility in mouse and human tissues

Deng

Bartošovič

et al. 2022

Nature

195

126

View full text Add to dashboard Cite

Cellular function in tissue is dependent on the local environment, requiring new methods for spatial mapping of biomolecules and cells in the tissue context1. The emergence of spatial transcriptomics has enabled genome-scale gene expression mapping2–5, but the ability to capture spatial epigenetic information of tissue at the cellular level and genome scale is lacking. Here we describe a method for spatially resolved chromatin accessibility profiling of tissue sections using next-generation sequencing (spatial-ATAC-seq) by combining in situ Tn5 transposition chemistry6 and microfluidic deterministic barcoding5. Profiling mouse embryos using spatial-ATAC-seq delineated tissue-region-specific epigenetic landscapes and identified gene regulators involved in the development of the central nervous system. Mapping the accessible genome in the mouse and human brain revealed the intricate arealization of brain regions. Applying spatial-ATAC-seq to tonsil tissue resolved the spatially distinct organization of immune cell types and states in lymphoid follicles and extrafollicular zones. This technology progresses spatial biology by enabling spatially resolved chromatin accessibility profiling to improve our understanding of cell identity, cell state and cell fate decision in relation to epigenetic underpinnings in development and disease.

show abstract

Section: Spatial Mapping Of the E13 Mouse Embryomentioning

confidence: 99%

Spatial profiling of chromatin accessibility in mouse and human tissues

Deng

Bartošovič

et al. 2022

Nature

195

126

View full text Add to dashboard Cite

show abstract

“…This dysregulation can result in aberrant neural progenitor dynamics, potentially leading to the generation of non-functional or improperly differentiated neurons. Impaired ASCL1 function may lead to disrupted synaptic formation and connectivity [225]. This disruption could contribute to cognitive and functional de cits observed in neurodegenerative conditions.…”

Section: Role Of Neuroin Ammation In Fueling Neurodegenerationmentioning

confidence: 99%

Investigating How Inflammation Involving NF-κB Signaling Disrupts the Genetic Architecture of Neurons/Neural Stem Cells and Fuels Neurodegeneration

Shafi,

Rajpar,

Yaqoob

et al. 2024

Preprint

View full text Add to dashboard Cite

Background: Understanding how inflammation disrupts neural stem cells and neuronal genetic architecture is crucial. This investigation explores these mechanisms, aiming to decipher the role of inflammation in disrupting neuronal genetic architecture. Unraveling these complexities may reveal therapeutic targets, offering hope for precision interventions to impede or slow the progression of debilitating neurodegenerative conditions.Methods: Databases including PubMed, MEDLINE and Google Scholar were searched for published articles without any date restrictions, involving NF-κB and neurogenic genes/signaling pathways/transcription factors. They were investigated in the study to unravel how inflammation disrupts the neural stem cells (NSCs) and neuronal genetic architecture, and how this process fuels the development of neurodegeneration. This study adheres to relevant PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses).Results: This study reveals how NF-κB activation plays a central role in inflammation-induced disruption, mediating transcriptional dysregulation of key neurogenic factors like Ngn1, NeuroD, and PDGF, compromising the neurogenic code. Downregulation of neurotrophic factors, notably BDNF, increases neuronal vulnerability to apoptotic pathways, accelerating neurodegeneration. Inflammatory processes extend to the genomic landscape, affecting genes crucial for neurogenesis and synaptic function, contributing to observed synaptic dysfunction in neurodegenerative diseases. Furthermore, inflammation disrupts NSCs, impairing neurogenesis and compromising neural progenitor dynamics, diminishing the regenerative potential of the nervous system. Identified therapeutic strategies include precision targeting of NF-κB, restoration of neurotrophic support, and interventions promoting proper gene expression and neurogenesis, offering promising avenues for mitigating inflammation-induced damage and halting neurodegenerative progression.Conclusion: This study investigates the intricate impact of inflammation on neural stem cells (NSCs) and neuronal genetic architecture, providing insights into the pathogenesis disrupting neuronal architecture. NF-κB-mediated disruptions compromise neurotrophic support, impair neurogenesis, induce synaptic dysfunction, and enhance vulnerability to apoptosis. This orchestrated genomic dysregulation contributes to the progression of neurodegenerative diseases. Therapeutically, precision targeting of NF-κB, restoration of neurotrophic support, and promotion of neurogenesis emerge as promising strategies to mitigate inflammation-induced damage, offering potential avenues for interventions to impede the neurodegenerative cascade.

show abstract

“…Conversely, examples of pioneer TFs that do not display MCB (at least in tested conditions), have started to emerge. Ascl1 is a well-characterized pioneer TF with a master regulatory function in neurogenesis, and which was recently shown to be excluded from mitotic chromatin in neural stem cells [ 20 , 40 , 41 ]. Another example is the pioneer TF Zelda, shown to be excluded from mitotic chromatin during zygotic genome activation in D. melanogaster [ 42 ].…”

Section: Mitotic Chromosome Binding: An Intrinsic or Regulated Proper...mentioning

confidence: 99%

Function and regulation of transcription factors during mitosis-to-G1 transition

2022

Self Cite

View full text Add to dashboard Cite

During cell division, drastic cellular changes characteristic of mitosis result in the inactivation of the transcriptional machinery, and global downregulation of transcription. Sequence-specific transcription factors (TFs) have thus been considered mere bystanders, devoid of any regulatory function during mitosis. This view changed significantly in recent years, upon the conclusion that many TFs associate with condensed chromosomes during cell division, even occupying a fraction of their genomic target sites in mitotic chromatin. This finding was at the origin of the concept of mitotic bookmarking by TFs, proposed as a mechanism to propagate gene regulatory information across cell divisions, by facilitating the reactivation of specific bookmarked genes. While the underlying mechanisms and biological significance of this model remain elusive, recent developments in this fast-moving field have cast new light into TF activity during mitosis, beyond a bookmarking role. Here, we start by reviewing the most recent findings on the complex nature of TF–chromatin interactions during mitosis, and on mechanisms that may regulate them. Next, and in light of recent reports describing how transcription is reinitiated in temporally distinct waves during mitosis-to-G1 transition, we explore how TFs may contribute to defining this hierarchical gene expression process. Finally, we discuss how TF activity during mitotic exit may impact the acquisition of cell identity upon cell division, and propose a model that integrates dynamic changes in TF–chromatin interactions during this cell-cycle period, with the execution of cell-fate decisions.

show abstract

Function of Proneural Genes Ascl1 and Asense in Neurogenesis: How Similar Are They?

Cited by 12 publications

References 78 publications

Spatial profiling of chromatin accessibility in mouse and human tissues

Spatial profiling of chromatin accessibility in mouse and human tissues

Investigating How Inflammation Involving NF-κB Signaling Disrupts the Genetic Architecture of Neurons/Neural Stem Cells and Fuels Neurodegeneration

Function and regulation of transcription factors during mitosis-to-G1 transition

Contact Info

Product

Resources

About