Notch Signaling Controls Oligodendrocyte Regeneration in the Injured Telencephalon of Adult Zebrafish

Kim, Hwan Ki; Lee, Dong-Won; Kim, Eun‐Mi; Jeong, Inyoung; Kim, Suhyun; Kim, Bumjoon J.; Park, Hae Chul

doi:10.5607/en20050

Cited by 10 publications

(5 citation statements)

References 29 publications

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“…Surprisingly, in contrast to mammals, there is no increase in the proliferation rate of olig2-positive cells in the injured hemisphere, compared to the uninjured hemisphere (März et al, 2011, Baumgart et al, 2012. However, recent data suggest a higher number of proliferating parenchymal and ventricular olig2-positive cells at 4 dpl [117]. This study also suggests that olig2-positive RGCs from the medial telencephalic ventricular zone can generate new oligodendrocytes following brain injury [117].…”

Section: Oligodendrocyte/oligodendrocyte Progenitor Cell Recruitment mentioning

confidence: 47%

“…However, recent data suggest a higher number of proliferating parenchymal and ventricular olig2-positive cells at 4 dpl [117]. This study also suggests that olig2-positive RGCs from the medial telencephalic ventricular zone can generate new oligodendrocytes following brain injury [117]. Consequently, the proliferation of the olig2-positive cells appears to be moderate after stab wound injury of the zebrafish telencephalon.…”

Section: Oligodendrocyte/oligodendrocyte Progenitor Cell Recruitment mentioning

confidence: 49%

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Cellular Mechanisms Participating in Brain Repair of Adult Zebrafish and Mammals after Injury

Ghaddar

Lübke

Couret

et al. 2021

Cells

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Adult neurogenesis is an evolutionary conserved process occurring in all vertebrates. However, striking differences are observed between the taxa, considering the number of neurogenic niches, the neural stem cell (NSC) identity, and brain plasticity under constitutive and injury-induced conditions. Zebrafish has become a popular model for the investigation of the molecular and cellular mechanisms involved in adult neurogenesis. Compared to mammals, the adult zebrafish displays a high number of neurogenic niches distributed throughout the brain. Furthermore, it exhibits a strong regenerative capacity without scar formation or any obvious disabilities. In this review, we will first discuss the similarities and differences regarding (i) the distribution of neurogenic niches in the brain of adult zebrafish and mammals (mainly mouse) and (ii) the nature of the neural stem cells within the main telencephalic niches. In the second part, we will describe the cascade of cellular events occurring after telencephalic injury in zebrafish and mouse. Our study clearly shows that most early events happening right after the brain injury are shared between zebrafish and mouse including cell death, microglia, and oligodendrocyte recruitment, as well as injury-induced neurogenesis. In mammals, one of the consequences following an injury is the formation of a glial scar that is persistent. This is not the case in zebrafish, which may be one of the main reasons that zebrafish display a higher regenerative capacity.

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Section: Oligodendrocyte/oligodendrocyte Progenitor Cell Recruitment mentioning

confidence: 47%

Section: Oligodendrocyte/oligodendrocyte Progenitor Cell Recruitment mentioning

confidence: 49%

Cellular Mechanisms Participating in Brain Repair of Adult Zebrafish and Mammals after Injury

Ghaddar

Lübke

Couret

et al. 2021

Cells

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“…Thus, we speculate that AVP can compensate for the dysregulation of PI3K/AKT and Wnt pathways by regulating the NOTCH, MAPK, and focal adhesion signaling pathways, thus promoting OL development and myelin formation and improving autism-like behavior. A large number of studies have confirmed that activation of NOTCH (Kim et al, 2020;Li et al, 2021), MAPK (Ishii et al, 2016;Lorenzati et al, 2021), and Focal adhesion (Forrest et al, 2009;Lafrenaye and Fuss, 2010) signaling pathway can regulate the proliferation, differentiation, and migration of OL and myelin formation. In addition, crosstalk between these pathways and PI3K/AKT and Wnt pathway has been reported in many neurological or non-neurological disorders (Bai et al, 2019;Ishii et al, 2019Ishii et al, , 2021Worthmuller and Ruegg, 2020;Acar et al, 2021).…”

Section: Pi3k/akt Signaling Pathway Represents An Essentialmentioning

confidence: 97%

The Changes of Amygdala Transcriptome in Autism Rat Model After Arginine Vasopressin Treatment

et al. 2022

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BackgroundSome studies have shown that arginine vasopressin (AVP) can significantly improve the social interaction disorder of autism, but the mechanism remains unclear.MethodsFemale Wistar rats were intraperitoneally injected with VPA or normal saline at embryonic day 12.5 to establish an autism model or normal control in their offspring. Male offspring prenatally exposed to VPA were randomly assigned to two groups: the VPA-induced autism model group and the AVP group. The rats in the AVP group were treated with intranasal AVP at postnatal day (PND) 21 and for 3 weeks. The VPA-induced autism model group was given the same dose of normal saline in the same way. Behavioral responses were evaluated in the open field and three-chambered social test apparatus; the expression levels of AVP in serum were detected by enzyme-linked immunosorbent assay kit, and the gene expression levels on the amygdala were measured by RNA-seq at PND42.ResultsIntranasal administration of AVP can significantly improve the social interaction disorder and elevate the levels of AVP in serum. Transcriptome sequencing results showed that 518 differently expressed genes (DEGs) were identified in the VPA-induced autism model group compared with the control in this study. Gene Ontology biological process enrichment analysis of DEGs showed that the VPA-induced autism model group had significant nervous system developmental impairments compared with the normal group, particularly in gliogenesis, glial cell differentiation, and oligodendrocyte differentiation. Gene Set Enrichment Analysis (GSEA) enrichment analysis also showed that biological process of oligodendrocyte differentiation, axoneme assembly, and axon ensheathment were inhibited in the VPA-induced autism model group. Pathway enrichment analysis of DEGs between the control and VPA-induced autism model group showed that the PI3K/AKT and Wnt pathways were significantly dysregulated in the VPA-induced autism model group. Few DEGs were found when compared with the transcriptome between the VPA-induced autism model group and the AVP treatment group. GSEA enrichment analysis showed deficits in oligodendrocyte development and function were significantly improved after AVP treatment; the pathways were mainly enriched in the NOTCH, mitogen-activated protein kinase, and focal adhesion signaling pathways, but not in the PI3K/AKT and Wnt pathways. The expression patterns analysis also showed the same results.ConclusionAVP can significantly improve the social interaction disorder of VPA-induced autism model, and AVP may target behavioral symptoms in autism by modulating the vasopressin pathways, rather than primary disease mechanisms.

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“…Thus, although her4.3 expression at the time of cell isolation at 21-23 dpf does not fully resemble her4.3:switchCas9 transgene expression in all ancestral cells when the inherited SABER barcodes were generated, our data and past literature 31,40,41 strongly suggest that it can be used as a proxy to identify Notch-active founder cell types and trace their descendants at later stages. Notably, Notch signaling has been shown to be important for cell fate specification of the aforementioned non-neuronal cell types in development and regeneration [42][43][44][45][46] . Regulation of her4.3 expression is orchestrated via notch1a, notch1b and notch3 receptor genes 31 .…”

Section: Signal Tracing Reveals That Notch Stimulated Progenitors Giv...mentioning

confidence: 99%

Barcoding Notch signaling in the developing brain

Siniscalco,

Perera,

Greenslade

et al. 2024

Preprint

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Developmental signaling inputs are fundamental for shaping cell fates and behavior. However, traditional fluorescent-based signaling reporters have limitations in scalability and molecular resolution of cell types. We present SABER-seq, a CRISPR-Cas molecular recorder that stores transient developmental signaling cues as permanent mutations in cellular genomes for deconstruction at later stages via single-cell transcriptomics. We applied SABER-seq to record Notch signaling in developing zebrafish brains. SABER-seq has two components: a signaling sensor and a barcode recorder. The sensor activates Cas9 in a Notch-dependent manner with inducible control while the recorder accumulates mutations that represent Notch activity in founder cells. We combine SABER-seq with an expanded juvenile brain atlas to define cell types whose fates are determined downstream of Notch signaling. We identified examples wherein Notch signaling may have differential impact on terminal cell fates. SABER-seq is a novel platform for rapid, scalable and high-resolution mapping of signaling activity during development.

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Notch Signaling Controls Oligodendrocyte Regeneration in the Injured Telencephalon of Adult Zebrafish

Cited by 10 publications

References 29 publications

Cellular Mechanisms Participating in Brain Repair of Adult Zebrafish and Mammals after Injury

Cellular Mechanisms Participating in Brain Repair of Adult Zebrafish and Mammals after Injury

The Changes of Amygdala Transcriptome in Autism Rat Model After Arginine Vasopressin Treatment

Barcoding Notch signaling in the developing brain

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