SRSF10 regulates proliferation of neural progenitor cells and affects neurogenesis in developing mouse neocortex

Li, Junjie; Jiang, Hanyang; Mu, Ya-Wei; Wei, Zixuan; Ma, Anlun; Sun, Ming; Zhao, Jingjing; Zhu, Changhong; Chen, Xianhua

doi:10.1016/j.isci.2023.107042

Cited by 4 publications

(5 citation statements)

References 62 publications

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“…Microtubule-associated protein 2 (Map2) in neural progenitor cells (Li et al, 2023). We confirmed Map2 expression to correlate with embryonic ISH expression data of Map2 from the online database Genepaint (Visel et al, 2004).…”

Section: 54supporting

confidence: 61%

“…Map2 isoforms were confirmed to have specific bands via western blot at 280, 270, 70, and 75 kDa (manufacturer information). A previous study used this antibody to label Map2 in neural progenitor cells (Li et al., 2023). We confirmed Map2 expression to correlate with embryonic ISH expression data of Map2 from the online database Genepaint (Visel et al., 2004).…”

Section: Methodsmentioning

confidence: 99%

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Illuminating the terminal nerve: Uncovering the link between GnRH‐1 neuron and olfactory development

Amato,

Taroc,

Forni

2024

J of Comparative Neurology

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During embryonic development, the olfactory placode (OP) generates migratory neurons, including olfactory pioneer neurons, cells of the terminal nerve (TN), gonadotropin‐releasing hormone‐1 (GnRH‐1) neurons, and other uncharacterized neurons. Pioneer neurons from the OP induce olfactory bulb (OB) morphogenesis. In mice, GnRH‐1 neurons appear in the olfactory system around mid‐gestation and migrate via the TN axons to different brain regions. The GnRH‐1 neurons are crucial in controlling the hypothalamic‐pituitary‐gonadal axis. Kallmann syndrome is characterized by impaired olfactory system development, defective OBs, secretion of GnRH‐1, and infertility. The precise mechanistic link between the olfactory system and GnRH‐1 development remains unclear. Studies in humans and mice highlight the importance of the prokineticin‐2/prokineticin‐receptor‐2 (Prokr2) signaling pathway in OB morphogenesis and GnRH‐1 neuronal migration. Prokr2 loss‐of‐function mutations can cause Kallmann syndrome (KS), and hence the Prokr2 signaling pathway represents a unique model to decipher the olfactory/GnRH‐1 connection. We discovered that Prokr2 is expressed in the TN neurons during the critical period of GnRH‐1 neuron formation, migration, and induction of OB morphogenesis. Single‐cell RNA sequencing identified that the TN is formed by neurons distinct from the olfactory neurons. The TN neurons express multiple genes associated with KS. Our study suggests that the aberrant development of pioneer/TN neurons might cause the KS spectrum.

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Section: 54supporting

confidence: 61%

Section: Methodsmentioning

confidence: 99%

Illuminating the terminal nerve: Uncovering the link between GnRH‐1 neuron and olfactory development

Amato,

Taroc,

Forni

2024

J of Comparative Neurology

View full text Add to dashboard Cite

show abstract

“…Map2 isoforms were confirmed to have specific bands via western blot at 280,270,70 and 75 kDa (manufacturer information). A previous study used this antibody to label Map2 in neural progenitor cells (Li et al, 2023). We confirmed Map2 expression to correlate with embryonic ISH expression data of Map2 from the online database Genepaint (Visel et al, 2004).…”

Section: Methodsmentioning

confidence: 99%

“…ISH was performed as described (Forni et al, 2013) and visualized with an alkaline phosphatase conjugated anti-DIG (1:1000), and NBT/BCIP developer solution (Roche Diagnostics). SW Rabbit anti-GnRH-1 Susan WRAY, NINDS/NIH 1:6000 (Wray et al, 1988) Rabbit anti-Map2 Cell Signaling Technology #4542 1:200 (Li et al, 2023).…”

Section: Ishmentioning

confidence: 99%

Illuminating the Terminal Nerve: Uncovering the Link between GnRH-1 and Olfactory Development

Amato,

Taroc,

Forni

2023

Preprint

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During embryonic development, the olfactory placode (OP) generates migratory neurons, including olfactory pioneer neurons, cells of the terminal nerve (TN), Gonadotropin-releasing hormone-1 (GnRH-1) neurons, and other uncharacterized neurons. Pioneer neurons from the olfactory placode induce olfactory bulb morphogenesis.In mice, GnRH-1 neurons appear in the olfactory system around mid-gestation and migrate via the terminal nerve axons to different brain regions. The GnRH-1 neurons are crucial in controlling the hypothalamic-pituitary-gonadal (HPG) axis. Kallmann syndrome is characterized by impaired olfactory system development, defective olfactory bulbs, defective secretion of GnRH-1, and infertility. The precise mechanistic link between the olfactory system and GnRH-1 development remains unclear. Studies in humans and mice highlight the importance of the Prokineticin-2/Prokineticin-Receptor-2 (Prokr2) signaling pathway in olfactory bulb morphogenesis and GnRH-1 neuronal migration.Prokr2loss-of-function mutations can cause Kallmann syndrome, and hence the Prokr2 signaling pathway represents a unique model to decipher the olfactory/GnRH-1 connection. We discovered that Prokr2 is expressed in the TN neurons during the critical period of GnRH-1 neuron formation, migration, and induction of olfactory bulb morphogenesis. Single-cell RNA sequencing identified that the TN is formed by neurons that are distinct from the olfactory neurons. The TN neurons express multiple genes associated with KS. Our study suggests that the aberrant development of pioneer/TN neurons might cause the KS spectrum.Key Points1) Pioneer or terminal nerve neurons play a crucial role in initiating the development of the olfactory bulbs. We found that the Prokineticin Receptor-2 gene, associated with Kallmann syndrome, is expressed by the olfactory pioneer/terminal nerve neurons.2) We genetically traced, isolated, and conducted Single-cell RNA sequencing on terminal nerve neurons of rodents. This analysis revealed a significant enrichment of gene expression related to Kallmann syndrome.3) Our study indicates that the investigation of Pioneer/terminal nerve neurons should be a pivotal focal point for comprehending developmental defects affecting olfactory and GnRH-1 systems.

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“…They might be associated with skin tumours and proliferative skin diseases. [77][78][79] The Over Representation Analysis indicates that the package identified module M11 (Figure 5E). The top 12 genes were linked with two primary mechanisms: inherited skin diseases and metabolism and oxidative stress mechanisms.…”

Section: Mclustermentioning

confidence: 99%

Comprehensive modular analyses of scar subtypes illuminate underlying molecular mechanisms and potential therapeutic targets

Liu,

Lu,

Qiu

et al. 2023

International Wound Journal

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Pathological scarring resulting from traumas and wounds, such as hypertrophic scars and keloids, pose significant aesthetic, functional and psychological challenges. This study provides a comprehensive transcriptomic analysis of these conditions, aiming to illuminate underlying molecular mechanisms and potential therapeutic targets. We employed a co‐expression and module analysis tool to identify significant gene clusters associated with distinct pathophysiological processes and mechanisms, notably lipid metabolism, sebum production, cellular energy metabolism and skin barrier function. This examination yielded critical insights into several skin conditions including folliculitis, skin fibrosis, fibrosarcoma and congenital ichthyosis. Particular attention was paid to Module Cluster (MCluster) 3, encompassing genes like BLK, TRPV1 and GABRD, all displaying high expression and potential implications in immune modulation. Preliminary immunohistochemistry validation supported these findings, showing elevated expression of these genes in non‐fibrotic samples rich in immune activity. The complex interplay of different cell types in scar formation, such as fibroblasts, myofibroblasts, keratinocytes and mast cells, was also explored, revealing promising therapeutic strategies. This study underscores the promise of targeted gene therapy for pathological scars, paving the way for more personalised therapeutic approaches. The results necessitate further research to fully ascertain the roles of these identified genes and pathways in skin disease pathogenesis and potential therapeutics. Nonetheless, our work forms a strong foundation for a new era of personalised medicine for patients suffering from pathological scarring.

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SRSF10 regulates proliferation of neural progenitor cells and affects neurogenesis in developing mouse neocortex

Cited by 4 publications

References 62 publications

Illuminating the terminal nerve: Uncovering the link between GnRH‐1 neuron and olfactory development

Illuminating the terminal nerve: Uncovering the link between GnRH‐1 neuron and olfactory development

Illuminating the Terminal Nerve: Uncovering the Link between GnRH-1 and Olfactory Development

Comprehensive modular analyses of scar subtypes illuminate underlying molecular mechanisms and potential therapeutic targets

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