Comparative role of SOX10 gene in the gliogenesis of central, peripheral, and enteric nervous systems

Bhattarai, Chacchu; Poudel, Phanindra Prasad; Ghosh, Arnab; Kalthur, Sneha Guruprasad

doi:10.1016/j.diff.2022.09.001

Cited by 9 publications

(3 citation statements)

References 141 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We can only speculate as to how the absence of COMMD10 may lead to lower expression of Sox10 and, sequentially, other genes during embryogenesis. During normal embryogenesis, Sox10 mRNA appears in late gastrulating embryos (mouse E7.5) in the neural crest-forming region, and its gene expression depends on Wnt signaling [ 57 , 58 ]. Sox10 protein was also found to directly interact with β-catenin [ 59 ], which is activated in the canonical Wnt signaling pathway (reviewed in [ 60 ]).…”

Section: Resultsmentioning

confidence: 99%

COMMD10 Is Essential for Neural Plate Development during Embryogenesis

Phan

Pelargos

Tsytsykova

et al. 2023

JDB

View full text Add to dashboard Cite

The COMMD (copper metabolism MURR1 domain containing) family includes ten structurally conserved proteins (COMMD1 to COMMD10) in eukaryotic multicellular organisms that are involved in a diverse array of cellular and physiological processes, including endosomal trafficking, copper homeostasis, and cholesterol metabolism, among others. To understand the role of COMMD10 in embryonic development, we used Commd10Tg(Vav1-icre)A2Kio/J mice, where the Vav1-cre transgene is integrated into an intron of the Commd10 gene, creating a functional knockout of Commd10 in homozygous mice. Breeding heterozygous mice produced no COMMD10-deficient (Commd10Null) offspring, suggesting that COMMD10 is required for embryogenesis. Analysis of Commd10Null embryos demonstrated that they displayed stalled development by embryonic day 8.5 (E8.5). Transcriptome analysis revealed that numerous neural crest-specific gene markers had lower expression in mutant versus wild-type (WT) embryos. Specifically, Commd10Null embryos displayed significantly lower expression levels of a number of transcription factors, including a major regulator of the neural crest, Sox10. Moreover, several cytokines/growth factors involved in early embryonic neurogenesis were also lower in mutant embryos. On the other hand, Commd10Null embryos demonstrated higher expression of genes involved in tissue remodeling and regression processes. Taken together, our findings show that Commd10Null embryos die by day E8.5 due to COMMD10-dependent neural crest failure, revealing a new and critical role for COMMD10 in neural development.

show abstract

Section: Resultsmentioning

confidence: 99%

COMMD10 Is Essential for Neural Plate Development during Embryogenesis

Phan

Pelargos

Tsytsykova

et al. 2023

JDB

View full text Add to dashboard Cite

show abstract

“…A study on diabetes peripheral neuropathy by Jiao et al found that miR-7a-5p regulation ameliorated mitochondrial dysfunction and reduced apoptosis via the VDAC1/JNK/c-JUN pathway [ 48 ]. The SOX10 gene and SOX10 protein are responsible for the gliogenesis of glial cells in neural crest cells [ 49 ]. Furthermore, Xie et al found that downregulation of Sp1 alleviated neuropathic pain-like behaviors after neutral alignment via the HDAC1/SOX10 axis [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Expression Profiles of Long Noncoding RNAs and Messenger RNAs in a Rat Model of Spinal Cord Injury

Cao

Tang²,

Tan

et al. 2023

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

Spinal cord injury (SCI) is a serious disorder of the central nervous system with a high disability rate. Long noncoding RNAs (lncRNAs) are reported to mediate many biological processes. The aim of this study was to explore lncRNA and mRNA expression profiles and functional networks after SCI. Differentially expressed genes between SCI model rats and sham controls were identified by microarray assays and analyzed by functional enrichment. Key lncRNAs were identified using a support vector machine- (SVM-) recursive feature elimination (RFE) algorithm. A trans and cis regulation model was used to analyze the regulatory relationships between lncRNAs and their targets. An lncRNA-related ceRNA network was established. We identified 5465 differentially expressed lncRNAs (DE lncRNAs) and 8366 differentially expressed mRNAs (DE mRNAs) in the SCI group compared with the sham group ( fold change > 2.0 , p < 0.05 ). Four genes were confirmed by qRT-PCR which were consistent with the microarray data. GSEA analysis showed that most marked changes occurred in pathways related to immune inflammation and nerve cell function, including cytokine-cytokine receptor interaction, neuroactive ligand-receptor interaction, and GABAergic synapse. Enrichment analysis identified 30 signaling pathways, including those associated with immune inflammation response. A total of 40 key lncRNAs were identified using the SVM-RFE algorithm. A key lncRNA-mRNAs coexpression network was generated for 230 951 lncRNA-mRNA pairs with half showing positive correlations. Several key DE lncRNAs were predicted to have “cis”- or “trans”-regulated target genes. The transcription factors, Sp1, JUN, and SOX10, may regulate the interaction between XR_001837123.1 and ETS 1. In addition, five pairs of ceRNA regulatory sequences were constructed. Many mRNAs and lncRNAs were found to be dysregulated after SCI. Bioinformatic analysis showed that DE lncRNAs may play crucial roles in SCI. It is anticipated that these findings will provide new insights into the underlying mechanisms and potential therapeutic targets for SCI.

show abstract

“…In these studies, the primary readout of gliogenesis was astrogliogenesis, using either morphology or molecular markers to identify glial fate. Although a few factors, such as Sox10, have been reported to promote oligodendrocyte precursor cell (OPC) fate (23, 24), the progenitor-level mechanisms that govern astrocyte-to-oligodendrocyte transition remain poorly understood. Furthermore, how mechanisms that maintain ongoing neurogenesis crosstalk with those that promote gliogenesis remains to be understood.…”

Section: Introductionmentioning

confidence: 99%

Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signaling pathway

Bose,

Talwar,

Suresh

et al. 2023

Preprint

View full text Add to dashboard Cite

In the developing vertebrate central nervous system, neurons and glia typically arise sequentially from common progenitors. Here, we report that the transcription factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via distinct cell-autonomous roles in progenitors and in postmitotic neurons that regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate that loss ofFoxg1in cortical progenitors at neurogenic stages causes premature astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway componentFgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis. Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the augmentation of FGF signalling. We identify a second novel function of FOXG1 in regulating the expression of gliogenic ligand FGF18 in new born neocortical upper-layer neurons. Loss of FOXG1 in postmitotic neurons increasesFgf18expression and enhances gliogenesis in the progenitors. These results fit well with the model that new born neurons secrete cues that trigger progenitors to produce the next wave of cell types, astrocytes. If FGF signalling is attenuated inFoxg1null progenitors, they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic signalling via the FGF pathway to regulate the sequential generation of neurons, astrocytes, and oligodendrocytes in the cerebral cortex.Significance StatementFunctional brain circuitry requires the correct numbers and subtypes of neurons and glia. A fundamental feature of the vertebrate central nervous system is that common progenitors produce first neurons and then glia. Cell-intrinsic factors modulate how a progenitor responds to cell-extrinsic cues to achieve this transition. Here, we report that the transcription factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortexin vivoby regulating different aspects of the gliogenic FGF signalling pathway in progenitors and in postmitotic neurons. Loss ofFoxg1results in premature gliogenesis via regulation of novel targetsFgfr3in progenitors andFgf18in postmitotic neurons. Our findings offer mechanistic insight into FOXG1 syndrome, an Autism Spectrum Disorder caused byFoxg1mutations in humans.

show abstract

Comparative role of SOX10 gene in the gliogenesis of central, peripheral, and enteric nervous systems

Cited by 9 publications

References 141 publications

COMMD10 Is Essential for Neural Plate Development during Embryogenesis

COMMD10 Is Essential for Neural Plate Development during Embryogenesis

Expression Profiles of Long Noncoding RNAs and Messenger RNAs in a Rat Model of Spinal Cord Injury

Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signaling pathway

Contact Info

Product

Resources

About