Transcriptional regulation of peripheral glial cell differentiation in the embryonic nervous system of drosophila

Glia ◽  
2011 ◽  
Vol 59 (9) ◽  
pp. 1264-1272 ◽  
Author(s):  
Imke Schmidt ◽  
Sigrídur Rut Franzdóttir ◽  
Gundula Edenfeld ◽  
Floriano Rodrigues ◽  
Ariane Zierau ◽  
...  
Keyword(s):  
Nervous System ◽  
Transcriptional Regulation ◽  
Cell Differentiation ◽  
Glial Cell ◽  
Embryonic Nervous System

scholarly journals Enteric nervous system specific deletion of Foxd3 disrupts glial cell differentiation and activates compensatory enteric progenitors

2012 ◽  
Vol 363 (2) ◽  
pp. 373-387 ◽  
Author(s):  
Nathan A. Mundell ◽  
Jennifer L. Plank ◽  
Alison W. LeGrone ◽  
Audrey Y. Frist ◽  
Lei Zhu ◽  
...  
Keyword(s):  
Nervous System ◽  
Cell Differentiation ◽  
Enteric Nervous System ◽  
Glial Cell ◽  
Specific Deletion

scholarly journals METTL3-dependent m6A modification programs T follicular helper cell differentiation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yingpeng Yao ◽  
Ying Yang ◽  
Wenhui Guo ◽  
Lifan Xu ◽  
Menghao You ◽  
...  
Keyword(s):  
T Cells ◽  
Transcriptional Regulation ◽  
Cell Differentiation ◽  
Ectopic Expression ◽  
Signature Genes ◽  
Follicular Helper ◽  
Conditional Deletion ◽  
A Cell ◽  
A Site ◽  
Post Transcriptional Regulation

AbstractT follicular helper (TFH) cells are specialized effector CD4+ T cells critical to humoral immunity. Whether post-transcriptional regulation has a function in TFH cells is unknown. Here, we show conditional deletion of METTL3 (a methyltransferase catalyzing mRNA N6-methyladenosine (m6A) modification) in CD4+ T cells impairs TFH differentiation and germinal center responses in a cell-intrinsic manner in mice. METTL3 is necessary for expression of important TFH signature genes, including Tcf7, Bcl6, Icos and Cxcr5 and these effects depend on intact methyltransferase activity. m6A-miCLIP-seq shows the 3′ UTR of Tcf7 mRNA is subjected to METTL3-dependent m6A modification. Loss of METTL3 or mutation of the Tcf7 3′ UTR m6A site results in accelerated decay of Tcf7 transcripts. Importantly, ectopic expression of TCF-1 (encoded by Tcf7) rectifies TFH defects owing to METTL3 deficiency. Our findings indicate that METTL3 stabilizes Tcf7 transcripts via m6A modification to ensure activation of a TFH transcriptional program, indicating a pivotal function of post-transcriptional regulation in promoting TFH cell differentiation.

scholarly journals Electrospun Fiber Scaffolds for Engineering Glial Cell Behavior to Promote Neural Regeneration

2020 ◽  
Vol 8 (1) ◽  
pp. 4
Author(s):  
Devan L. Puhl ◽  
Jessica L. Funnell ◽  
Derek W. Nelson ◽  
Manoj K. Gottipati ◽  
Ryan J. Gilbert
Keyword(s):  
Nervous System ◽  
Glial Cell ◽  
Cell Response ◽  
Electrospun Fiber ◽  
Neural Regeneration ◽  
Cell Phenotype ◽  
Comprehensive Overview ◽  
Fiber Alignment ◽  
Wide Range ◽  
Fiber Scaffolds

Electrospinning is a fabrication technique used to produce nano- or micro- diameter fibers to generate biocompatible, biodegradable scaffolds for tissue engineering applications. Electrospun fiber scaffolds are advantageous for neural regeneration because they mimic the structure of the nervous system extracellular matrix and provide contact guidance for regenerating axons. Glia are non-neuronal regulatory cells that maintain homeostasis in the healthy nervous system and regulate regeneration in the injured nervous system. Electrospun fiber scaffolds offer a wide range of characteristics, such as fiber alignment, diameter, surface nanotopography, and surface chemistry that can be engineered to achieve a desired glial cell response to injury. Further, electrospun fibers can be loaded with drugs, nucleic acids, or proteins to provide the local, sustained release of such therapeutics to alter glial cell phenotype to better support regeneration. This review provides the first comprehensive overview of how electrospun fiber alignment, diameter, surface nanotopography, surface functionalization, and therapeutic delivery affect Schwann cells in the peripheral nervous system and astrocytes, oligodendrocytes, and microglia in the central nervous system both in vitro and in vivo. The information presented can be used to design and optimize electrospun fiber scaffolds to target glial cell response to mitigate nervous system injury and improve regeneration.

Glioblastoma Multiforme with Hypodipsic Hypernatremia in a Seven-Month-Old Golden Retriever

2016 ◽  
Vol 52 (5) ◽  
pp. 319-324 ◽  
Author(s):  
Stephanie Engel ◽  
Karen Marie Hilling ◽  
Travis Kuder Meuten ◽  
Chad Brendan Frank ◽  
Angela J. Marolf
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glioblastoma Multiforme ◽  
Glial Cell ◽  
Congenital Malformations ◽  
Cell Tumor ◽  
Golden Retriever ◽  
Neoplastic Process ◽  
Underlying Causes ◽  
The Central Nervous System

ABSTRACT Primary hypodipsic hypernatremia is a rarely reported disease in dogs. Reported underlying causes associated with this disease in dogs include congenital malformations, encephalitis, intracranial neoplasia, and pressure atrophy of the hypothalamus secondary to hydrocephalus. The dog in this report had an infiltrative neoplastic disorder, likely causing damage to the hypothalamic osmoreceptors responsible for the thirst generation. The neoplastic process was identified histopathologically as glioblastoma multiforme, an unusual tumor to occur in a dog this young. A tumor of the central nervous system causing physical destruction of the osmoreceptors has rarely been reported in dogs and none of the previously reported cases involved a glial cell tumor.

scholarly journals Origins of glial cell populations in the insect nervous system

2016 ◽  
Vol 18 ◽  
pp. 96-104 ◽  
Author(s):  
Jaison J Omoto ◽  
Jennifer K Lovick ◽  
Volker Hartenstein
Keyword(s):  
Nervous System ◽  
Glial Cell ◽  
Cell Populations ◽  
Insect Nervous System

scholarly journals Sufu regulation of Hedgehog signaling in P19 cells is required for proper glial cell differentiation

2021 ◽  
Author(s):  
Danielle M. Spice ◽  
Joshua Dierolf ◽  
Gregory M. Kelly
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
Glial Cell ◽  
Neural Differentiation ◽  
Hedgehog Signaling ◽  
Target Genes ◽  
Cell Model ◽  
Ectopic Expression ◽  
Negative Regulator ◽  
Embryonal Carcinoma Cell

AbstractHedgehog signaling is essential for vertebrate development, however, less is known about the negative regulators that influence this pathway during the differentiation of cell fates. Using the mouse P19 embryonal carcinoma cell model, Suppressor of Fused (SUFU), a negative regulator of the Hedgehog pathway, was investigated during retinoic acid-induced neural differentiation. We found Hedgehog signaling was activated in the early phase of neural differentiation and became inactive during terminal differentiation of neurons and astrocytes. SUFU, which regulates signaling at the level of GLI, remained relatively unchanged during the differentiation process, however SUFU loss through CRISPIR-Cas9 gene editing resulted in decreased cell proliferation and ectopic expression of Hedgehog target genes. Interestingly, SUFU-deficient cells were unable to differentiate in the absence of retinoic acid, but when differentiated in its presence they showed delayed and decreased astrocyte differentiation; neuron differentiation did not appear to be affected. Retinoic acid-induced differentiation also caused ectopic activation of Hh target genes in SUFU-deficient cells and while the absence of the GLI3 transcriptional inhibitor suggested the pathway was active, no full-length GLI3 was detected even though the message encoding Gli3 was present. Thus, the study would indicate the proper timing and proportion of glial cell differentiation requires SUFU, and its normal regulation of GLI3 to maintain Hh signaling in an inactive state.

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