Pax3 function is required specifically for inner ear structures with melanogenic fates

Kim, Hong Kyung; Ankamreddy, Harinarayana; Lee, Dong Jin; Kong, Kyoung Ah; Ko, Hyuk Wan; Kim, Myoung Hee; Bok, Jinwoong

doi:10.1016/j.bbrc.2014.02.047

Cited by 24 publications

(14 citation statements)

References 32 publications

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“…For example, Pax3 regulates cell phenotypic mesenchymal–epithelial interconversion in vitro (Wiggan et al, ). Mouse inner ear components with melanogenic fates require Pax3 function (Kim et al, ). Moreover, conditional expression of Pax7 controls the derivation of skeletal myogenic precursors from differentiating human pluripotent stem cells (Darabi and Perlingeiro, ).…”

Section: Discussionmentioning

confidence: 99%

Pax3 and Pax7 interact reciprocally and regulate the expression of cadherin‐7 through inducing neuron differentiation in the developing chicken spinal cord

Lin

Wang

Yang

et al. 2015

J of Comparative Neurology

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Pax3 and Pax7 are closely related transcription factors that are widely expressed in the developing nervous system and somites. In the CNS, both genes are expressed in the dorsal part of the neural tube during development. Pax3 and Pax7 are involved in the sonic hedgehog (Shh) signaling pathway and are inhibited by Shh overexpression. The present study confirms in vivo that Pax3 overexpression represses the expression of Pax7, whereas Pax7 overexpression endogenously enhances and ectopically induces the expression of Pax3 in the developing chicken spinal cord. Overexpression of Pax3 and Pax7 represses the endogenous expression of cadherin-7, a member of the cadherin family of morphogenetic genes, and induces its ectopic expression. The present study also shows that overexpression of Pax3 and Pax7 changes the fate and morphology of cells in the neuroepithelial layer and induces the expression of postmitotic neuronal markers. We show that both Pax3 and Pax7 promote the differentiation of neural progenitor cells into neurons. Furthermore, the downregulation of Pax3 and Pax7 with specific shRNAs results in apoptosis in the developing spinal cord. Collectively, these results suggest that the transcription factors Pax3 and Pax7 play important roles in regulating morphogenesis and cell differentiation in the developing spinal cord.

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Section: Discussionmentioning

confidence: 99%

Pax3 and Pax7 interact reciprocally and regulate the expression of cadherin‐7 through inducing neuron differentiation in the developing chicken spinal cord

Lin

Wang

Yang

et al. 2015

J of Comparative Neurology

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“…In addition, epithelial mesenchymal transition (EMT), or the differentiation from the ectoderm into mesoderm, is also critical for the migration and differentiation of neural crest cells, and is controlled by PAX3, which plays a key role in the development of embryonic nerve cells. PAX3 and Msx1 induce Snail1 and Snail2 to down-regulate the expression of adhesion proteins, thereby allowing the neural crest cells to migrate and differentiate into mesenchymal cells [14]. The transcription factor GBX2 antagonizes OTX2, which inhibits PAX6 expression and induces the production of post-brain neural progenitor cells.…”

Section: Discussionmentioning

confidence: 99%

SV40T reprograms Schwann cells into stem-like cells that can re-differentiate into terminal nerve cells.

Nan

Wang

et al. 2020

Preprint

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Background : The effects of Simian virus 40 T antigen (SV40T) on various kinds of cells are different. Previous researchers failed to use SV40T immortalized nerve cells. However, they argued that SV40T caused nerve cell transformation. No one further study what is the specific effect of SV40T on nerve cells. We transfected Schwann cells (SCs) that did not have differentiation ability with MPH 86 plasmid containing SV40T in order to explore the effects of SV40T on Schwann cells. Methods : SCs were transfected with MPH 86 plasmid carrying the SV40T gene and cultured in different media, as well as co-cultured with neural stem cells (NSCs). In our study, SCs overexpressing SV40T were defined as SV40T-SCs. The proliferation of these cells was detected by WST-1, and the expression of different biomarkers was analyzed by qPCR and immunohistochemistry. Results: SV40T induced the characteristics of NSCs, such as the ability to grow in suspension, form spheroid colonies and proliferate rapidly, in the SCs, which were reversed by knocking out SV40T by the Flip-adenovirus . In addition, SV40T up-regulated the neurocrest markers Nestin, Pax3 and Slug, and down-regulated S100b as well as the late differentiation markers MBP, GFAP and Olig1/2. These cells also expressed NSC markers like Nestin, Sox2, CD133 and SSEA-1, as well as early development markers of embryonic stem cells (ESCs) like BMP4, c-Myc, OCT4 and Gbx2. Co-culturing with NSCs induced differentiation of the SV40T-SCs into neuronal and glial cells. Conclusions: SV40T reprograms Schwann cells to stem-like cells at the stage of neural crest cells that can differentiate to terminal nerve cells.

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“…Reissner's membrane is more medial within the duct and separates the scala media from the scala vestibuli compartment. The fully differentiated stria is more lateral and is created by a merger between cochlear duct epithelium and neural crest‐derived cells originating beyond the duct . It becomes highly vascularized, and it plays a key role in maintaining the ionic homeostasis of endolymph, the fluid that resides in scala media .…”

Section: Transcription Factors Expressed On the Roof Of The Cochlear mentioning

confidence: 99%

“…The fully differentiated stria is more lateral and is created by a merger between cochlear duct epithelium and neural crest-derived cells originating beyond the duct. 44,45 It becomes highly vascularized, and it plays a key role in maintaining the ionic homeostasis of endolymph, the fluid that resides in scala media. [46][47][48] The high potassium and calcium concentrations of endolymph carry the electrical currents underlying mechanotransduction.…”

Section: Transcription Factors Expressed On the Roof Of The Cochleamentioning

confidence: 99%

The acquisition of positional information across the radial axis of the cochlea

Munnamalai

Fekete

2019

Developmental Dynamics

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The mammalian cochlea detects sound and transmits this information to the brain. A cross section through the cochlea reveals functionally distinct epithelial domains arrayed around the circumference of a fluid‐filled duct. Six major domains include two on the roof of the duct (Reissner's membrane medially and the stria vascularis laterally) and four across the floor of the duct, including the medial and lateral halves of the sensory domain, the organ of Corti. These radial domains are distinguishable in the embryonic cochlea by differential expression of transcription factors, and we focus here on a subset of the factors that can influence cochlear fates. We then move upstream of these genes to identify which of five signaling pathways (Notch, Fgf, Wnt, Bmp, and Shh) controls their spatial patterns of expression. We link the signaling pathways to their downstream genes, separating them by their radial position, to create putative gene regulatory networks (GRNs) from two time points, before and during the time when six radial compartments arise. These GRNs offer a framework for understanding the acquisition of positional information across the radial axis of the cochlea, and to guide therapeutic approaches to repair or regenerate distinct cochlear components that may contribute to hearing loss.

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Pax3 function is required specifically for inner ear structures with melanogenic fates

Cited by 24 publications

References 32 publications

Pax3 and Pax7 interact reciprocally and regulate the expression of cadherin‐7 through inducing neuron differentiation in the developing chicken spinal cord

Pax3 and Pax7 interact reciprocally and regulate the expression of cadherin‐7 through inducing neuron differentiation in the developing chicken spinal cord

SV40T reprograms Schwann cells into stem-like cells that can re-differentiate into terminal nerve cells.

The acquisition of positional information across the radial axis of the cochlea

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