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Desert hedgehog links transcription factor Sox10 to perineurial development.

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Desert hedgehog links transcription factor Sox10 to perineurial development. / Küspert, Melanie; Weider, Matthias; Müller, Jana; Hermans-Borgmeyer, Irmgard; Meijer, Dies; Wegner, Michael.

in: J NEUROSCI, Jahrgang 32, Nr. 16, 16, 2012, S. 5472-5480.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Küspert, M, Weider, M, Müller, J, Hermans-Borgmeyer, I, Meijer, D & Wegner, M 2012, 'Desert hedgehog links transcription factor Sox10 to perineurial development.', J NEUROSCI, Jg. 32, Nr. 16, 16, S. 5472-5480. <http://www.ncbi.nlm.nih.gov/pubmed/22514309?dopt=Citation>

APA

Küspert, M., Weider, M., Müller, J., Hermans-Borgmeyer, I., Meijer, D., & Wegner, M. (2012). Desert hedgehog links transcription factor Sox10 to perineurial development. J NEUROSCI, 32(16), 5472-5480. [16]. http://www.ncbi.nlm.nih.gov/pubmed/22514309?dopt=Citation

Vancouver

Küspert M, Weider M, Müller J, Hermans-Borgmeyer I, Meijer D, Wegner M. Desert hedgehog links transcription factor Sox10 to perineurial development. J NEUROSCI. 2012;32(16):5472-5480. 16.

Bibtex

@article{47d1b092f7c646af9a1d0a48483aad66,
title = "Desert hedgehog links transcription factor Sox10 to perineurial development.",
abstract = "Schwann cells are the main glial cell type in the PNS. They develop along nerves during embryogenesis and rely on the HMG domain containing Sox10 transcription factor for specification, lineage progression, and terminal differentiation. Sox10 deletion in immature Schwann cells caused peripheral nerve defects in mice that were not restricted to this glial cell type, although expression in the nerve and gene loss were. Formation of the perineurium as the protecting sheath was, for instance, heavily compromised. This resembled the defect observed after loss of Desert hedgehog (Dhh) in mice. Here we show that Sox10 activates Dhh expression in Schwann cells via an enhancer that is located in intron 1 of the Dhh gene. Sox10 binds this enhancer in monomeric form via several sites. Mutation of these sites abolishes both Schwann-cell-specific activity and Sox10 responsiveness in vitro and in transgenic mouse embryos. This argues that Sox10 activates Dhh expression by direct binding to the enhancer and by increasing Dhh levels promotes formation of the perineurial sheath. This represents the first mechanism for a non-cell-autonomous function of Sox10 during peripheral nerve development.",
keywords = "Animals, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Transfection, Chromatin Immunoprecipitation, Mutation/genetics, RNA, Small Interfering/genetics/metabolism, Cell Line, Transformed, Green Fluorescent Proteins/genetics, Schwann Cells/metabolism, Gene Expression Regulation, Developmental/genetics/*physiology, Protein Binding/genetics, Hedgehog Proteins/genetics/*metabolism, Exons/genetics, DNA-Binding Proteins/genetics/metabolism, Peripheral Nervous System/cytology/*embryology/metabolism, Plant Proteins/genetics/metabolism, SOXE Transcription Factors/genetics/*metabolism, Animals, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Transfection, Chromatin Immunoprecipitation, Mutation/genetics, RNA, Small Interfering/genetics/metabolism, Cell Line, Transformed, Green Fluorescent Proteins/genetics, Schwann Cells/metabolism, Gene Expression Regulation, Developmental/genetics/*physiology, Protein Binding/genetics, Hedgehog Proteins/genetics/*metabolism, Exons/genetics, DNA-Binding Proteins/genetics/metabolism, Peripheral Nervous System/cytology/*embryology/metabolism, Plant Proteins/genetics/metabolism, SOXE Transcription Factors/genetics/*metabolism",
author = "Melanie K{\"u}spert and Matthias Weider and Jana M{\"u}ller and Irmgard Hermans-Borgmeyer and Dies Meijer and Michael Wegner",
year = "2012",
language = "English",
volume = "32",
pages = "5472--5480",
journal = "J NEUROSCI",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "16",

}

RIS

TY - JOUR

T1 - Desert hedgehog links transcription factor Sox10 to perineurial development.

AU - Küspert, Melanie

AU - Weider, Matthias

AU - Müller, Jana

AU - Hermans-Borgmeyer, Irmgard

AU - Meijer, Dies

AU - Wegner, Michael

PY - 2012

Y1 - 2012

N2 - Schwann cells are the main glial cell type in the PNS. They develop along nerves during embryogenesis and rely on the HMG domain containing Sox10 transcription factor for specification, lineage progression, and terminal differentiation. Sox10 deletion in immature Schwann cells caused peripheral nerve defects in mice that were not restricted to this glial cell type, although expression in the nerve and gene loss were. Formation of the perineurium as the protecting sheath was, for instance, heavily compromised. This resembled the defect observed after loss of Desert hedgehog (Dhh) in mice. Here we show that Sox10 activates Dhh expression in Schwann cells via an enhancer that is located in intron 1 of the Dhh gene. Sox10 binds this enhancer in monomeric form via several sites. Mutation of these sites abolishes both Schwann-cell-specific activity and Sox10 responsiveness in vitro and in transgenic mouse embryos. This argues that Sox10 activates Dhh expression by direct binding to the enhancer and by increasing Dhh levels promotes formation of the perineurial sheath. This represents the first mechanism for a non-cell-autonomous function of Sox10 during peripheral nerve development.

AB - Schwann cells are the main glial cell type in the PNS. They develop along nerves during embryogenesis and rely on the HMG domain containing Sox10 transcription factor for specification, lineage progression, and terminal differentiation. Sox10 deletion in immature Schwann cells caused peripheral nerve defects in mice that were not restricted to this glial cell type, although expression in the nerve and gene loss were. Formation of the perineurium as the protecting sheath was, for instance, heavily compromised. This resembled the defect observed after loss of Desert hedgehog (Dhh) in mice. Here we show that Sox10 activates Dhh expression in Schwann cells via an enhancer that is located in intron 1 of the Dhh gene. Sox10 binds this enhancer in monomeric form via several sites. Mutation of these sites abolishes both Schwann-cell-specific activity and Sox10 responsiveness in vitro and in transgenic mouse embryos. This argues that Sox10 activates Dhh expression by direct binding to the enhancer and by increasing Dhh levels promotes formation of the perineurial sheath. This represents the first mechanism for a non-cell-autonomous function of Sox10 during peripheral nerve development.

KW - Animals

KW - Humans

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Transfection

KW - Chromatin Immunoprecipitation

KW - Mutation/genetics

KW - RNA, Small Interfering/genetics/metabolism

KW - Cell Line, Transformed

KW - Green Fluorescent Proteins/genetics

KW - Schwann Cells/metabolism

KW - Gene Expression Regulation, Developmental/genetics/physiology

KW - Protein Binding/genetics

KW - Hedgehog Proteins/genetics/metabolism

KW - Exons/genetics

KW - DNA-Binding Proteins/genetics/metabolism

KW - Peripheral Nervous System/cytology/embryology/metabolism

KW - Plant Proteins/genetics/metabolism

KW - SOXE Transcription Factors/genetics/metabolism

KW - Animals

KW - Humans

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Transfection

KW - Chromatin Immunoprecipitation

KW - Mutation/genetics

KW - RNA, Small Interfering/genetics/metabolism

KW - Cell Line, Transformed

KW - Green Fluorescent Proteins/genetics

KW - Schwann Cells/metabolism

KW - Gene Expression Regulation, Developmental/genetics/physiology

KW - Protein Binding/genetics

KW - Hedgehog Proteins/genetics/metabolism

KW - Exons/genetics

KW - DNA-Binding Proteins/genetics/metabolism

KW - Peripheral Nervous System/cytology/embryology/metabolism

KW - Plant Proteins/genetics/metabolism

KW - SOXE Transcription Factors/genetics/metabolism

M3 - SCORING: Journal article

VL - 32

SP - 5472

EP - 5480

JO - J NEUROSCI

JF - J NEUROSCI

SN - 0270-6474

IS - 16

M1 - 16

ER -