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Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration.

Injured peripheral sensory neurons switch to a regenerative state after axon injury, which requires transcriptional and epigenetic changes. However, the roles and mechanisms of gene inactivation after injury are poorly understood. Here, we show that DNA methylation, which generally leads to gene sil... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America December 26, 2018, Vol.115(52), pp.E12417-E12426
Main Author: Oh, Young Mi
Other Authors: Mahar, Marcus , Ewan, Eric E , Leahy, Kathleen M , Zhao, Guoyan , Cavalli, Valeria
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1812518115
Link: http://search.proquest.com/docview/2155151805/?pq-origsite=primo
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recordid: proquest2155151805
title: Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration.
format: Article
creator:
  • Oh, Young Mi
  • Mahar, Marcus
  • Ewan, Eric E
  • Leahy, Kathleen M
  • Zhao, Guoyan
  • Cavalli, Valeria
subjects:
  • Animals–Metabolism
  • Axons–Physiology
  • Ccaat-Enhancer-Binding Proteins–Metabolism
  • DNA Methylation–Genetics
  • Epigenesis, Genetic–Genetics
  • Epigenomics–Methods
  • Female–Genetics
  • Gene Expression Regulation–Genetics
  • Gene Expression Regulation, Neoplastic–Physiology
  • Gene Silencing–Metabolism
  • Histones–Genetics
  • Male–Physiology
  • Mice–Genetics
  • Mice, Inbred C57bl–Physiology
  • Nerve Regeneration–Genetics
  • Nuclear Proteins–Metabolism
  • Promoter Regions, Genetic–Injuries
  • Repressor Proteins–Injuries
  • Sciatic Nerve–Injuries
  • Ccaat-Enhancer-Binding Proteins
ispartof: Proceedings of the National Academy of Sciences of the United States of America, December 26, 2018, Vol.115(52), pp.E12417-E12426
description: Injured peripheral sensory neurons switch to a regenerative state after axon injury, which requires transcriptional and epigenetic changes. However, the roles and mechanisms of gene inactivation after injury are poorly understood. Here, we show that DNA methylation, which generally leads to gene silencing, is required for robust axon regeneration after peripheral nerve lesion. Ubiquitinlike containing PHD ring finger 1 (UHRF1), a critical epigenetic regulator involvedinDNA methylation, increases upon axon injury and is required for robust axon regeneration. The increased level of UHRF1 results from a decrease in miR-9. The level of another target of miR-9, the transcriptional regulator RE1 silencing transcription factor (REST), transiently increases after injury and is required for axon regeneration. Mechanistically, UHRF1 interacts with DNA methyltransferases (DNMTs) and H3K9me3 at the promoter region to repress the expression ofthe tumor suppressor gene phosphatase andtensinhomolog(PTEN) andREST.Ourstudyrevealsanepigenetic mechanism that silences tumor suppressor genes and restricts REST expression in time after injury to promote axon regeneration. axon regeneration | epigenetic | UHRF1 | REST | DNMT
language: eng
source:
identifier: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1812518115
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleEpigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration.
creatorOh, Young Mi ; Mahar, Marcus ; Ewan, Eric E ; Leahy, Kathleen M ; Zhao, Guoyan ; Cavalli, Valeria
contributorOh, Young Mi (correspondence author) ; Oh, Young Mi (record owner)
ispartofProceedings of the National Academy of Sciences of the United States of America, December 26, 2018, Vol.115(52), pp.E12417-E12426
identifierE-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1812518115
subjectAnimals–Metabolism ; Axons–Physiology ; Ccaat-Enhancer-Binding Proteins–Metabolism ; DNA Methylation–Genetics ; Epigenesis, Genetic–Genetics ; Epigenomics–Methods ; Female–Genetics ; Gene Expression Regulation–Genetics ; Gene Expression Regulation, Neoplastic–Physiology ; Gene Silencing–Metabolism ; Histones–Genetics ; Male–Physiology ; Mice–Genetics ; Mice, Inbred C57bl–Physiology ; Nerve Regeneration–Genetics ; Nuclear Proteins–Metabolism ; Promoter Regions, Genetic–Injuries ; Repressor Proteins–Injuries ; Sciatic Nerve–Injuries ; Ccaat-Enhancer-Binding Proteins
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descriptionInjured peripheral sensory neurons switch to a regenerative state after axon injury, which requires transcriptional and epigenetic changes. However, the roles and mechanisms of gene inactivation after injury are poorly understood. Here, we show that DNA methylation, which generally leads to gene silencing, is required for robust axon regeneration after peripheral nerve lesion. Ubiquitinlike containing PHD ring finger 1 (UHRF1), a critical epigenetic regulator involvedinDNA methylation, increases upon axon injury and is required for robust axon regeneration. The increased level of UHRF1 results from a decrease in miR-9. The level of another target of miR-9, the transcriptional regulator RE1 silencing transcription factor (REST), transiently increases after injury and is required for axon regeneration. Mechanistically, UHRF1 interacts with DNA methyltransferases (DNMTs) and H3K9me3 at the promoter region to repress the expression ofthe tumor suppressor gene phosphatase andtensinhomolog(PTEN) andREST.Ourstudyrevealsanepigenetic mechanism that silences tumor suppressor genes and restricts REST expression in time after injury to promote axon regeneration. axon regeneration | epigenetic | UHRF1 | REST | DNMT
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