The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium

Dnmt1 is critical for immediate postnatal intestinal development, but is not required for the survival of the adult intestinal epithelium, the only rapidly dividing somatic tissue for which this has been shown. Acute Dnmt1 deletion elicits dramatic hypomethylation and genomic instability. Recovery o...

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Detalles Bibliográficos
Autores principales: Elliott, Ellen N, Sheaffer, Karyn L, Kaestner, Klaus H
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2016
Materias:
Developmental Biology and Stem Cells
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4786433/
https://www.ncbi.nlm.nih.gov/pubmed/26808831
http://dx.doi.org/10.7554/eLife.12975
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author Elliott, Ellen N
Sheaffer, Karyn L
Kaestner, Klaus H
author_facet Elliott, Ellen N
Sheaffer, Karyn L
Kaestner, Klaus H
author_sort Elliott, Ellen N
collection PubMed
description Dnmt1 is critical for immediate postnatal intestinal development, but is not required for the survival of the adult intestinal epithelium, the only rapidly dividing somatic tissue for which this has been shown. Acute Dnmt1 deletion elicits dramatic hypomethylation and genomic instability. Recovery of DNA methylation state and intestinal health is dependent on the de novo methyltransferase Dnmt3b. Ablation of both Dnmt1 and Dnmt3b in the intestinal epithelium is lethal, while deletion of either Dnmt1 or Dnmt3b has no effect on survival. These results demonstrate that Dnmt1 and Dnmt3b cooperate to maintain DNA methylation and genomic integrity in the intestinal epithelium. DOI: http://dx.doi.org/10.7554/eLife.12975.001
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spelling pubmed-47864332016-03-17 The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium Elliott, Ellen N Sheaffer, Karyn L Kaestner, Klaus H eLife Developmental Biology and Stem Cells Dnmt1 is critical for immediate postnatal intestinal development, but is not required for the survival of the adult intestinal epithelium, the only rapidly dividing somatic tissue for which this has been shown. Acute Dnmt1 deletion elicits dramatic hypomethylation and genomic instability. Recovery of DNA methylation state and intestinal health is dependent on the de novo methyltransferase Dnmt3b. Ablation of both Dnmt1 and Dnmt3b in the intestinal epithelium is lethal, while deletion of either Dnmt1 or Dnmt3b has no effect on survival. These results demonstrate that Dnmt1 and Dnmt3b cooperate to maintain DNA methylation and genomic integrity in the intestinal epithelium. DOI: http://dx.doi.org/10.7554/eLife.12975.001 eLife Sciences Publications, Ltd 2016-01-25 /pmc/articles/PMC4786433/ /pubmed/26808831 http://dx.doi.org/10.7554/eLife.12975 Text en © 2016, Elliott et al http://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Developmental Biology and Stem Cells
Elliott, Ellen N
Sheaffer, Karyn L
Kaestner, Klaus H
The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium
title The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium
title_full The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium
title_fullStr The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium
title_full_unstemmed The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium
title_short The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium
title_sort ‘de novo’ dna methyltransferase dnmt3b compensates the dnmt1-deficient intestinal epithelium
topic Developmental Biology and Stem Cells
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4786433/
https://www.ncbi.nlm.nih.gov/pubmed/26808831
http://dx.doi.org/10.7554/eLife.12975
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