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Article ; Online: ChIP-Seq: Library Preparation and Sequencing.

Sheaffer, Karyn L / Schug, Jonathan

Methods in molecular biology (Clifton, N.J.)

2016 Volume 1402, Page(s) 101–117

Abstract: Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-Seq) has been used extensively to determine the genome-wide location of DNA-binding factors, such as transcription factors, posttranscriptionally modified histones, and members of ...

Abstract	Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-Seq) has been used extensively to determine the genome-wide location of DNA-binding factors, such as transcription factors, posttranscriptionally modified histones, and members of the transcription complex, to assess regulatory input, epigenetic modifications, and transcriptional activity, respectively. Here we describe methods to isolate chromatin from tissues, immunoprecipitate DNA bound to a protein of interest, and perform next-generation sequencing to identify a genome-wide DNA-binding pattern.
MeSH term(s)	Animals ; Chromatin/genetics ; Chromatin/isolation & purification ; Chromatin/metabolism ; Chromatin Immunoprecipitation/methods ; DNA/genetics ; DNA/isolation & purification ; DNA/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/isolation & purification ; DNA-Binding Proteins/metabolism ; Gene Library ; Genome ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Sequence Analysis, DNA/methods
Chemical Substances	Chromatin ; DNA-Binding Proteins ; DNA (9007-49-2)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-3378-5_9
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Article ; Online: The 'de novo' DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium.

Elliott, Ellen N / Sheaffer, Karyn L / Kaestner, Klaus H

eLife

2016 Volume 5

Abstract: 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 ... ...

Abstract	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.
MeSH term(s)	Animals ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/deficiency ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; Gene Deletion ; Intestinal Mucosa/enzymology ; Intestinal Mucosa/physiology ; Mice, Knockout ; Survival Analysis ; DNA Methyltransferase 3B
Chemical Substances	DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37)
Language	English
Publishing date	2016-01-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.12975
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Article ; Online: DNA Hypomethylation Contributes to Genomic Instability and Intestinal Cancer Initiation.

Sheaffer, Karyn L / Elliott, Ellen N / Kaestner, Klaus H

Cancer prevention research (Philadelphia, Pa.)

2016 Volume 9, Issue 7, Page(s) 534–546

Abstract: Intestinal cancer is a heterogeneous disease driven by genetic mutations and epigenetic changes. Approximately 80% of sporadic colorectal cancers are initiated by mutation and inactivation of the adenomatous polyposis coli (APC) gene, which results in ... ...

Abstract	Intestinal cancer is a heterogeneous disease driven by genetic mutations and epigenetic changes. Approximately 80% of sporadic colorectal cancers are initiated by mutation and inactivation of the adenomatous polyposis coli (APC) gene, which results in unrestrained intestinal epithelial growth and formation of adenomas. Aberrant DNA methylation promotes cancer progression by the inactivation of tumor suppressor genes via promoter methylation. In addition, global DNA hypomethylation is often seen before the formation of adenomas, suggesting that it contributes to neoplastic transformation. Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the Apc(Min/+) mouse model of intestinal cancer. However, the consequences of intestinal epithelial-specific acute hypomethylation during Apc(Min/+) tumor initiation have not been reported. Using temporally controlled intestinal epithelial-specific gene ablation, we show that total loss of Dnmt1 in the Apc(Min/+) mouse model of intestinal cancer causes accelerated adenoma initiation. Deletion of Dnmt1 precipitates an acute response characterized by hypomethylation of repetitive elements and genomic instability, which surprisingly is followed by remethylation with time. Two months post-Dnmt1 ablation, mice display increased macroadenoma load, consistent with a role for Dnmt1 and DNA methylation in maintaining genomic stability. These data suggest that DNA hypomethylation plays a previously unappreciated role in intestinal adenoma initiation. Cancer Prev Res; 9(7); 534-46. ©2016 AACRSee related article by Lee and Laird, p. 509.
MeSH term(s)	Adenoma/genetics ; Adenoma/pathology ; Animals ; Carcinogenesis/genetics ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methylation/genetics ; Genomic Instability/genetics ; Intestinal Neoplasms/genetics ; Intestinal Neoplasms/pathology ; Mice
Chemical Substances	DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37)
Language	English
Publishing date	2016-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2434717-6
ISSN	1940-6215 ; 1940-6207
ISSN (online)	1940-6215
ISSN	1940-6207
DOI	10.1158/1940-6207.CAPR-15-0349
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Article ; Online: Transcriptional networks in liver and intestinal development.

Sheaffer, Karyn L / Kaestner, Klaus H

Cold Spring Harbor perspectives in biology

2012 Volume 4, Issue 9, Page(s) a008284

Abstract: The development of the gastrointestinal tract is a complex process that integrates signaling processes with downstream transcriptional responses. Here, we discuss the regionalization of the primitive gut and formation of the intestine and liver. Anterior- ...

Abstract	The development of the gastrointestinal tract is a complex process that integrates signaling processes with downstream transcriptional responses. Here, we discuss the regionalization of the primitive gut and formation of the intestine and liver. Anterior-posterior position in the primitive gut is important for establishing regions that will become functional organs. Coordination of signaling between the epithelium and mesenchyme and downstream transcriptional responses is required for intestinal development and homeostasis. Liver development uses a complex transcriptional network that controls the establishment of organ domains, cell differentiation, and adult function. Discussion of these transcriptional mechanisms gives us insight into how the primitive gut, composed of simple endodermal cells, develops into multiple diverse cell types that are organized into complex mature organs.
MeSH term(s)	Animals ; Body Patterning/genetics ; Cell Differentiation ; Embryonic Development/genetics ; Gene Regulatory Networks ; Homeostasis ; Intestinal Mucosa/metabolism ; Intestines/growth & development ; Liver/growth & development ; Liver/metabolism ; Transcription Factors/physiology
Chemical Substances	Transcription Factors
Language	English
Publishing date	2012-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1943-0264
ISSN (online)	1943-0264
DOI	10.1101/cshperspect.a008284
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Article ; Online: The ‘de novo’ DNA methyltransferase Dnmt3b compensates the Dnmt1-deficient intestinal epithelium

Ellen N Elliott / Karyn L Sheaffer / Klaus H Kaestner

eLife, Vol

2016 Volume 5

Abstract	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.
Keywords	DNA methylation ; intestinal epithelium ; dnmt1 ; dnmt3 ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
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Article ; Online: Epigenetic regulation of intestinal stem cells by Tet1-mediated DNA hydroxymethylation.

Kim, Rinho / Sheaffer, Karyn L / Choi, Inchan / Won, Kyoung-Jae / Kaestner, Klaus H

Genes & development

2016 Volume 30, Issue 21, Page(s) 2433–2442

Abstract: Methylated cytosines are associated with gene silencing. The ten-eleven translocation (TET) hydroxylases, which oxidize methylated cytosines to 5-hydroxymethylcytosine (5hmC), are essential for cytosine demethylation. Gene silencing and activation are ... ...

Abstract	Methylated cytosines are associated with gene silencing. The ten-eleven translocation (TET) hydroxylases, which oxidize methylated cytosines to 5-hydroxymethylcytosine (5hmC), are essential for cytosine demethylation. Gene silencing and activation are critical for intestinal stem cell (ISC) maintenance and differentiation, but the potential role of TET hydroxylases in these processes has not yet been examined. Here, we generated genome-wide maps of the 5hmC mark in ISCs and their differentiated progeny. Genes with high levels of hydroxymethylation in ISCs are strongly associated with Wnt signaling and developmental processes. We found Tet1 to be the most abundantly expressed Tet gene in ISCs; therefore, we analyzed intestinal development in Tet1-deficient mice and determined that these mice are growth-retarded, exhibit partial postnatal lethality, and have significantly reduced numbers of proliferative cells in the intestinal epithelium. In addition, the Tet1-deficient intestine displays reduced organoid-forming capacity. In the Tet1-deficient crypt, decreased expression of Wnt target genes such as Axin2 and Lgr5 correlates with lower 5hmC levels at their promoters. These data demonstrate that Tet1-mediated DNA hydroxymethylation plays a critical role in the epigenetic regulation of the Wnt pathway in intestinal stem and progenitor cells and consequently in the self-renewal of the intestinal epithelium.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cells, Cultured ; DNA Methylation ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental/genetics ; Intestines/cytology ; Intestines/growth & development ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Receptors, G-Protein-Coupled/genetics ; Sequence Deletion ; Stem Cells/cytology ; Stem Cells/physiology ; Wnt Signaling Pathway/genetics
Chemical Substances	DNA-Binding Proteins ; Lgr5 protein, mouse ; Proto-Oncogene Proteins ; Receptors, G-Protein-Coupled ; TET1 protein, mouse
Language	English
Publishing date	2016-11-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.288035.116
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Article: The BisPCR(2) method for targeted bisulfite sequencing.

Bernstein, Diana L / Kameswaran, Vasumathi / Le Lay, John E / Sheaffer, Karyn L / Kaestner, Klaus H

Epigenetics & chromatin

2015 Volume 8, Page(s) 27

Abstract: Background: DNA methylation has emerged as an important regulator of development and disease, necessitating the design of more efficient and cost-effective methods for detecting and quantifying this epigenetic modification. Next-generation sequencing ( ... ...

Abstract	Background: DNA methylation has emerged as an important regulator of development and disease, necessitating the design of more efficient and cost-effective methods for detecting and quantifying this epigenetic modification. Next-generation sequencing (NGS) techniques offer single base resolution of CpG methylation levels with high statistical significance, but are also high cost if performed genome-wide. Here, we describe a simplified targeted bisulfite sequencing approach in which DNA sequencing libraries are prepared following sodium bisulfite conversion and two rounds of PCR for target enrichment and sample barcoding, termed BisPCR(2). Results: We have applied the BisPCR(2) technique to validate differential methylation at several type 2 diabetes risk loci identified in genome-wide studies of human islets. We confirmed some previous findings while not others, in addition to identifying novel differentially methylated CpGs at these genes of interest, due to the much higher depth of sequencing coverage in BisPCR(2) compared to prior array-based approaches. Conclusion: This study presents a robust, efficient, and cost-effective technique for targeted bisulfite NGS, and illustrates its utility by reanalysis of prior findings from genome-wide studies.
Language	English
Publishing date	2015-08-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2462129-8
ISSN	1756-8935
ISSN	1756-8935
DOI	10.1186/s13072-015-0020-x
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Article ; Online: Dnmt1 is essential to maintain progenitors in the perinatal intestinal epithelium.

Elliott, Ellen N / Sheaffer, Karyn L / Schug, Jonathan / Stappenbeck, Thaddeus S / Kaestner, Klaus H

Development (Cambridge, England)

2015 Volume 142, Issue 12, Page(s) 2163–2172

Abstract: The DNA methyltransferase Dnmt1 maintains DNA methylation patterns and genomic stability in several in vitro cell systems. Ablation of Dnmt1 in mouse embryos causes death at the post-gastrulation stage; however, the functions of Dnmt1 and DNA methylation ...

Abstract	The DNA methyltransferase Dnmt1 maintains DNA methylation patterns and genomic stability in several in vitro cell systems. Ablation of Dnmt1 in mouse embryos causes death at the post-gastrulation stage; however, the functions of Dnmt1 and DNA methylation in organogenesis remain unclear. Here, we report that Dnmt1 is crucial during perinatal intestinal development. Loss of Dnmt1 in intervillus progenitor cells causes global hypomethylation, DNA damage, premature differentiation, apoptosis and, consequently, loss of nascent villi. We further confirm the crucial role of Dnmt1 during crypt development using the in vitro organoid culture system, and illustrate a clear differential requirement for Dnmt1 in immature versus mature organoids. These results demonstrate an essential role for Dnmt1 in maintaining genomic stability during intestinal development and the establishment of intestinal crypts.
MeSH term(s)	Animals ; Apoptosis/genetics ; Cell Proliferation/genetics ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/physiology ; DNA Damage/genetics ; DNA Methylation/genetics ; Gene Expression Regulation, Developmental ; Genomic Instability/genetics ; Intestinal Mucosa/cytology ; Intestinal Mucosa/embryology ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Organogenesis/genetics ; Stem Cells/cytology
Chemical Substances	DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37)
Language	English
Publishing date	2015-06-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.117341
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Article: The Target of Rapamycin pathway antagonizes pha-4/FoxA to control development and aging.

Sheaffer, Karyn L / Updike, Dustin L / Mango, Susan E

Current biology : CB

2008 Volume 18, Issue 18, Page(s) 1355–1364

Abstract: Background: FoxA factors are critical regulators of embryonic development and postembryonic life, but little is know about the upstream pathways that modulate their activity. C. elegans pha-4 encodes a FoxA transcription factor that is required to ... ...

Abstract	Background: FoxA factors are critical regulators of embryonic development and postembryonic life, but little is know about the upstream pathways that modulate their activity. C. elegans pha-4 encodes a FoxA transcription factor that is required to establish the foregut in embryos and to control growth and longevity after birth. We previously identified the AAA+ ATPase homolog ruvb-1 as a potent suppressor of pha-4 mutations. Results: Here we show that ruvb-1 is a component of the Target of Rapamycin (TOR) pathway in C. elegans (CeTOR). Both ruvb-1 and let-363/TOR control nucleolar size and promote localization of box C/D snoRNPs to nucleoli, suggesting a role in rRNA maturation. Inactivation of let-363/TOR or ruvb-1 suppresses the lethality associated with reduced pha-4 activity. The CeTOR pathway controls protein homeostasis and also contributes to adult longevity. We find that pha-4 is required to extend adult lifespan in response to reduced CeTOR signaling. Mutations in the predicted CeTOR target rsks-1/S6 kinase or in ife-2/eIF4E also reduce protein biosynthesis and extend lifespan, but only rsks-1 mutations require pha-4 for adult longevity. In addition, rsks-1, but not ife-2, can suppress the larval lethality associated with pha-4 loss-of-function mutations. Conclusions: The data suggest that pha-4 and the CeTOR pathway antagonize one another to regulate postembryonic development and adult longevity. We suggest a model in which nutrients promote TOR and S6 kinase signaling, which represses pha-4/FoxA, leading to a shorter lifespan. A similar regulatory hierarchy may function in other animals to modulate metabolism, longevity, or disease.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/growth & development ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/antagonists & inhibitors ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/physiology ; Larva/physiology ; Longevity ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/physiology ; Phenotype ; Phosphotransferases (Alcohol Group Acceptor)/genetics ; Phosphotransferases (Alcohol Group Acceptor)/physiology ; RNA/genetics ; RNA Interference ; Ribonucleoproteins/physiology ; Trans-Activators/antagonists & inhibitors ; Trans-Activators/genetics
Chemical Substances	Caenorhabditis elegans Proteins ; Nuclear Proteins ; Pha-4 protein, C elegans ; Ribonucleoproteins ; Trans-Activators ; RNA (63231-63-0) ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; let-363 protein, C elegans (EC 2.7.1.-)
Language	English
Publishing date	2008-09-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2008.07.097
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Article ; Online: DNA methylation is required for the control of stem cell differentiation in the small intestine.

Sheaffer, Karyn L / Kim, Rinho / Aoki, Reina / Elliott, Ellen N / Schug, Jonathan / Burger, Lukas / Schübeler, Dirk / Kaestner, Klaus H

Genes & development

2014 Volume 28, Issue 6, Page(s) 652–664

Abstract: The mammalian intestinal epithelium has a unique organization in which crypts harboring stem cells produce progenitors and finally clonal populations of differentiated cells. Remarkably, the epithelium is replaced every 3-5 d throughout adult life. ... ...

Abstract	The mammalian intestinal epithelium has a unique organization in which crypts harboring stem cells produce progenitors and finally clonal populations of differentiated cells. Remarkably, the epithelium is replaced every 3-5 d throughout adult life. Disrupted maintenance of the intricate balance of proliferation and differentiation leads to loss of epithelial integrity or barrier function or to cancer. There is a tight correlation between the epigenetic status of genes and expression changes during differentiation; however, the mechanism of how changes in DNA methylation direct gene expression and the progression from stem cells to their differentiated descendants is unclear. Using conditional gene ablation of the maintenance methyltransferase Dnmt1, we demonstrate that reducing DNA methylation causes intestinal crypt expansion in vivo. Determination of the base-resolution DNA methylome in intestinal stem cells and their differentiated descendants shows that DNA methylation is dynamic at enhancers, which are often associated with genes important for both stem cell maintenance and differentiation. We establish that the loss of DNA methylation at intestinal stem cell gene enhancers causes inappropriate gene expression and delayed differentiation.
MeSH term(s)	Animals ; Cell Differentiation ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Methylation/genetics ; Gene Deletion ; Gene Expression Regulation, Developmental ; Intestine, Small/cytology ; Mice ; Stem Cells/cytology
Chemical Substances	DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37)
Language	English
Publishing date	2014-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.230318.113
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