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Article ; Online: OCT4 and SOX2 Work as Transcriptional Activators in Reprogramming Human Fibroblasts.

Narayan, Santosh / Bryant, Gene / Shah, Shivangi / Berrozpe, Georgina / Ptashne, Mark

2017 Volume 20, Issue 7, Page(s) 1585–1596

Abstract: SOX2 and OCT4, in conjunction with KLF4 and cMYC, are sufficient to reprogram human fibroblasts to induced pluripotent stem cells (iPSCs), but it is unclear if they function as transcriptional activators or as repressors. We now show that, like OCT4, ... ...

Abstract	SOX2 and OCT4, in conjunction with KLF4 and cMYC, are sufficient to reprogram human fibroblasts to induced pluripotent stem cells (iPSCs), but it is unclear if they function as transcriptional activators or as repressors. We now show that, like OCT4, SOX2 functions as a transcriptional activator. We substituted SOX2-VP16 (a strong activator) for wild-type (WT) SOX2, and we saw an increase in the efficiency and rate of reprogramming, whereas the SOX2-HP1 fusion (a strong repressor) eliminated reprogramming. We report that, at an early stage of reprogramming, virtually all DNA-bound OCT4, SOX2, and SOX2-VP16 were embedded in putative enhancers, about half of which were created de novo. Those associated with SOX2-VP16 were, on average, stronger than those bearing WT SOX2. Many newly created putative enhancers were transient, and many transcription factor locations on DNA changed as reprogramming progressed. These results are consistent with the idea that, during reprogramming, there is an intermediate state that is distinct from both parental cells and iPSCs.
MeSH term(s)	Cell Differentiation ; Cellular Reprogramming ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Herpes Simplex Virus Protein Vmw65/genetics ; Herpes Simplex Virus Protein Vmw65/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Octamer Transcription Factor-3/genetics ; Octamer Transcription Factor-3/metabolism ; Primary Cell Culture ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; SOXB1 Transcription Factors/genetics ; SOXB1 Transcription Factors/metabolism ; Signal Transduction ; Transcriptional Activation
Chemical Substances	GKLF protein ; Herpes Simplex Virus Protein Vmw65 ; Kruppel-Like Transcription Factors ; MYC protein, human ; Octamer Transcription Factor-3 ; POU5F1 protein, human ; Proto-Oncogene Proteins c-myc ; Recombinant Fusion Proteins ; SOX2 protein, human ; SOXB1 Transcription Factors
Language	English
Publishing date	2017-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2017.07.071
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Article ; Online: OCT4 and SOX2 Work as Transcriptional Activators in Reprogramming Human Fibroblasts

Santosh Narayan / Gene Bryant / Shivangi Shah / Georgina Berrozpe / Mark Ptashne

Cell Reports, Vol 20, Iss 7, Pp 1585-

2017 Volume 1596

Abstract	SOX2 and OCT4, in conjunction with KLF4 and cMYC, are sufficient to reprogram human fibroblasts to induced pluripotent stem cells (iPSCs), but it is unclear if they function as transcriptional activators or as repressors. We now show that, like OCT4, SOX2 functions as a transcriptional activator. We substituted SOX2-VP16 (a strong activator) for wild-type (WT) SOX2, and we saw an increase in the efficiency and rate of reprogramming, whereas the SOX2-HP1 fusion (a strong repressor) eliminated reprogramming. We report that, at an early stage of reprogramming, virtually all DNA-bound OCT4, SOX2, and SOX2-VP16 were embedded in putative enhancers, about half of which were created de novo. Those associated with SOX2-VP16 were, on average, stronger than those bearing WT SOX2. Many newly created putative enhancers were transient, and many transcription factor locations on DNA changed as reprogramming progressed. These results are consistent with the idea that, during reprogramming, there is an intermediate state that is distinct from both parental cells and iPSCs.
Keywords	reprogramming ; iPSCs ; enhancers ; transcription ; transcription factors ; stem cells ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Polycomb Responds to Low Levels of Transcription.

Berrozpe, Georgina / Bryant, Gene O / Warpinski, Katherine / Spagna, Dan / Narayan, Santosh / Shah, Shivangi / Ptashne, Mark

Cell reports

2017 Volume 20, Issue 4, Page(s) 785–793

Abstract: How is Polycomb (Pc), a eukaryotic negative regulator of transcription, targeted to specific mammalian genes? Our genome-wide analysis of the Pc mark H3K27me3 in murine cells revealed that Pc is preferentially associated with CpG island promoters of ... ...

Abstract	How is Polycomb (Pc), a eukaryotic negative regulator of transcription, targeted to specific mammalian genes? Our genome-wide analysis of the Pc mark H3K27me3 in murine cells revealed that Pc is preferentially associated with CpG island promoters of genes that are transcribed at a low level and less so with promoters of genes that are either silent or more highly expressed. Studies of the CpG island promoter of the Kit gene demonstrate that Pc is largely absent when the gene is silent in myeloid cells, as well as when the gene is highly expressed in mast cells. Manipulations that increase transcription in the former case, and reduce it in the latter, increase Pc occupancy. The average negative effect of Pc, we infer, is about 2-fold. We suggest possible biological roles for such negative effects and propose a mechanism by which Pc might be recruited to weakly transcribed genes.
MeSH term(s)	Animals ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; CpG Islands/genetics ; Humans ; Mice ; Myeloid Cells/metabolism ; Polycomb-Group Proteins/genetics ; Polycomb-Group Proteins/metabolism ; Promoter Regions, Genetic/genetics ; Transcription, Genetic/genetics
Chemical Substances	Polycomb-Group Proteins
Language	English
Publishing date	2017-07-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2017.06.076
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Article ; Online: Regulation of a mammalian gene bearing a CpG island promoter and a distal enhancer.

Berrozpe, Georgina / Bryant, Gene O / Warpinski, Katherine / Ptashne, Mark

Cell reports

2013 Volume 4, Issue 3, Page(s) 445–453

Abstract: A quantitative nucleosome occupancy assay revealed rules for nucleosome disposition in yeast and showed how disposition affects regulation of the GAL genes. Here, we show how those findings apply to the control of Kit, a mammalian gene. The Kit promoter ... ...

Abstract	A quantitative nucleosome occupancy assay revealed rules for nucleosome disposition in yeast and showed how disposition affects regulation of the GAL genes. Here, we show how those findings apply to the control of Kit, a mammalian gene. The Kit promoter lies in a CpG island, and its enhancer (active in mast cells) lies some 150 kb upstream. Nucleosomes form with especially high avidities at the Kit promoter, a reaction that, we surmise, ensures extremely low basal expression. In mast cells, transcriptional activators displace nucleosomes that are less tightly formed at the Kit enhancer. In turn, the active enhancer replaces a single Kit promoter nucleosome with the transcriptional machinery, thereby inducing transcription over 1,000-fold. As at the yeast GAL genes, the inhibitory effects of nucleosomes facilitate high factors of induction by mammalian activators working in the absence of specific repressors.
MeSH term(s)	Alleles ; Animals ; Base Sequence ; CpG Islands ; DNA Methylation ; Mast Cells/physiology ; Mice ; Molecular Sequence Data ; Myogenin/genetics ; Nucleosomes/genetics ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-kit/biosynthesis ; Proto-Oncogene Proteins c-kit/genetics ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Yeasts/genetics
Chemical Substances	Myogenin ; Nucleosomes ; RNA, Messenger ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2013-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2013.07.001
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Article ; Online: Regulation of a Mammalian Gene Bearing a CpG Island Promoter and a Distal Enhancer

Georgina Berrozpe / Gene O. Bryant / Katherine Warpinski / Mark Ptashne

Cell Reports, Vol 4, Iss 3, Pp 445-

2013 Volume 453

Abstract	A quantitative nucleosome occupancy assay revealed rules for nucleosome disposition in yeast and showed how disposition affects regulation of the GAL genes. Here, we show how those findings apply to the control of Kit, a mammalian gene. The Kit promoter lies in a CpG island, and its enhancer (active in mast cells) lies some 150 kb upstream. Nucleosomes form with especially high avidities at the Kit promoter, a reaction that, we surmise, ensures extremely low basal expression. In mast cells, transcriptional activators displace nucleosomes that are less tightly formed at the Kit enhancer. In turn, the active enhancer replaces a single Kit promoter nucleosome with the transcriptional machinery, thereby inducing transcription over 1,000-fold. As at the yeast GAL genes, the inhibitory effects of nucleosomes facilitate high factors of induction by mammalian activators working in the absence of specific repressors.
Keywords	Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2013-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Polycomb Responds to Low Levels of Transcription

Georgina Berrozpe / Gene O. Bryant / Katherine Warpinski / Dan Spagna / Santosh Narayan / Shivangi Shah / Mark Ptashne

Cell Reports, Vol 20, Iss 4, Pp 785-

2017 Volume 793

Abstract	How is Polycomb (Pc), a eukaryotic negative regulator of transcription, targeted to specific mammalian genes? Our genome-wide analysis of the Pc mark H3K27me3 in murine cells revealed that Pc is preferentially associated with CpG island promoters of genes that are transcribed at a low level and less so with promoters of genes that are either silent or more highly expressed. Studies of the CpG island promoter of the Kit gene demonstrate that Pc is largely absent when the gene is silent in myeloid cells, as well as when the gene is highly expressed in mast cells. Manipulations that increase transcription in the former case, and reduce it in the latter, increase Pc occupancy. The average negative effect of Pc, we infer, is about 2-fold. We suggest possible biological roles for such negative effects and propose a mechanism by which Pc might be recruited to weakly transcribed genes.
Keywords	Polycomb ; Kit gene ; genome-wide ; transcription ; CpG island promoters ; CRISPR ; shRAD21 ; enhancers ; Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2017-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Direct engagement of the PI3K pathway by mutant KIT dominates oncogenic signaling in gastrointestinal stromal tumor.

Bosbach, Benedikt / Rossi, Ferdinand / Yozgat, Yasemin / Loo, Jennifer / Zhang, Jennifer Q / Berrozpe, Georgina / Warpinski, Katherine / Ehlers, Imke / Veach, Darren / Kwok, Andrew / Manova, Katia / Antonescu, Cristina R / DeMatteo, Ronald P / Besmer, Peter

Proceedings of the National Academy of Sciences of the United States of America

2017 Volume 114, Issue 40, Page(s) E8448–E8457

Abstract: Gastrointestinal stromal tumors (GISTs) predominantly harbor activating mutations in the receptor tyrosine kinase KIT. To genetically dissect in vivo the requirement of different signal transduction pathways emanating from KIT for tumorigenesis, the ... ...

Abstract	Gastrointestinal stromal tumors (GISTs) predominantly harbor activating mutations in the receptor tyrosine kinase KIT. To genetically dissect in vivo the requirement of different signal transduction pathways emanating from KIT for tumorigenesis, the oncogenic
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Drug Resistance, Neoplasm/genetics ; Female ; Gastrointestinal Neoplasms/genetics ; Gastrointestinal Neoplasms/metabolism ; Gastrointestinal Neoplasms/pathology ; Gastrointestinal Stromal Tumors/genetics ; Gastrointestinal Stromal Tumors/metabolism ; Gastrointestinal Stromal Tumors/pathology ; Humans ; Imatinib Mesylate/pharmacology ; Male ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Signal Transduction ; Tumor Cells, Cultured
Chemical Substances	Protein Kinase Inhibitors ; Imatinib Mesylate (8A1O1M485B) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2017--03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1711449114
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Article: A distant upstream locus control region is critical for expression of the Kit receptor gene in mast cells.

Berrozpe, Georgina / Agosti, Valter / Tucker, Christine / Blanpain, Cedric / Manova, Katia / Besmer, Peter

Molecular and cellular biology

2006 Volume 26, Issue 15, Page(s) 5850–5860

Abstract: The Kit receptor tyrosine kinase functions in hematopoiesis, melanogenesis, and gametogenesis and in interstitial cells of Cajal. We previously identified two upstream hypersensitive site (HS) clusters in mast cells and melanocytes. Here we investigated ... ...

Abstract	The Kit receptor tyrosine kinase functions in hematopoiesis, melanogenesis, and gametogenesis and in interstitial cells of Cajal. We previously identified two upstream hypersensitive site (HS) clusters in mast cells and melanocytes. Here we investigated the roles of these 5' HS sequences in Kit expression using transgenic mice carrying Kit-GFP reporter constructs. In these mice there is close correspondence between Kit-GFP reporter and endogenous Kit gene expression in most tissues analyzed. Deletion analysis defined the 5' upstream HS cluster region as critical for Kit expression in mast cells. Furthermore, chromatin immunoprecipitation analysis in mast cells showed that H3 and H4 histone hyperacetylation and RNA polymerase II recruitment within the Kit promoter and in the 5' HS region were associated with Kit expression. Therefore, the 5' upstream hypersensitivity sites appear to be critical components of locus control region-mediated Kit gene activation in mast cells.
MeSH term(s)	Animals ; Bone Marrow Cells/cytology ; Bone Marrow Cells/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Cerebellum/metabolism ; Chromatin/chemistry ; Chromatin/metabolism ; Female ; Gene Expression Regulation ; Genes, Reporter ; Histones/metabolism ; Locus Control Region ; Male ; Mast Cells/cytology ; Mast Cells/physiology ; Mice ; Mice, Transgenic ; Nucleic Acid Conformation ; Ovary/cytology ; Ovary/metabolism ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; RNA Polymerase II/metabolism ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; Testis/cytology ; Testis/metabolism ; Transcriptional Activation
Chemical Substances	Chromatin ; Histones ; Recombinant Fusion Proteins ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2006-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.01854-05
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Article ; Online: A RSC/nucleosome complex determines chromatin architecture and facilitates activator binding.

Floer, Monique / Wang, Xin / Prabhu, Vidya / Berrozpe, Georgina / Narayan, Santosh / Spagna, Dan / Alvarez, David / Kendall, Jude / Krasnitz, Alexander / Stepansky, Asya / Hicks, James / Bryant, Gene O / Ptashne, Mark

Cell

2010 Volume 141, Issue 3, Page(s) 407–418

Abstract: How is chromatin architecture established and what role does it play in transcription? We show that the yeast regulatory locus UASg bears, in addition to binding sites for the activator Gal4, sites bound by the RSC complex. RSC positions a nucleosome, ... ...

Abstract	How is chromatin architecture established and what role does it play in transcription? We show that the yeast regulatory locus UASg bears, in addition to binding sites for the activator Gal4, sites bound by the RSC complex. RSC positions a nucleosome, evidently partially unwound, in a structure that facilitates Gal4 binding to its sites. The complex comprises a barrier that imposes characteristic features of chromatin architecture. In the absence of RSC, ordinary nucleosomes encroach over the UASg and compete with Gal4 for binding. Taken with our previous work, the results show that both prior to and following induction, specific DNA-binding proteins are the predominant determinants of chromatin architecture at the GAL1/10 genes. RSC/nucleosome complexes are also found scattered around the yeast genome. Higher eukaryotic RSC lacks the specific DNA-binding determinants found on yeast RSC, and evidently Gal4 works in those organisms despite whatever obstacle broadly positioned nucleosomes present.
MeSH term(s)	Chromatin/metabolism ; DNA-Binding Proteins/metabolism ; Galactokinase/genetics ; HeLa Cells ; Humans ; Nucleosomes/metabolism ; Regulatory Elements, Transcriptional ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Trans-Activators/genetics ; Transcription Factors/metabolism
Chemical Substances	Chromatin ; DNA-Binding Proteins ; GAL10 protein, S cerevisiae ; Nucleosomes ; RSC complex, S cerevisiae ; Saccharomyces cerevisiae Proteins ; Trans-Activators ; Transcription Factors ; GAL1 protein, S cerevisiae (EC 2.7.1.6) ; Galactokinase (EC 2.7.1.6)
Language	English
Publishing date	2010-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2010.03.048
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Critical role for Kit-mediated Src kinase but not PI 3-kinase signaling in pro T and pro B cell development.

Agosti, Valter / Corbacioglu, Selim / Ehlers, Imke / Waskow, Claudia / Sommer, Gunhild / Berrozpe, Georgina / Kissel, Holger / Tucker, Christine M / Manova, Katia / Moore, Malcolm A S / Rodewald, Hans-Reimer / Besmer, Peter

The Journal of experimental medicine

2004 Volume 199, Issue 6, Page(s) 867–878

Abstract: The Kit receptor functions in hematopoiesis, lymphocyte development, gastrointestinal tract motility, melanogenesis, and gametogenesis. To investigate the roles of different Kit signaling pathways in vivo, we have generated knock-in mice in which docking ...

Abstract	The Kit receptor functions in hematopoiesis, lymphocyte development, gastrointestinal tract motility, melanogenesis, and gametogenesis. To investigate the roles of different Kit signaling pathways in vivo, we have generated knock-in mice in which docking sites for PI 3-kinase (KitY719) or Src kinase (KitY567) have been mutated. Whereas steady-state hematopoiesis is normal in KitY719F/Y719F and KitY567F/Y567F mice, lymphopoiesis is affected differentially. The KitY567F mutation, but not the KitY719F mutation, blocks pro T cell and pro B cell development in an age-dependent manner. Thus, the Src family kinase, but not the PI 3-kinase docking site in Kit, mediates a critical signal for lymphocyte development. In agreement with these results, treatment of normal mice with the Kit tyrosine kinase inhibitor imatinib (Gleevec) leads to deficits in pro T and pro B cell development, similar to those seen in KitY567F/Y567F and KitW/W mice. The two mutations do not affect embryonic gametogenesis but the KitY719F mutation blocks spermatogenesis at the spermatogonial stages and in contrast the KitY567F mutation does not affect this process. Therefore, Kit-mediated PI 3-kinase signaling and Src kinase family signaling is highly specific for different cellular contexts in vivo.
MeSH term(s)	Age Factors ; Animals ; B-Lymphocytes/drug effects ; B-Lymphocytes/physiology ; Benzamides ; Blotting, Western ; DNA Primers ; Flow Cytometry ; Histological Techniques ; Imatinib Mesylate ; Lymphopoiesis/drug effects ; Lymphopoiesis/genetics ; Male ; Mast Cells/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutagenesis, Insertional ; Mutagenesis, Site-Directed ; Mutation/genetics ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Piperazines/pharmacology ; Polymerase Chain Reaction ; Precipitin Tests ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Pyrimidines/pharmacology ; Signal Transduction/physiology ; Spermatogenesis/genetics ; T-Lymphocytes/drug effects ; T-Lymphocytes/physiology ; Testis/anatomy & histology ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
Chemical Substances	Benzamides ; DNA Primers ; Piperazines ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2004-03-15
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20031983
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