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Article: TLX1/HOX11-mediated disruption of primary thymocyte differentiation prior to the CD4+CD8+ double-positive stage.

Owens, Bronwyn M / Hawley, Teresa S / Spain, Lisa M / Kerkel, Kristi A / Hawley, Robert G

2006 Volume 132, Issue 2, Page(s) 216–229

Abstract: The TLX1/HOX11 homeobox gene is frequently activated in T-cell acute lymphoblastic leukaemia (T-ALL) by the t(10;14)(q24;q11) and t(7;10)(q35;q24) chromosomal translocations or by as yet unknown transcriptional mechanisms in the absence of 10q24 ... ...

Abstract	The TLX1/HOX11 homeobox gene is frequently activated in T-cell acute lymphoblastic leukaemia (T-ALL) by the t(10;14)(q24;q11) and t(7;10)(q35;q24) chromosomal translocations or by as yet unknown transcriptional mechanisms in the absence of 10q24 cytogenetic abnormalities. Almost all TLX1(+) T-ALLs exhibit a CD4(+)CD8(+) double-positive (DP) phenotype. To investigate the role of TLX1 as an initiating oncogene in T-ALL pathogenesis, we assessed the consequences of retroviral vector-directed TLX1 expression during the differentiation of murine and human thymocytes in fetal thymic organ cultures. Interestingly, enforced expression of TLX1 disrupted the differentiation of murine fetal liver precursors and human cord blood CD34(+) stem/progenitor cells prior to the DP thymocyte stage. Although differentiation arrest was associated with an increased percentage of apoptotic thymocytes, it could only be partially bypassed by coexpression of transgenic BCL2. Mutation of the invariant asparagine residue at position 51 of the homeodomain - which is required for efficient DNA binding - released the block, consistent with the notion that TLX1 inhibits thymocyte differentiation and promotes T-cell oncogenesis by functioning as a transcription factor. The relevance of these findings is discussed in the context of activating NOTCH1 mutations and the other genetic lesions implicated in the multistep transformation process of TLX1(+) T-ALL.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/immunology ; Genes, Homeobox ; Genes, bcl-2/immunology ; Genetic Vectors ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Immunophenotyping ; Leukemia-Lymphoma, Adult T-Cell/genetics ; Leukemia-Lymphoma, Adult T-Cell/immunology ; Mice ; Mice, Inbred BALB C ; Organ Culture Techniques ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Retroviridae/genetics ; Thymus Gland/immunology ; Transduction, Genetic
Chemical Substances	Homeodomain Proteins ; Proto-Oncogene Proteins ; TLX1 protein, human (143275-75-6)
Language	English
Publishing date	2006-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/j.1365-2141.2005.05850.x
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Article: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models

Genome biology. 2015 Dec., v. 16, no. 1

2015

Abstract: BACKGROUND: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood. RESULTS: Here, we profile CpG methylation in DS and control cerebral and ... ...

Abstract	BACKGROUND: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood. RESULTS: Here, we profile CpG methylation in DS and control cerebral and cerebellar cortex of adults and cerebrum of fetuses. We purify neuronal and non-neuronal nuclei and T lymphocytes and find biologically relevant genes with DS-specific methylation (DS-DM) in each of these cell types. Some genes show brain-specific DS-DM, while others show stronger DS-DM in T cells. Both 5-methyl-cytosine and 5-hydroxy-methyl-cytosine contribute to the DS-DM. Thirty percent of genes with DS-DM in adult brain cells also show DS-DM in fetal brains, indicating early onset of these epigenetic changes, and we find early maturation of methylation patterns in DS brain and lymphocytes. Some, but not all, of the DS-DM genes show differential expression. DS-DM preferentially affected CpGs in or near specific transcription factor binding sites (TFBSs), implicating a mechanism involving altered TFBS occupancy. Methyl-seq of brain DNA from mouse models with sub-chromosomal duplications mimicking DS reveals partial but significant overlaps with human DS-DM and shows that multiple chromosome 21 genes contribute to the downstream epigenetic effects. CONCLUSIONS: These data point to novel biological mechanisms in DS and have general implications for trans effects of chromosomal duplications and aneuploidies on epigenetic patterning.
Keywords	DNA ; DNA methylation ; Down syndrome ; T-lymphocytes ; adults ; animal models ; binding sites ; cerebral cortex ; chromosomes ; early development ; epigenetics ; fetus ; gene expression regulation ; genes ; humans ; immune response ; neurons ; transcription factors ; trisomics
Language	English
Dates of publication	2015-12
Size	p. 263.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-015-0827-6
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Article ; Online: Erratum to: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

Genome biology

2016 Volume 17, Issue 1, Page(s) 123

Language	English
Publishing date	2016-06-09
Publishing country	England
Document type	Published Erratum
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6914 ; 1465-6906
ISSN (online)	1474-760X ; 1465-6914
ISSN	1465-6906
DOI	10.1186/s13059-016-0949-5
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Article ; Online: Comparative anatomy of chromosomal domains with imprinted and non-imprinted allele-specific DNA methylation.

Paliwal, Anupam / Temkin, Alexis M / Kerkel, Kristi / Yale, Alexander / Yotova, Iveta / Drost, Natalia / Lax, Simon / Nhan-Chang, Chia-Ling / Powell, Charles / Borczuk, Alain / Aviv, Abraham / Wapner, Ronald / Chen, Xiaowei / Nagy, Peter L / Schork, Nicholas / Do, Catherine / Torkamani, Ali / Tycko, Benjamin

PLoS genetics

2013 Volume 9, Issue 8, Page(s) e1003622

Abstract: Allele-specific DNA methylation (ASM) is well studied in imprinted domains, but this type of epigenetic asymmetry is actually found more commonly at non-imprinted loci, where the ASM is dictated not by parent-of-origin but instead by the local haplotype. ...

Abstract	Allele-specific DNA methylation (ASM) is well studied in imprinted domains, but this type of epigenetic asymmetry is actually found more commonly at non-imprinted loci, where the ASM is dictated not by parent-of-origin but instead by the local haplotype. We identified loci with strong ASM in human tissues from methylation-sensitive SNP array data. Two index regions (bisulfite PCR amplicons), one between the C3orf27 and RPN1 genes in chromosome band 3q21 and the other near the VTRNA2-1 vault RNA in band 5q31, proved to be new examples of imprinted DMRs (maternal alleles methylated) while a third, between STEAP3 and C2orf76 in chromosome band 2q14, showed non-imprinted haplotype-dependent ASM. Using long-read bisulfite sequencing (bis-seq) in 8 human tissues we found that in all 3 domains the ASM is restricted to single differentially methylated regions (DMRs), each less than 2kb. The ASM in the C3orf27-RPN1 intergenic region was placenta-specific and associated with allele-specific expression of a long non-coding RNA. Strikingly, the discrete DMRs in all 3 regions overlap with binding sites for the insulator protein CTCF, which we found selectively bound to the unmethylated allele of the STEAP3-C2orf76 DMR. Methylation mapping in two additional genes with non-imprinted haplotype-dependent ASM, ELK3 and CYP2A7, showed that the CYP2A7 DMR also overlaps a CTCF site. Thus, two features of imprinted domains, highly localized DMRs and allele-specific insulator occupancy by CTCF, can also be found in chromosomal domains with non-imprinted ASM. Arguing for biological importance, our analysis of published whole genome bis-seq data from hES cells revealed multiple genome-wide association study (GWAS) peaks near CTCF binding sites with ASM.
MeSH term(s)	Alleles ; Aryl Hydrocarbon Hydroxylases/genetics ; Blood Proteins/genetics ; CCCTC-Binding Factor ; Chromosomes/genetics ; Cytochrome P450 Family 2 ; DNA Methylation/genetics ; Fetal Proteins/genetics ; Genome-Wide Association Study ; Genomic Imprinting ; Haplotypes ; Humans ; Oncogene Proteins/genetics ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-ets ; RNA, Long Noncoding/genetics ; Repressor Proteins/genetics ; Sensitivity and Specificity ; Transcription Factors/genetics
Chemical Substances	Blood Proteins ; CCCTC-Binding Factor ; CTCF protein, human ; Elk3 protein, human ; Fetal Proteins ; LINC01565 protein, human ; Oncogene Proteins ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-ets ; RNA, Long Noncoding ; Repressor Proteins ; Transcription Factors ; Aryl Hydrocarbon Hydroxylases (EC 1.14.14.1) ; CYP2A7 protein, human (EC 1.14.14.1) ; Cytochrome P450 Family 2 (EC 1.14.14.1)
Language	English
Publishing date	2013-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1003622
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Article ; Online: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

Genome biology

2015 Volume 16, Page(s) 263

Abstract: Background: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood.: Results: Here, we profile CpG methylation in DS and control cerebral and ... ...

Abstract	Background: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood. Results: Here, we profile CpG methylation in DS and control cerebral and cerebellar cortex of adults and cerebrum of fetuses. We purify neuronal and non-neuronal nuclei and T lymphocytes and find biologically relevant genes with DS-specific methylation (DS-DM) in each of these cell types. Some genes show brain-specific DS-DM, while others show stronger DS-DM in T cells. Both 5-methyl-cytosine and 5-hydroxy-methyl-cytosine contribute to the DS-DM. Thirty percent of genes with DS-DM in adult brain cells also show DS-DM in fetal brains, indicating early onset of these epigenetic changes, and we find early maturation of methylation patterns in DS brain and lymphocytes. Some, but not all, of the DS-DM genes show differential expression. DS-DM preferentially affected CpGs in or near specific transcription factor binding sites (TFBSs), implicating a mechanism involving altered TFBS occupancy. Methyl-seq of brain DNA from mouse models with sub-chromosomal duplications mimicking DS reveals partial but significant overlaps with human DS-DM and shows that multiple chromosome 21 genes contribute to the downstream epigenetic effects. Conclusions: These data point to novel biological mechanisms in DS and have general implications for trans effects of chromosomal duplications and aneuploidies on epigenetic patterning.
MeSH term(s)	Adult ; Aneuploidy ; Animals ; Brain/growth & development ; Brain/metabolism ; Brain/pathology ; Chromosomes, Human, Pair 21/genetics ; CpG Islands/genetics ; DNA Methylation/genetics ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/pathology ; Epigenesis, Genetic ; Fetus ; Humans ; Mice ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology
Language	English
Publishing date	2015-11-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-015-0827-6
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Article ; Online: Genomic surveys by methylation-sensitive SNP analysis identify sequence-dependent allele-specific DNA methylation.

Kerkel, Kristi / Spadola, Alexandra / Yuan, Eric / Kosek, Jolanta / Jiang, Le / Hod, Eldad / Li, Kerry / Murty, Vundavalli V / Schupf, Nicole / Vilain, Eric / Morris, Mitzi / Haghighi, Fatemeh / Tycko, Benjamin

Nature genetics

2008 Volume 40, Issue 7, Page(s) 904–908

Abstract: Allele-specific DNA methylation (ASM) is a hallmark of imprinted genes, but ASM in the larger nonimprinted fraction of the genome is less well characterized. Using methylation-sensitive SNP analysis (MSNP), we surveyed the human genome at 50K and 250K ... ...

Abstract	Allele-specific DNA methylation (ASM) is a hallmark of imprinted genes, but ASM in the larger nonimprinted fraction of the genome is less well characterized. Using methylation-sensitive SNP analysis (MSNP), we surveyed the human genome at 50K and 250K resolution, identifying ASM as recurrent genotype call conversions from heterozygosity to homozygosity when genomic DNAs were predigested with the methylation-sensitive restriction enzyme HpaII. Using independent assays, we confirmed ASM at 16 SNP-tagged loci distributed across various chromosomes. At 12 of these loci (75%), the ASM tracked strongly with the sequence of adjacent SNPs. Further analysis showed allele-specific mRNA expression at two loci from this methylation-based screen--the vanin and CYP2A6-CYP2A7 gene clusters--both implicated in traits of medical importance. This recurrent phenomenon of sequence-dependent ASM has practical implications for mapping and interpreting associations of noncoding SNPs and haplotypes with human phenotypes.
MeSH term(s)	Alleles ; Base Sequence ; Chromosome Mapping/methods ; Cluster Analysis ; DNA Methylation ; Female ; Humans ; Lymphocytes/metabolism ; Microarray Analysis ; Organ Specificity ; Placenta/metabolism ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA/methods
Language	English
Publishing date	2008-06-22
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/ng.174
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Zs.A 3613: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 46: Show issues

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Article ; Online: Altered DNA methylation in leukocytes with trisomy 21.

Kerkel, Kristi / Schupf, Nicole / Hatta, Kota / Pang, Deborah / Salas, Martha / Kratz, Alexander / Minden, Mark / Murty, Vundavalli / Zigman, Warren B / Mayeux, Richard P / Jenkins, Edmund C / Torkamani, Ali / Schork, Nicholas J / Silverman, Wayne / Croy, B Anne / Tycko, Benjamin

PLoS genetics

2010 Volume 6, Issue 11, Page(s) e1001212

Abstract: The primary abnormality in Down syndrome (DS), trisomy 21, is well known; but how this chromosomal gain produces the complex DS phenotype, including immune system defects, is not well understood. We profiled DNA methylation in total peripheral blood ... ...

Abstract	The primary abnormality in Down syndrome (DS), trisomy 21, is well known; but how this chromosomal gain produces the complex DS phenotype, including immune system defects, is not well understood. We profiled DNA methylation in total peripheral blood leukocytes (PBL) and T-lymphocytes from adults with DS and normal controls and found gene-specific abnormalities of CpG methylation in DS, with many of the differentially methylated genes having known or predicted roles in lymphocyte development and function. Validation of the microarray data by bisulfite sequencing and methylation-sensitive Pyrosequencing (MS-Pyroseq) confirmed strong differences in methylation (p<0.0001) for each of 8 genes tested: TMEM131, TCF7, CD3Z/CD247, SH3BP2, EIF4E, PLD6, SUMO3, and CPT1B, in DS versus control PBL. In addition, we validated differential methylation of NOD2/CARD15 by bisulfite sequencing in DS versus control T-cells. The differentially methylated genes were found on various autosomes, with no enrichment on chromosome 21. Differences in methylation were generally stable in a given individual, remained significant after adjusting for age, and were not due to altered cell counts. Some but not all of the differentially methylated genes showed different mean mRNA expression in DS versus control PBL; and the altered expression of 5 of these genes, TMEM131, TCF7, CD3Z, NOD2, and NPDC1, was recapitulated by exposing normal lymphocytes to the demethylating drug 5-aza-2'deoxycytidine (5aza-dC) plus mitogens. We conclude that altered gene-specific DNA methylation is a recurrent and functionally relevant downstream response to trisomy 21 in human cells.
MeSH term(s)	Adult ; Aging/genetics ; Azacitidine/pharmacology ; Child ; Child, Preschool ; DNA Methylation/drug effects ; DNA Methylation/genetics ; Down Syndrome/genetics ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Humans ; Infant ; Jurkat Cells ; Leukocyte Count ; Leukocytes/drug effects ; Leukocytes/metabolism ; Lymphocytes/drug effects ; Lymphocytes/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nod2 Signaling Adaptor Protein/genetics ; Nod2 Signaling Adaptor Protein/metabolism ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Reproducibility of Results ; Sequence Analysis, DNA ; Sulfites
Chemical Substances	NOD2 protein, human ; NPDC1 protein, human ; Nerve Tissue Proteins ; Nod2 Signaling Adaptor Protein ; RNA, Messenger ; Sulfites ; Azacitidine (M801H13NRU) ; hydrogen sulfite (OJ9787WBLU)
Language	English
Publishing date	2010-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1001212
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Article ; Online: TrkB receptor signaling regulates developmental death dynamics, but not final number, of retinal ganglion cells.

Pollock, Graeme S / Robichon, Regine / Boyd, Kristina A / Kerkel, Kristi A / Kramer, Melissa / Lyles, Johnalyn / Ambalavanar, Ranjini / Khan, Asema / Kaplan, David R / Williams, Robert W / Frost, Douglas O

The Journal of neuroscience : the official journal of the Society for Neuroscience

2003 Volume 23, Issue 31, Page(s) 10137–10145

Abstract: We investigated the effects of endogenous neurotrophin signaling on the death-survival of immature retinal ganglion cells (RGCs) in vivo. Null mutation of brain-derived neurotrophic factor [(BDNF) alone or in combination with neurotrophin 4 (NT4)] ... ...

Abstract	We investigated the effects of endogenous neurotrophin signaling on the death-survival of immature retinal ganglion cells (RGCs) in vivo. Null mutation of brain-derived neurotrophic factor [(BDNF) alone or in combination with neurotrophin 4 (NT4)] increases the peak rate of developmental RGC death as compared with normal. Null mutation of NT4 alone is ineffective. Null mutation of the full-length trkB (trkBFL) receptor catalytic domain produces a dose-dependent increase in the peak RGC death rate that is negatively correlated with retinal levels of trkBFL protein and phosphorylated (activated) trkBFL. Depletion of target-derived trkB ligands by injection of trkB-Fc fusion protein into the superior colliculus increases the peak rate of RGC death compared with trkA-Fc-treated and normal animals. Adult trkBFL+/- mice have a normal number of RGCs, despite an elevated peak death rate of immature RGCs. Thus, target-derived BDNF modulates the dynamics of developmental RGC death through trkBFL activation, but BDNF/trkB-independent mechanisms determine the final number of RGCs.
MeSH term(s)	Animals ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Count ; Cell Death/drug effects ; Cell Death/genetics ; Cell Survival/drug effects ; Cell Survival/genetics ; Cricetinae ; Immunoglobulin Fc Fragments/genetics ; Injections, Spinal ; Ligands ; Mesocricetus ; Mice ; Mice, Mutant Strains ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Receptor, trkB/genetics ; Receptor, trkB/metabolism ; Recombinant Fusion Proteins/administration & dosage ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; Retina/cytology ; Retina/growth & development ; Retina/metabolism ; Retinal Ganglion Cells/cytology ; Retinal Ganglion Cells/drug effects ; Retinal Ganglion Cells/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Superior Colliculi/drug effects
Chemical Substances	Brain-Derived Neurotrophic Factor ; Immunoglobulin Fc Fragments ; Ligands ; Nerve Growth Factors ; Recombinant Fusion Proteins ; Receptor, trkB (EC 2.7.10.1) ; neurotrophin 4 (P658DCA9XD)
Language	English
Publishing date	2003-10-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
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Article: TLX1/HOX11-mediated disruption of primary thymocyte differentiation prior to the CD4+CD8+ double-positive stage.

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Article: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models

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Article ; Online: Erratum to: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

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Article ; Online: Comparative anatomy of chromosomal domains with imprinted and non-imprinted allele-specific DNA methylation.

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Article ; Online: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

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Article ; Online: Genomic surveys by methylation-sensitive SNP analysis identify sequence-dependent allele-specific DNA methylation.

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Article ; Online: Altered DNA methylation in leukocytes with trisomy 21.

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Article ; Online: TrkB receptor signaling regulates developmental death dynamics, but not final number, of retinal ganglion cells.

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