Expression Profiling on Human Cell Lines with Different Acetylation Levels
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE49640 | GEO | 2014/08/06
SECONDARY ACCESSION(S): PRJNA214579
REPOSITORIES: GEO
Similar Datasets
Project description:Expression Profiling on Human Cell Lines with Different Acetylation Levels Expression profiling of human cell lines with different acetylation levels.
2014-08-06 | E-GEOD-49640 | biostudies-arrayexpress
Project description:PLZF acetylation levels regulate NKT cell differentiation
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Project description:PLZF acetylation levels regulate NKT cell diffrentiation
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Project description:The transcription factor PLZF (promyelocytic leukemia zinc finger) is encoded by the BTB domain-containing 16 (Zbtb16) gene. Its repressor function regulates specific transcriptional programs. During the development of invariant natural killer T (NKT) cells, PLZF is expressed and directs their effector program but the detailed mechanisms underlying PLZF regulation of multi-stage NKT cell developmental program are not well understood. This study investigated the role of acetylation-induced PLZF activation on NKT cell development by analyzing mice expressing a mutant form of PLZF mimicking constitutive acetylation (PLZFON mice). NKT populations in PLZFON mice were reduced in proportion and numbers of cells, and the cells present were blocked at the transition from developmental stage 1 to stage 2. NKT cell subset differentiation was also altered, with T-bet+ NKT1 and RORt+ NKT17 subsets dramatically reduced, and the emergence of a T-bet-RORt- NKT cell subset with features of cells in early developmental stages rather than mature NKT2 cells. Preliminary analysis of DNA methylation patterns suggested that activated PLZF acts on the DNA methylation signature to regulate NKT cells’ entry into the early stages of development, while repressing maturation. In wild-type NKT cells, deacetylation of PLZF is possible, allowing subsequent NKT cell differentiation. Interestingly, development of other innate lymphoid and myeloid cells, that are dependent on PLZF for their generation, is not altered in PLZFON mice highlighting lineage specific regulation. Overall, we propose that specific epigenetic control of PLZF through acetylation levels is required to regulate normal NKT cell differentiation. Key points: Constitutive acetylation of PLZF (PLZFON) blocks NKT cell development. PLZFON might act on the DNA methylation signature to control gene expression. PLZF acetylation levels regulate normal NKT cell differentiation.
2021-05-24 | GSE128558 | GEO
Project description:The N6-methyadenosine (m6A) levels in PC9 cell lines.
| PRJNA694641 | ENA
Project description:Comparison of aneuploidy levels in OVCAR8 cancer cell lines
| PRJEB70866 | ENA
Project description:Identification of genes and functions regulated by DDIT3/GADD153/CHOP by transcriptional profiling of cell lines expressing high levels of tamoxifen induced DDIT3.
2010-09-01 | E-MEXP-2709 | biostudies-arrayexpress
Project description:H2A.Z is a conserved histone variant that plays essential roles in various DNA-templated processes across eukaryotes. H2A.Z and histone post-translational modifications (PTMs) exert a bidirectional and context-dependent influence on each other. Nevertheless, the functions of the interplay between PTMs and H2A.Z level and the underlying molecular mechanism remain poorly understood. Here, we found that the loss of the histone acetyltransferase GCN5 impedes the overexpression of BSU1 typically observed in nrp1-1 nrp2-2, accompanied by changes in H3 acetylation and H2A.Z levels. Interestingly, the increment in H2A.Z levels typical of nrp1-1 nrp2-2 mutant alleviates the morphological and molecular phenotypes of gcn5. Conversely, H2A.Z-depleted mutants aggravate the phenotype of gcn5. In the gcn5 mutant, the H2A.Z level is globally reduced in the gene bodies, and this reduction is dependent on the histone chaperones NRP1 and NRP2. Additionally, the reduction of H3 acetylation levels caused by GCN5 depletion can be recovered in the nrp1-1 nrp2-2 mutant background, likely due to the over-accumulation of H2A.Z. In conclusion, our genetic, molecular, and genomic findings demonstrate that GCN5-mediated H3 acetylation promotes H2A.Z deposition, H2A.Z over-accumulation recovers the loss of GCN5-mediated H3 acetylation, and this interplay is crucial for regulating gene expression and plant development.
2025-05-20 | GSE297261 | GEO
Project description:Expression Profiling on Human Cell Lines with Different Acetylation Levels
| PRJNA214579 | ENA
Project description:The transcription factor PLZF (promyelocytic leukemia zinc finger) is encoded by the BTB 42 domain-containing 16 (Zbtb16) gene. Its repressor function regulates specific transcriptional 43 programs. During the development of invariant natural killer T (NKT) cells, PLZF is 44 expressed and directs their effector program but the detailed mechanisms underlying PLZF 45 regulation of multi-stage NKT cell developmental program are not well understood. This 46 study investigated the role of acetylation-induced PLZF activation on NKT cell development 47 by analyzing mice expressing a mutant form of PLZF mimicking constitutive acetylation (PLZFON mice). NKT populations in PLZFON 48 mice were reduced in proportion and numbers 49 of cells, and the cells present were blocked at the transition from developmental stage 1 to stage 2. NKT cell subset differentiation was also altered, with T-bet+ NKT1 and RORJt + 50 NKT17 subsets dramatically reduced, and the emergence of a T-bet - RORJt - 51 NKT cell subset 52 with features of cells in early developmental stages rather than mature NKT2 cells. Analysis 53 of DNA methylation patterns indicated that activated PLZF establishes a unique DNA 54 methylation signature to regulate NKT cells’ entry into the early stages of development, while 55 repressing maturation. In wild-type NKT cells, deacetylation of PLZF alleviates this 56 repression and allows subsequent NKT cell differentiation. Interestingly, development of 57 other innate lymphoid and myeloid cells, that are dependent on PLZF for their generation, is not altered in PLZFON 58 mice highlighting lineage specific regulation. Overall, we propose that 59 specific epigenetic control of PLZF through acetylation levels is required to regulate normal 60 NKT cell differentiation.
2021-04-21 | GSE171984 | GEO