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Cross-species meta-analysis of regulatory networks of the Pax5 transcription factor

ABSTRACT: Transcription profiling of chicken Pax5 deficient DT40 B cell line to investigate the targets of Pax5 which is required for B-cell differentiation Used in cross-species comparison to investigate evolutionarily conserved regulatory circuits in B cell development Pax5 deficient DT40 B cells (3 biological replicates) were compared to DT40 wild-type cells (3 biological replicates).

ORGANISM(S): Gallus gallus

SUBMITTER: Pekka Kohonen

PROVIDER: E-GEOD-34687 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of chicken Pax5 deficient DT40 B cell line

Project description:PAx5 is indispensible for the committment if early lymphoid progenitors to the B cell lineage as well as for the development and maintenance of B cells. To better understand the functional importance of Pax5 in the later stages of B cell development and investigate the targets of Pax5 regulation, we established a novel Pax5 deficient DT40 B cell line.

2005-04-17 | E-MEXP-270 | biostudies-arrayexpress

Transcription profiling of chicken Bcl6 deficient DT40 B cell line to investigate the targets of Bcl6 which is required for germinal center formation

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2010-02-17 | E-MEXP-2062 | biostudies-arrayexpress

Transcription profiling by array of chicken wild type and tumor supressor 53Bp1 knockout lymphoblast cells

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2008-11-04 | E-GEOD-8483 | biostudies-arrayexpress

RNA-seq of H3.3 knockout and wild type chicken DT40 cells

Project description:RNA-seq was performed for transcriptional analysis of wild-type DT40 cells (Gallus gallus, B-cell line) and a H3.3 knockout line (h3.3a-/-, h3.3b-/-). H3.3 is a H3 histone variant encoded on two genes (H3.3A and H3.3B) in chickens.

2014-08-31 | E-MTAB-2754 | biostudies-arrayexpress

Condensin plays a role in both interphase nuclei and premature chromosome condensation

Project description:Purpose: to identify how condensin I removal affects gene expression globally. Methods: Chicken DT40 CAP-H KO cells were treated with or without dox for 36 h. Total RNA samples were extracted and subjected to sequencing using an Illumina Hiseq2000 platform. Library preparation and Illumina sequencing were performed by Macrogen (South Korea). The sequence tags were spliced-mapped onto the chicken genome galGal4 using Tophat and Bowtie2 following quality test using FASTQC. Differential expression of genes was analyzed using the Bioconductor v2.3 package edgeR v3.2.3. Tag enrichment in NCBI RefSeq genes was calculated between dox-treated and untreated cells using edgeR exact test with tag-wise dispersion estimation. Results: We identified a total of 3798 genes to be differentially expressed in G1 condensin I-depleted chicken DT40 cells: 2495 down regulated and 1303 up regulated. Conclusions: Removal of CAP-H leads to significant misregulation of gene expression, suggesting a key role for condensin I in transcription during interphase. Total RNA profiles of CAP-H KO cells with or without Dox were generated by sequencing using Illumina Hiseq2000 platform.

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Expression profiling of DT40 chicken B cell line by RNA-seq

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2015-09-04 | E-GEOD-58766 | biostudies-arrayexpress

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Project description:In lymphomas derived from mature B cells the expression of the transcription factor PAX5 is maintained whereas classical Hodgkin lymphoma displays significantly reduced PAX5 expression despite its derivation from mature B cells. To elucidate the functional role of PAX5 in classical Hodgkin lymphoma, we re-established the PAX5 expression in the Hodgkin cell line L428 with and without epigenetic modulation. To this end, we stably transfected the Hodgkin cell line L428 with an inducible PAX5 expression construct. Although the overexpressed PAX5 was transcriptionally active as demonstrated by synthetic reporter constructs, no induction of the B-cell phenotype was achieved. PAX5 chromatin immunoprecipitation with subsequent next generation sequencing in B-cell lines and the PAX5 overexpressing L428 cell line showed different binding patterns. Since epigenetic restrictions might affect PAX5 binding, combined DNA demethylation and histone acetylation was performed. However, no re-expression of B-cell genes was observed also under these conditions. Thus, PAX5 is not sufficient for the re-activation of the B-cell program in Hodgkin cells despite epigenetic opening of the chromatin. This clearly indicates that the repression of the B-cell identity of the Hodgkin cells is caused and secured by complex molecular mechanisms. Analysis of genome-wide PAX5 binding sites in B-cell lines (Raji, Namalwa) and the PAX5-producing Hodgkin cell line L428-PAX5 by ChIP-Seq

2013-07-30 | E-GEOD-44551 | biostudies-arrayexpress

Profile of gene expression signatures on DT40 cell for bursal-derived peptides

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2011-07-06 | E-GEOD-30396 | biostudies-arrayexpress

PAX5 overexpression is not enough to reestablish the mature B-cell phenotype in classical Hodgkin lymphoma

Project description:In lymphomas derived from mature B cells the expression of the transcription factor PAX5 is maintained whereas classical Hodgkin lymphoma displays significantly reduced PAX5 expression despite its derivation from mature B cells. To elucidate the functional role of PAX5 in classical Hodgkin lymphoma, we re-established the PAX5 expression in the Hodgkin cell line L428 with and without epigenetic modulation. To this end, we stably transfected the Hodgkin cell line L428 with an inducible PAX5 expression construct. Although the overexpressed PAX5 was transcriptionally active as demonstrated by synthetic reporter constructs, no induction of the B-cell phenotype was achieved. PAX5 chromatin immunoprecipitation with subsequent next generation sequencing in B-cell lines and the PAX5 overexpressing L428 cell line showed different binding patterns. Since epigenetic restrictions might affect PAX5 binding, combined DNA demethylation and histone acetylation was performed. However, no re-expression of B-cell genes was observed also under these conditions. Thus, PAX5 is not sufficient for the re-activation of the B-cell program in Hodgkin cells despite epigenetic opening of the chromatin. This clearly indicates that the repression of the B-cell identity of the Hodgkin cells is caused and secured by complex molecular mechanisms. 2 Burkitt lymphoma cell lines (Raji, Namalwa), the Hodgkin lymphoma cell line L428 and the PAX5-producing L428 (L428-PAX5) with or without 5-aza-2M-bM-^@M-2-deoxycytidine/Trichostatin A treatment were analysed in triplicate.

2013-07-30 | E-GEOD-44244 | biostudies-arrayexpress

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