Genome-wide survey of transcriptional differences between males and females of Tribolium castaneum, the red flour beetle
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ABSTRACT: Genome-wide survey of transcriptional differences between males and females of Tribolium castaneum, the red flour beetle Four biological replicates for male and female beetles with 20 individuals per replicate. Two technical replicates, one replicate per sex. 16,434 genes/expressed non-coding regions represented twice on each array. Three 60 mer probes for most exons/expressed non-coding regions. 167,538 unique genomic probes replicated twice per array.
Project description:Mutant p53 (mtp53) promotes chemotherapy resistance through multiple mechanisms including disabling pro-apoptotic proteins and by regulating gene expression. Analysis of promoter regions identified through CHIP-on-CHIP and CHIP-SEQ platforms reveal that the ETS motif (EBS) is prevalent within predicted mtp53 binding sites. We demonstrate that mtp53 regulates gene expression through EBS in promoters, and that ETS2 mediates the interaction with this motif. Importantly, we identified TDP2, a 5’-tyrosyl DNA phosphodiesterase involved in the repair of DNA damage caused by etoposide, as a transcriptional target of mtp53. We demonstrate that suppression of TDP2 sensitizes mtp53 expressing cells to etoposide, and that mtp53 and TDP2 are frequently overexpressed in human lung cancer; thus, our analysis identifies a potentially “druggable” component of mtp53’s gain-of-function activity. Comparison of two different transcriptional binding analysis (ChIP-on-ChIP and ChIP-Seq) for the identification of novel mutant p53 (R248W) binding.
Project description:In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics, C. elegans ChIP-chip with DPY-27
Project description:Pregnant rats were randomly divided into two groups. Dams were then housed individually and fed throughout gestation a 22 % protein diet, representing the control group (C, n=5), or an 9% isocaloric protein diet, representing the low-protein (LP, n=6). Both diets were isocaloric, because the protein deficiency in the LP diet was compensated by the addition of carbohydrates. Feeding of LP diet began on the day of conception and continuing throughout pregnancy. The low-protien diet resulted in Intra-Uterine Growth Restriction (IUGR) of the fetuses.<br><br> An additional processed data file, E-MEXP-1015_all_norm_calls.txt, is available for download from <a href="ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/MEXP/E-MEXP-1015/">ftp://ftp.ebi.ac.uk/pub/databases/microarray/data/experiment/MEXP/E-MEXP-1015/</a>
Project description:The tomato (Solanum lycopersicum) MADS-box transcription factor RIN, one of the earliest-acting fruit-ripening regulators, is required for both ethylene-dependent and -independent regulatory pathways for fruit ripeing. Here, we performed chromatin immunoprecipitation coupled with a DNA microarray (ChIP-chip) for the putative promoters of whole tomato predicted genes (ITAG2) for the genome-wide identification of the direct RIN targets. The ChIP-chip with anti-RIN antibody resulted in detection of 1,046 RIN-binding sites, each of which was assigned a significantly high peak score (FDRM-bM-^IM-$0.05) in at least two of the three biologically independent analyses. Using the information about genomic position of the RIN-binding sites, we found 1,200 genes as potential direct RIN targets that carried one or more RIN-binding sites in the transcription regulatory region (2-kb upstream putative promoter) or in other gene regions, such as exons, introns or a downstream region from the translation termination site (1-kb), where the promoter region of a neighbor gene are overlapped. Three biologically independent samples (chromatin-immunoprecipitated DNA and input DNA) recovered from the ripening tomato fruits.
Project description:In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics, C. elegans ChIP-chip experiments included: biological duplicates of SDC-3, a single DPY-27 IP, and a mock IP.
Project description:In many species, a dosage compensation complex (DCC) is targeted to X chromosomes of one sex to equalize levels of X gene products between males (1X) and females (2X). Here we identify cis-acting regulatory elements that target the C. elegans X chromosome for repression by the DCC. The DCC binds to discrete, dispersed sites on X of two types. rex sites recruit the DCC in an autonomous, DNA sequence-dependent manner using a 12 bp consensus motif that is enriched on X. This motif is critical for DCC binding, is clustered in rex sites, and confers much of X-chromosome specificity. Motif variants enriched on X by 3.8-fold or more are highly predictive (95%) for rex sites. In contrast, dox sites lack the X-enriched variants and cannot bind the DCC when detached from X. dox sites are more prevalent than rex sites and, unlike rex sites, reside preferentially in promoters of some expressed genes. These findings fulfill predictions for a targeting model in which the DCC binds to recruitment sites on X and disperses to discrete sites lacking autonomous recruitment ability. To relate DCC binding to function, we identified dosage-compensated and non-compensated genes on X. Unexpectedly, many genes of both types have bound DCC, but many do not, suggesting the DCC acts over long distances to repress X gene expression. Remarkably, the DCC binds to autosomes, but at far fewer sites and rarely at consensus motifs. DCC disruption causes opposite effects on expression of X and autosomal genes. The DCC thus acts at a distance to impact expression throughout the genome. Keywords: dosage compensation, condensin, X chromosome, gene expression, epigenetics, C. elegans ChIP-chip experiments included: biological duplicates of SDC-3 and MIX-1 IPs, a single DPY-27 IP, and 3 mock IPs.
Project description:This SuperSeries is composed of the following subset Series: GSE36749: Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-Seq] GSE36751: Mutant p53 cooperates with ETS2 to promote etoposide resistance [ChIP-chip] Refer to individual Series
Project description:MCL1 is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared to germinal center B-cell-like (GCB) DLBCL patient samples (p=2.7 x 10(-10)) [PMID 23257783]. Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; p=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization (aCGH) data of 203 DLBCL samples [GSE11318] and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1 positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs. This GEO dataset is comprised of aCGH measurements for DLBCL cell lines, which are used in the above-mentioned paper. Cell lines were measured against the DNA of a healthy male donor who in turn was measured against a pool of healthy DNAs to correct for individual CNVs of the donor.
Project description:Tomato (Solanum lycopersicum) has two MADS-box FRUITFULL homologs, FUL1 and FUL2, both of which are able to interact with the master ripening regulator RIN. Here, we performed chromatin immunoprecipitation coupled with a DNA microarray (ChIP-chip) for the 2-kb upstream putative promoters of whole tomato predicted genes (ITAG2) for a large-scale identification of the direct target genes of FUL1 and FUL2 during ripening. The ChIP-chip with antibodies of FUL1 and FUL2 identified 1,877 and 1,919 of FUL1- and FUL2-binding sites, respectively, each of which was assigned a significantly high peak score (FDR<0.05) in at least two of the three biologically independent analyses. Using the information about genomic position of the FUL1- and FUL2-binding sites, we found 1,943 and 2,051 potential direct targets of FUL1 and FUL2, respectively, that carried one or more binding sites in the putative promoter or in other gene regions, such as exons, introns or a downstream region from the translation termination site (1-kb), where the promoter region of a neighbor gene are overlapped. The majority of the direct target genes are common between FUL1, FUL2 and RIN, suggesting that FUL1 and FUL2 act redundantly in the regulation of fruit ripening, and that these factors regulate the expression of their targets in a form of heteromer complex. Interestingly, the analysis also found direct targets unique to each of FUL1, FUL2 and RIN, implying their exclusive roles during ripening. Three biologically independent samples (chromatin-immunoprecipitated DNA and input DNA) recovered from the ripening tomato fruits.
Project description:LNCaP cells were grown in charcoal stripped media for 48hrs and then treated for 1hr with the synthetic androgen R1881 or ethanol (vehicle). Cell extracts from both treatment conditions were then subjected to chromatin-immunoprecipitation using an anti-androgen receptor antibody, before labeling and hybridisation to a microarray containing 24,000 gene promoter regions.