CHANCE: comprehensive software for quality control and validation of ChIP-seq data

Diaz, Aaron A.; Nellore, Abhinav; Song, Jun S.

doi:10.1186/gb-2012-13-10-r98

Cited by 61 publications

(60 citation statements)

References 11 publications

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“…We confirmed the quality of the ChIP-seq data with CHANCE (Supplemental Fig. S9; Diaz et al 2012). In addition, we found that 51%-55% of GBM H3K4me3 peaks overlap with the ChromHMM promoter state in at least one of the nine ENCODE cell lines analyzed in Ernst et al (2011) (Supplemental Fig.…”

Section: Acquisition Of H3k4me3 In Primary Gbm At a Subset Of Recurresupporting

confidence: 54%

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Recurrent epimutations activate gene body promoters in primary glioblastoma

Nagarajan¹,

Zhang²,

Bell³

et al. 2014

Genome Res.

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Aberrant DNA hypomethylation may play an important role in the growth rate of glioblastoma (GBM), but the functional impact on transcription remains poorly understood. We assayed the GBM methylome with MeDIP-seq and MREseq, adjusting for copy number differences, in a small set of non-glioma CpG island methylator phenotype (non-G-CIMP) primary tumors. Recurrent hypomethylated loci were enriched within a region of chromosome 5p15 that is specified as a cancer amplicon and also encompasses TERT, encoding telomerase reverse transcriptase, which plays a critical role in tumorigenesis. Overall, 76 gene body promoters were recurrently hypomethylated, including TERT and the oncogenes GLI3 and TP73. Recurring hypomethylation also affected previously unannotated alternative promoters, and luciferase reporter assays for three of four of these promoters confirmed strong promoter activity in GBM cells. Histone H3 lysine 4 trimethylation (H3K4me3) ChIP-seq on tissue from the GBMs uncovered peaks that coincide precisely with tumor-specific decrease of DNA methylation at 200 loci, 133 of which are in gene bodies. Detailed investigation of TP73 and TERT gene body hypomethylation demonstrated increased expression of corresponding alternate transcripts, which in TP73 encodes a truncated p73 protein with oncogenic function and in TERT encodes a putative reverse transcriptase-null protein. Our findings suggest that recurring gene body promoter hypomethylation events, along with histone H3K4 trimethylation, alter the transcriptional landscape of GBM through the activation of a limited number of normally silenced promoters within gene bodies, in at least one case leading to expression of an oncogenic protein.[Supplemental material is available for this article.]

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Section: Acquisition Of H3k4me3 In Primary Gbm At a Subset Of Recurresupporting

confidence: 54%

“…The sequencing libraries were aligned as single-end samples to ensure equal mapping bias across the samples. ChIP enrichment was further verified using CHANCE (Diaz et al 2012). Peak calling was performed using MACS at a 1% false discovery rate and a P-value < 1 3 10 À10 ).…”

Section: Chromatin Immunoprecipitation-sequencing (Chip-seq)mentioning

confidence: 99%

Recurrent epimutations activate gene body promoters in primary glioblastoma

Nagarajan¹,

Zhang²,

Bell³

et al. 2014

Genome Res.

Self Cite

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“…Quality control of the Nano-ChIP-seq data was performed using two independent methods: ChIP enrichment at known promoters and employing the ChIP-seq quality control and validation tool ChIP-seq analytics and confidence estimation (CHANCE; ref. 41). Comparisons of Nano-ChIP-seq read densities at 1,000 promoters associated with highly expressed protein-coding genes confirmed successful enrichment in all H3K27ac and H3K4me3 libraries.…”

Section: Identifying Epigenomic Promoter Alterations In Gastric Cancermentioning

confidence: 71%

Epigenomic Promoter Alterations Amplify Gene Isoform and Immunogenic Diversity in Gastric Adenocarcinoma

et al. 2017

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Promoter elements play important roles in isoform and cell type-specific expression. We surveyed the epigenomic promoter landscape of gastric adenocarcinoma, analyzing 110 chromatin profiles (H3K4me3, H3K4me1, H3K27ac) of primary gastric cancers, gastric cancer lines, and nonmalignant gastric tissues. We identified nearly 2,000 promoter alterations (somatic promoters), many deregulated in various epithelial malignancies and mapping frequently to alternative promoters within the same gene, generating potential pro-oncogenic isoforms (RASA3). Somatic promoterassociated N-terminal peptides displaying relative depletion in tumors exhibited high-affinity MHC binding predictions and elicited potent T-cell responses in vitro, suggesting a mechanism for reducing tumor antigenicity. In multiple patient cohorts, gastric cancers with high somatic promoter usage also displayed reduced T-cell cytolytic marker expression. Somatic promoters are enriched in PRC2 occupancy, display sensitivity to EZH2 therapeutic inhibition, and are associated with novel cancer-associated transcripts. By generating tumor-specific isoforms and decreasing tumor antigenicity, epigenomic promoter alterations may thus drive intrinsic tumorigenesis and also allow nascent cancers to evade host immunity. SIGNIFICANCE:We apply epigenomic profiling to demarcate the promoter landscape of gastric cancer. Many tumor-specific promoters activate different promoters in the same gene, some generating pro-oncogenic isoforms. Tumor-specific promoters also reduce tumor antigenicity by causing relative depletion of immunogenic peptides, contributing to cancer immunoediting and allowing tumors to evade host immune attack. Cancer Discov; 7(6);

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“…Only tags that passed the quality filter and mapped uniquely to the genome were used. ChIP enrichment was further verified using CHANCE (58). The H3K4me3 mark peaks were identified using MACS 2.0.1 (59) with two biological replicate samples, including corresponding input, shift-size window 73 bp, no model, with P -value threshold <10E−5.…”

Section: Methodsmentioning

confidence: 99%

Exposure to the widely used herbicide atrazine results in deregulation of global tissue-specific RNA transcription in the third generation and is associated with a global decrease of histone trimethylation in mice

et al. 2016

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The epigenetic events imposed during germline reprogramming and affected by harmful exposure can be inherited and transferred to subsequent generations via gametes inheritance. In this study, we examine the transgenerational effects promoted by widely used herbicide atrazine (ATZ). We exposed pregnant outbred CD1 female mice and the male progeny was crossed for three generations with untreated females. We demonstrate here that exposure to ATZ affects meiosis, spermiogenesis and reduces the spermatozoa number in the third generation (F3) male mice. We suggest that changes in testis cell types originate from modified transcriptional network in undifferentiated spermatogonia. Importantly, exposure to ATZ dramatically increases the number of transcripts with novel transcription initiation sites, spliced variants and alternative polyadenylation sites. We found the global decrease in H3K4me3 occupancy in the third generation males. The regions with altered H3K4me3 occupancy in F3 ATZ-derived males correspond to altered H3K4me3 occupancy of F1 generation and 74% of changed peaks in F3 generation are associated with enhancers. The regions with altered H3K4me3 occupancy are enriched in SP family and WT1 transcription factor binding sites. Our data suggest that the embryonic exposure to ATZ affects the development and the changes induced by ATZ are transferred up to three generations.

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CHANCE: comprehensive software for quality control and validation of ChIP-seq data

Cited by 61 publications

References 11 publications

Recurrent epimutations activate gene body promoters in primary glioblastoma

Recurrent epimutations activate gene body promoters in primary glioblastoma

Epigenomic Promoter Alterations Amplify Gene Isoform and Immunogenic Diversity in Gastric Adenocarcinoma

Exposure to the widely used herbicide atrazine results in deregulation of global tissue-specific RNA transcription in the third generation and is associated with a global decrease of histone trimethylation in mice

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