ChIP-seq study of inheritence of Myc in Drosophila
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE39521 | GEO | 2013/01/21
SECONDARY ACCESSION(S): PRJNA171026
REPOSITORIES: GEO
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Project description:Myc is an important oncogene. It is considered as a transcription factor, but the function of Myc in normal or cancer cells have not been fully understood. In addition, Myc plays a role in cell proliferation and differentiation. It is also important for cell identity and stay on chromatin throughout the cell cycle. However, the inheritance of Myc is still a mystery. Here we study the function and inheritance of Myc in D. melanogaster by mapping the binding sites of Myc during interphase and mitosis using ChIP-seq. DNA sample of ChIP for Myc are collected from Kc cells in interphase or mitosis. Input sequences from previous study in the same cell type (GSM762848, GSM762849) are used as control.
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Project description:During mitosis, TATA-binding protein(TBP), which remains bound to DNA during mitosis, recruits PP2A and also interacts with a subunit of the condensin complex to allow efficient dephosphorylation and inactivation of condensin near these promoters to inhibit their compaction. These result suggest that TBP function is not only important for expression of genes transcribed bDuring mitosis, TATA-binding protein(TBP), which remains bound to DNA during mitosis, recruits PP2A and also interacts with a subunit of the condensin complex to allow efficient dephosphorylation and inactivation of condensin near these promoters to inhibit their compaction. These result suggest that TBP function is not only important for expression of genes transcribed by all three RNA polymerase during interphase, but also for transmitting the memory of gene activity through mitosis to daughter cellsy all three RNA polymerase during interphase, but also for transmitting the memory of gene activity through mitosis to daughter cells We use ChIP-chip approach to identify TBP-bindind sites in mitotic Jurkat cells at genome-wide level. Input DNA fragments and DNA fragments immunoprecipitated by TBP antibodies by ChIP assay on mitotic Jurkat cells were used to probe the Affymetrix Genechip human tiling 2.0c to identift TBP-binding sites in mitotic Jurkat cells. Input and ChIP sample were replicated three times as following: Input rep1, TBP ChIP1, Input rep2, TBP ChIP2, Input rep3, TBP ChIP3.
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2013-01-21 | E-GEOD-32584 | biostudies-arrayexpress
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Project description:Background: During mitosis the cell depends on proper attachment and segregation of replicated chromosomes to generate two identical progeny. In cancers defined by overexpression or dysregulation of the MYC oncogene this process becomes impaired, leading to genomic instability and tumor evolution. Recently it was discovered that the chromatin regulator WDR5—a critical MYC cofactor—regulates expression of genes needed in mitosis through a direct interaction with the master kinase PDPK1. However, whether PDPK1 and WDR5 contribute to similar mitotic gene regulation in MYC-overexpressing cancers remains unclear. Therefore, to characterize the influence of WDR5 and PDPK1 on mitotic gene expression in cells with high MYC levels, we performed a comparative transcriptomic analysis in neuroblastoma cell lines defined by MYCN-amplification, which results in high cellular levels of the N-MYC protein. Results: Using RNA-seq analysis, we identify the genes regulated by N-MYC and PDPK1 in multiple engineered CHP-134 neuroblastoma cell lines and compare them to previously published gene expression data collected in CHP-134 cells following inhibition of WDR5. We find that as expected N-MYC regulates a multitude of genes, including those related to mitosis, but that PDPK1 regulates specific sets of genes involved in development, signaling, and mitosis. Analysis of N-MYC- and PDPK1-regulated genes reveals a small group of commonly controlled genes associated with spindle pole formation and chromosome segregation, which overlap with genes that are also regulated by WDR5. We also find that N-MYC physically interacts with PDPK1 through the WDR5-PDPK1 interaction suggesting regulation of mitotic gene expression may be achieved through a N-MYC-WDR5-PDPK1 nexus. Conclusions: Overall, we identify a small group of genes highly enriched within functional gene categories related to mitotic processes that are commonly regulated by N-MYC, WDR5, and PDPK1 and suggest that a tripartite interaction between the three regulators may be responsible for setting the level of mitotic gene regulation in N-MYC amplified cell lines. This study provides a foundation for future studies to determine the exact mechanism by which N-MYC, WDR5, and PDPK1 converge on cell cycle related processes.
2024-03-29 | GSE244899 | GEO
Project description:Background: During mitosis the cell depends on proper attachment and segregation of replicated chromosomes to generate two identical progeny. In cancers defined by overexpression or dysregulation of the MYC oncogene this process becomes impaired, leading to genomic instability and tumor evolution. Recently it was discovered that the chromatin regulator WDR5—a critical MYC cofactor—regulates expression of genes needed in mitosis through a direct interaction with the master kinase PDPK1. However, whether PDPK1 and WDR5 contribute to similar mitotic gene regulation in MYC-overexpressing cancers remains unclear. Therefore, to characterize the influence of WDR5 and PDPK1 on mitotic gene expression in cells with high MYC levels, we performed a comparative transcriptomic analysis in neuroblastoma cell lines defined by MYCN-amplification, which results in high cellular levels of the N-MYC protein. Results: Using RNA-seq analysis, we identify the genes regulated by N-MYC and PDPK1 in multiple engineered CHP-134 neuroblastoma cell lines and compare them to previously published gene expression data collected in CHP-134 cells following inhibition of WDR5. We find that as expected N-MYC regulates a multitude of genes, including those related to mitosis, but that PDPK1 regulates specific sets of genes involved in development, signaling, and mitosis. Analysis of N-MYC- and PDPK1-regulated genes reveals a small group of commonly controlled genes associated with spindle pole formation and chromosome segregation, which overlap with genes that are also regulated by WDR5. We also find that N-MYC physically interacts with PDPK1 through the WDR5-PDPK1 interaction suggesting regulation of mitotic gene expression may be achieved through a N-MYC-WDR5-PDPK1 nexus. Conclusions: Overall, we identify a small group of genes highly enriched within functional gene categories related to mitotic processes that are commonly regulated by N-MYC, WDR5, and PDPK1 and suggest that a tripartite interaction between the three regulators may be responsible for setting the level of mitotic gene regulation in N-MYC amplified cell lines. This study provides a foundation for future studies to determine the exact mechanism by which N-MYC, WDR5, and PDPK1 converge on cell cycle related processes.
2024-03-29 | GSE244835 | GEO
Project description:The genome is thought to be transcriptionally silent during mitosis. Technical limitations have prevented the sensitive mapping of mitotic transcription and transcription reactivation during mitotic exit, and thus the networks by which transcriptome dynamics govern the generation of daughter cells have been unclear. We used 5-ethynyluridine to pulse-label intact transcripts during mitosis and mitotic exit and find that the first round of transcription activates genes that are involved in macromolecular synthesis, rather than cell identity. Many interphase genes exhibit residual transcription in mitosis, as confirmed by different methods of assessment, and a subset of genes are more highly transcribed in mitosis than in interphase. We suggest that mitotic transcription may serve an epigenetic function in restoring proper transcription patterns during mitotic exit.
2017-09-20 | GSE87476 | GEO