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Gene expression of fly testes with dMi-2, kumgang (CG5204) knock downs and wild-type heads by RNA-Seq

ABSTRACT: The effect of different spermatocyte-specific loss of functions; kumgang (kmg or CG5204), dMi-2 in the gene expression in fly testes was assessed by RNA-Seq. Gene expression in wild-type heads were also measured to have a reference expression profile of 'somatic tissues'. / Title: Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression / Abstract: To selectively express cell type–specific transcripts during development, it is critical to maintain genes required for other lineages in a silent state. Here, we show in the Drosophila male germline stem cell lineage that a spermatocyte-specific zinc finger protein, Kumgang (Kmg), working with the chromatin remodeler dMi-2 prevents transcription of genes normally expressed only in somatic lineages. By blocking transcription from normally cryptic promoters, Kmg restricts activation by Aly, a component of the testis-meiotic arrest complex, to transcripts for male germ cell differentiation. Our results suggest that as new regions of the genome become open for transcription during terminal differentiation, blocking the action of a promiscuous activator on cryptic promoters is a critical mechanism for specifying precise gene activation.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE89380 | GEO | 2017/05/18

SECONDARY ACCESSION(S): PRJNA352407

REPOSITORIES: GEO

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Gene expression of fly testes with dMi-2, kumgang (CG5204) knock downs

Project description:The effect of different loss of functions; kumgang (kmg or CG5204), dMi-2, and kmg and always early (aly) double on the gene expression in spermatocyte differentation was assessed by microarray. TITLE: Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression ABSTRACT: To selectively express cell type–specific transcripts during development, it is critical to maintain genes required for other lineages in a silent state. Here, we show in the Drosophila male germline stem cell lineage that a spermatocyte-specific zinc finger protein, Kumgang (Kmg), working with the chromatin remodeler dMi-2 prevents transcription of genes normally expressed only in somatic lineages. By blocking transcription from normally cryptic promoters, Kmg restricts activation by Aly, a component of the testis-meiotic arrest complex, to transcripts for male germ cell differentiation. Our results suggest that as new regions of the genome become open for transcription during terminal differentiation, blocking the action of a promiscuous activator on cryptic promoters is a critical mechanism for specifying precise gene activation.

2017-05-18 | GSE68696 | GEO

ChIP-Seq with Kumgang (Kmg), dMi-2, and Aly from wild-type and kmg KD Drosophila melanogaster testes

Project description:Genome wide localization of Kumgang, dMi-2, and Aly in Drosophila melanogaster testes were evaluated by ChIP-Seq in wild-type and kmg knock down testes. / Title: Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression / Abstract: To selectively express cell type–specific transcripts during development, it is critical to maintain genes required for other lineages in a silent state. Here, we show in the Drosophila male germline stem cell lineage that a spermatocyte-specific zinc finger protein, Kumgang (Kmg), working with the chromatin remodeler dMi-2 prevents transcription of genes normally expressed only in somatic lineages. By blocking transcription from normally cryptic promoters, Kmg restricts activation by Aly, a component of the testis-meiotic arrest complex, to transcripts for male germ cell differentiation. Our results suggest that as new regions of the genome become open for transcription during terminal differentiation, blocking the action of a promiscuous activator on cryptic promoters is a critical mechanism for specifying precise gene activation.

2017-05-18 | GSE89381 | GEO

Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression

Project description:This SuperSeries is composed of the SubSeries listed below. Abstract To selectively express cell type–specific transcripts during development, it is critical to maintain genes required for other lineages in a silent state. Here, we show in the Drosophila male germline stem cell lineage that a spermatocyte-specific zinc finger protein, Kumgang (Kmg), working with the chromatin remodeler dMi-2 prevents transcription of genes normally expressed only in somatic lineages. By blocking transcription from normally cryptic promoters, Kmg restricts activation by Aly, a component of the testis-meiotic arrest complex, to transcripts for male germ cell differentiation. Our results suggest that as new regions of the genome become open for transcription during terminal differentiation, blocking the action of a promiscuous activator on cryptic promoters is a critical mechanism for specifying precise gene activation.

2017-05-18 | GSE89506 | GEO

Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression

Project description:Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression

| PRJNA352401 | ENA

Widespread transposable element-driven oncogene expression in cancers

Project description:Transposable elements act as promiscuous cryptic promoters that upregulate oncogenes (“onco-exaptation”) in many cancers.

2019-02-05 | GSE113946 | GEO

Sequential changes at differentiation gene promoters as they become active in a stem cell lineage

Project description:Transcriptional silencing of terminal differentiation genes by the Polycomb group (PcG) machinery is emerging as a key feature of precursor cells in stem cell lineages. How, then, is this epigenetic silencing reversed for proper cellular differentiation? Here we investigate how the developmental program reverses local PcG action to allow expression of terminal differentiation genes in the Drosophila male germline stem cell lineage. We find that the silenced state, set up in precursor cells, is relieved through developmentally regulated sequential events at promoters once cells commit to spermatocyte differentiation. The programmed events include global down-regulation of PRC2, recruitment of hypophosphorylated RNA Polymerase II (Pol II) to promoters, as well as expression and action of cell-type specific homologs of subunits of TFIID (tTAFs). In addition, action of tMAC, a tissue specific version of the MIP/dREAM complex, is required both for recruitment of tTAFs to target differentiation genes and for proper cell-type specific localization of PRC1 components and tTAFs to the spermatocyte nucleolus. Together, action of the tMAC and tTAF cell-type specific chromatin and transcription machinery leads to loss of Polycomb and release of Pol II from the promoter of terminal differentiation genes to elongation, allowing robust transcription of the terminal differentiation genes.

2011-07-15 | GSE28728 | GEO

set2 buratowski lab

Project description:H3K36 methylation by Set2 targets Rpd3S histone deacetylase to 3Ã¢ÂÂ transcribed regions, repressing internal cryptic promoters and slowing elongation. To further explore the function of this pathway, global transcription was analyzed in yeast experiencing a series of carbon source shifts. Many previously unreported cryptic ncRNAs are induced by specific carbon sources, showing that cryptic promoters can be environmentally regulated. Also, approximately 230 mRNA genes show altered induction or repression upon SET2 deletion. A majority of Set2-repressed genes have overlapping lncRNA transcription. At these promoters, H3K36me3 and deacetylation by Rpd3S leads to slower or reduced induction. Unexpectedly, Set2 derepresses 159 genes, apparently by mediating a balance between Rpd3S and Rpd3L. Therefore, in addition to repression of cryptic transcription, H3K36 methylation maintains optimal expression dynamics of many mRNAs.

2016-09-25 | E-MTAB-4268 | biostudies-arrayexpress

A fluorescent assay for cryptic transcription in Saccharomyces cerevisiae [RNA-seq]

Project description:The disruption of chromatin structure can result in transcription initiation from cryptic promoters within gene bodies. While the passage of RNA polymerase II is a well-characterized chromatin-disrupting force, numerous factors, including histone chaperones, normally stabilize chromatin on transcribed genes, thereby repressing cryptic transcription. DNA replication, which requires a partially overlapping set of histone chaperones, is also inherently disruptive to chromatin, but a role for DNA replication in cryptic transcription has never been examined. In this study, we tested the hypothesis that, in the absence of chromatin-stabilizing factors, DNA replication can promote cryptic transcription in S. cerevisiae. Using a novel fluorescent reporter assay, we show that multiple factors, including Asf1, CAF-1, Rtt106, Spt6, and FACT, block transcription from a cryptic promoter, but are entirely or partially dispensable in G1-arrested cells, suggesting a requirement for DNA replication in chromatin disruption. Collectively, these results demonstrate that transcription fidelity is dependent on numerous factors that function to assemble chromatin on nascent DNA.

2023-12-07 | GSE249580 | GEO

A fluorescent assay for cryptic transcription in Saccharomyces cerevisiae [MNase-seq]

2023-12-06 | GSE249469 | GEO

Identification of non-coding transcripts regulated by the transcription factor Rap1 by RNA-Seq analysis

Project description:Many active eukaryotic gene promoters exhibit divergent noncoding transcription, but the mechanisms restricting expression of these transcripts are not well understood. Here we demonstrate how a sequence-specific transcription factor represses divergent noncoding transcription at highly expressed genes in yeast. We find that depletion of the transcription factor Rap1 induces noncoding transcription in a large fraction of Rap1 regulated gene promoters. Specifically, Rap1 prevents transcription initiation at cryptic promoters near its binding sites, which is uncoupled from transcription regulation in the protein-coding direction. We further provide evidence that Rap1 acts independently of chromatin-based mechanisms to repress cryptic or divergent transcription. Finally, we show that divergent transcription in the absence of Rap1 is elicited by the RSC chromatin remodeller. We propose that a sequence-specific transcription factor limits access of basal transcription machinery to regulatory elements and adjacent sequences that act as divergent cryptic promoters, thereby providing directionality towards productive transcription.

2018-12-20 | GSE107813 | GEO

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