ZSCAN5B and its primate-specific paralogs bind RNA polymerase III genes and extra-TFIIIC (ETC) sites to modulate mitotic progression
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ABSTRACT:
PROVIDER: PRJNA336013 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3955280.fastq.gz | Fastqsanger.gz | |||
| SRR3955281.fastq.gz | Fastqsanger.gz | |||
| SRR3955282.fastq.gz | Fastqsanger.gz | |||
| SRR3955279.fastq.gz | Fastqsanger.gz | |||
| SRR3992190.fastq.gz | Fastqsanger.gz |
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Project description:Particularly in the context of differentiation and development, the importance of three-dimensional chromatin architecture to gene regulatory mechanisms is becoming increasingly clear. The most ancient known mechanism of chromatin organization involves TFIIIC, a transcription factor (TF) that recruits RNA polymerase III (Pol III) for transcription of tRNA and other types of non-coding RNA genes. From yeast to mammals, TFIIIC binds to tRNA genes (tDNAs) and scattered “extra-TFIIIC” (ETC) loci and serves to tether these loci together as anchors of chromatin loops. TFIIIC activities are modulated by MAF, MYC, and other TF proteins that are still unidentified. Here we identify the ZSCAN5 TF family - including mammalian ZSCAN5B and its primate-specific paralogs - as proteins that occupy mammalian Pol III promoters and ETC sites. We show that ZSCAN5B binds with high specificity to a conserved subset of tDNA loci and other Pol III genes in human and mouse and that primate-specific ZSCAN5A and ZSCAN5D also bind Pol III genes, although ZSCAN5D preferentially localizes to MIR SINE- and LINE2-associated ETC sites. ZSCAN5 genes are expressed in proliferating cell populations and are cell-cycle regulated, and gene expression data suggested that they might cooperate to regulate basic cellular functions including mitotic progression. Consistent with this predicted role, ZSCAN5A knockdown led to increasing numbers of cells in mitotic cells and aneuploidy in cultured cells. Together these data implicate ZSCAN5 genes in regulation of Pol III gene transcription and nearby Pol II genes, ultimately influencing cell cycle progression and differentiation in a variety of tissues.
2017-02-16 | GSE84884 | GEO
Project description:Particularly in the context of differentiation and development, the importance of three-dimensional chromatin architecture to gene regulatory mechanisms is becoming increasingly clear. The most ancient known mechanism of chromatin organization involves TFIIIC, a transcription factor (TF) that recruits RNA polymerase III (Pol III) for transcription of tRNA and other types of non-coding RNA genes. From yeast to mammals, TFIIIC binds to tRNA genes (tDNAs) and scattered “extra-TFIIIC” (ETC) loci and serves to tether these loci together as anchors of chromatin loops. TFIIIC activities are modulated by MAF, MYC, and other TF proteins that are still unidentified. Here we identify the ZSCAN5 TF family - including mammalian ZSCAN5B and its primate-specific paralogs - as proteins that occupy mammalian Pol III promoters and ETC sites. We show that ZSCAN5B binds with high specificity to a conserved subset of tDNA loci and other Pol III genes in human and mouse and that primate-specific ZSCAN5A and ZSCAN5D also bind Pol III genes, although ZSCAN5D preferentially localizes to MIR SINE- and LINE2-associated ETC sites. ZSCAN5 genes are expressed in proliferating cell populations and are cell-cycle regulated, and gene expression data suggested that they might cooperate to regulate basic cellular functions including mitotic progression. Consistent with this predicted role, ZSCAN5A knockdown led to increasing numbers of cells in mitotic cells and aneuploidy in cultured cells. Together these data implicate ZSCAN5 genes in regulation of Pol III gene transcription and nearby Pol II genes, ultimately influencing cell cycle progression and differentiation in a variety of tissues.
2017-02-16 | GSE85040 | GEO
Project description:Particularly in the context of differentiation and development, the importance of three-dimensional chromatin architecture to gene regulatory mechanisms is becoming increasingly clear. The most ancient known mechanism of chromatin organization involves TFIIIC, a transcription factor (TF) that recruits RNA polymerase III (Pol III) for transcription of tRNA and other types of non-coding RNA genes. From yeast to mammals, TFIIIC binds to tRNA genes (tDNAs) and scattered “extra-TFIIIC” (ETC) loci and serves to tether these loci together as anchors of chromatin loops. TFIIIC activities are modulated by MAF, MYC, and other TF proteins that are still unidentified. Here we identify the ZSCAN5 TF family - including mammalian ZSCAN5B and its primate-specific paralogs - as proteins that occupy mammalian Pol III promoters and ETC sites. We show that ZSCAN5B binds with high specificity to a conserved subset of tDNA loci and other Pol III genes in human and mouse and that primate-specific ZSCAN5A and ZSCAN5D also bind Pol III genes, although ZSCAN5D preferentially localizes to MIR SINE- and LINE2-associated ETC sites. ZSCAN5 genes are expressed in proliferating cell populations and are cell-cycle regulated, and gene expression data suggested that they might cooperate to regulate basic cellular functions including mitotic progression. Consistent with this predicted role, ZSCAN5A knockdown led to increasing numbers of cells in mitotic cells and aneuploidy in cultured cells. Together these data implicate ZSCAN5 genes in regulation of Pol III gene transcription and nearby Pol II genes, ultimately influencing cell cycle progression and differentiation in a variety of tissues.
2017-02-16 | GSE85009 | GEO
Project description:Mammalian genomes contain hundreds of genes transcribed by RNA Polymerase III (Pol III), encoding noncoding RNAs and especially the tRNAs specialized to carry specific amino acids to the ribosome for protein synthesis. In addition to this well-known function, tRNAs and their genes (tDNAs) serve a variety of other critical cellular functions. For example, tRNAs and other Pol III transcripts can be cleaved to yield small RNAs with potent regulatory activities. Furthermore, from yeast to mammals, active tDNAs and related "extra-TFIIIC" (ETC) loci provide the DNA scaffolds for the most ancient known mechanism of three-dimensional chromatin architecture. Here we identify the ZSCAN5 TF family - including mammalian ZSCAN5B and its primate-specific paralogs - as proteins that occupy mammalian Pol III promoters and ETC sites. We show that ZSCAN5B binds with high specificity to a conserved subset of Pol III genes in human and mouse. Furthermore, primate-specific ZSCAN5A and ZSCAN5D also bind Pol III genes, although ZSCAN5D preferentially localizes to MIR SINE- and LINE2-associated ETC sites. ZSCAN5 genes are expressed in proliferating cell populations and are cell-cycle regulated, and siRNA knockdown experiments suggested a cooperative role in regulation of mitotic progression. Consistent with this prediction, ZSCAN5A knockdown led to increasing numbers of cells in mitosis and the appearance of cells. Together, these data implicate the role of ZSCAN5 genes in regulation of Pol III genes and nearby Pol II loci, ultimately influencing cell cycle progression and differentiation in a variety of tissues.
| S-EPMC5340127 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-02-16 | GSE85045 | GEO
Project description:ZSCAN5B and its primate-specific paralogs bind RNA polymerase III genes and extra-TFIIIC (ETC) sites to modulate mitotic progression [SiRNA RNA-Seq data set]
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Project description:ZSCAN5B and its primate-specific paralogs bind RNA polymerase III genes and extra-TFIIIC (ETC) sites to modulate mitotic progression [Mouse Placenta ChIP-Seq data set]
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Project description:ZSCAN5B and its primate-specific paralogs bind RNA polymerase III genes and extra-TFIIIC (ETC) sites to modulate mitotic progression [Human cell line ChIP-Seq data set]
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Project description:MYC proteins bind to virtually all active promoters transcribed by RNA polymerase II (RNAPII), but whether they interact with the three-dimensional chromatin architecture is unknown. Here we used HiChIP sequencing of the MYCN oncoprotein and found that MYCN localizes to three-dimensional hubs formed by active promoters and enhancers. In these hubs, MYCN interacts with TFIIIC, an architectural protein complex. MYCN recruits TFIIIC to promoters when transcription elongation is inhibited, and the complex of both proteins induces premature transcription termination. Termination correlates closely with the TFIIIC-dependent removal of MYCN from promoter hubs and with corresponding alterations in the three-dimensional interactions of cohesin complexes. This limits DNA damage by removing RNAPII that stalls proximal to double-strand breaks. Binding of TFIIIC to MYCN is limited by competition with Aurora-A and this protects genes involved in mRNA processing from termination, arguing that MYCN contributes to the unusual proliferative capacity of neuroblastoma cells via removing stalled RNAPII from promoter hubs and via increasing the capacity for RNA processing.
2024-07-15 | GSE223054 | GEO
Project description:MYC proteins bind to virtually all active promoters transcribed by RNA polymerase II (RNAPII), but whether they interact with the three-dimensional chromatin architecture is unknown. Here we used HiChIP sequencing of the MYCN oncoprotein and found that MYCN localizes to three-dimensional hubs formed by active promoters and enhancers. In these hubs, MYCN interacts with TFIIIC, an architectural protein complex. MYCN recruits TFIIIC to promoters when transcription elongation is inhibited, and the complex of both proteins induces premature transcription termination. Termination correlates closely with the TFIIIC-dependent removal of MYCN from promoter hubs and with corresponding alterations in the three-dimensional interactions of cohesin complexes. This limits DNA damage by removing RNAPII that stalls proximal to double-strand breaks. Binding of TFIIIC to MYCN is limited by competition with Aurora-A and this protects genes involved in mRNA processing from termination, arguing that MYCN contributes to the unusual proliferative capacity of neuroblastoma cells via removing stalled RNAPII from promoter hubs and via increasing the capacity for RNA processing.
2024-07-15 | GSE223052 | GEO