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Precise modulation of transcription factor levels reveals drivers of dosage sensitivity

ABSTRACT: Precise modulation of transcription factor levels reveals drivers of dosage sensitivity

PROVIDER: PRJNA848202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19630900_1.fastq.gz	Fastqsanger.gz
	SRR19630900_2.fastq.gz	Fastqsanger.gz
	SRR19630901_1.fastq.gz	Fastqsanger.gz
	SRR19630901_2.fastq.gz	Fastqsanger.gz
	SRR19630902_1.fastq.gz	Fastqsanger.gz

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Precise modulation of transcription factor levels reveals drivers of dosage sensitivity

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-04 | GSE205904 | GEO

Precise modulation of transcription factor levels identifies features underlying dosage sensitivity.

Project description:Transcriptional regulation exhibits extensive robustness, but human genetics indicates sensitivity to transcription factor (TF) dosage. Reconciling such observations requires quantitative studies of TF dosage effects at trait-relevant ranges, largely lacking so far. TFs play central roles in both normal-range and disease-associated variation in craniofacial morphology; we therefore developed an approach to precisely modulate TF levels in human facial progenitor cells and applied it to SOX9, a TF associated with craniofacial variation and disease (Pierre Robin sequence (PRS)). Most SOX9-dependent regulatory elements (REs) are buffered against small decreases in SOX9 dosage, but REs directly and primarily regulated by SOX9 show heightened sensitivity to SOX9 dosage; these RE responses partially predict gene expression responses. Sensitive REs and genes preferentially affect functional chondrogenesis and PRS-like craniofacial shape variation. We propose that such REs and genes underlie the sensitivity of specific phenotypes to TF dosage, while buffering of other genes leads to robust, nonlinear dosage-to-phenotype relationships.

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [CUT&Run]

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [CUT&Run]

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [ATAC-Seq]

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [ATAC-Seq]

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [RNA-Seq]

Project description:Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [RNA-Seq]

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [CUT&Run]

Project description:ATP-dependent chromatin remodelers establish and arrange nucleosome distribution, modifying accessibility of DNA. Brg1 is exclusive ATPase subunit of mSWI/SNF complex. To understand the dosage dependent function of mSWI/SNF complex. We take an advantage of dTag system to precisely control abundancy of BRG1. We found overall Brg1-binding is sensitive to its abundance nevertheless OCT4-target or H3K27ac region, suggesting Brg1 genome-wide distribution rather than being actively recruited. We also reveal open chromatin dependency on BRG1. The chromatin accessibility of super enhancer shows buffered response on depletion of BRG1, whereas weak enhancer is sensitive. Finally, transcriptomic analysis identified that transcription shows buffered dependencies on BRG1 loss. Overall, our results highlight kinetics differences of BRG1-binding to transcriptome underline BRG1 dosage-sensitive mechanism.

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [ATAC-Seq]

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Precise modulation of mSWI/SNF identified dosage-sensitive chromatin regulation [RNA-Seq]

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Next-generation sequencing facilitates quantitative analysis of the transcriptomes of FOXG1 100% dosage, FOXG1 60% dosage, FOXG1 30% dosage, and FOXG1 0% dosage GABA interneurons derived from human embryonic stem cells

Project description:Next-generation sequencing facilitates quantitative analysis of the transcriptomes of FOXG1 100% dosage GABA interneurons, FOXG1 60% dosage GABA interneurons, FOXG1 30% dosage GABA interneurons, and FOXG1 0% dosage GABA interneurons derived from human embryonic stem cells. We report a genetic manipulation system that enable precise dosage control of FOXG1 protein in human pluripotent stem cells (hPSCs). Using this system, we explored how the various reduced dosage affect human ventrol GABA interneuron development. We employed RNA seq on hPSC-derived GABA interneurons (day 60) to invest the expression pattern under different FOXG1 dosage conditions. RNA-Seq on GABA interneurons (Day 60) indicates that compared to the FOXG1 100% group, variable insufficiency of FOXG1 produces more than 1000 differently expressed genes (DEGs), and more DEGs in the group with less FOXG1 dosage. Heat map on Pearson Correlation indicates that groups with more discriminated FOXG1 exhibit much weaker correlation. Venn diagram reveals that each group has a set of distinct DEGs, suggesting that each FOXG1 protein dosage could results in different expression pattern during differentiation. The DEGs can be divided into two clusters, with one showing dosage-dependent regulation by FOXG1 and the other one typical binary. Key regulatory genes for GABA interneuron induction (NKX2-1, NKX6-2, GAD1, etc.) and for functional GABAergic-speciﬁc synapse formation (GABBR1, GABRA1, GABRB1, GABRG1, GABRQ, SHANK1, etc.) are down regulated along with reduction of FOXG1 protein.

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