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Genome-wide analysis of Smad and Schnurri transcription factors in C. elegans

ABSTRACT: Genome-wide analysis of Smad and Schnurri transcription factors in C. elegans

PROVIDER: PRJNA1106907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28868047_1.fastq.gz	Fastqsanger.gz
	SRR28868047_2.fastq.gz	Fastqsanger.gz
	SRR28868048_1.fastq.gz	Fastqsanger.gz
	SRR28868048_2.fastq.gz	Fastqsanger.gz
	SRR28868049_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of Smad and Schnurri transcription factors in C. elegans

Project description:Smads and their transcription factor partners mediate the transcriptional responses of target cells to secreted ligands of the Transforming Growth Factor-β (TGF-β) family, including those of the conserved bone morphogenetic protein (BMP) family, yet only a small number of direct target genes have been well characterized. In C. elegans, the BMP2/4 ortholog DBL-1 regulates multiple biological functions, including body size, via a canonical receptor-Smad signaling cascade. Here, we identify functional binding sites for SMA-3/Smad and its transcriptional partner SMA-9/Schnurri based on ChIP-seq peaks (identified by modEncode) and expression differences of nearby genes identified from RNA-seq analysis of corresponding mutants. We found that SMA-3 and SMA-9 have both overlapping and unique target genes. At a genome-wide scale, SMA-3/Smad acts as a transcriptional activator, whereas SMA-9/Schnurri direct targets include both activated and repressed genes. Mutations in sma-9 partially suppress the small body size phenotype of sma-3, suggesting some level of antagonism between these factors and challenging the prevailing model for Schnurri function. A functional analysis of direct target genes revealed a novel role in body size for genes involved in one-carbon metabolism and in the endoplasmic reticulum (ER) secretory pathway, including the disulfide reductase dpy-11. Our findings indicate that Smads and SMA-9/Schnurri have previously unappreciated complex genetic and genomic regulatory interactions that in turn regulate the secretion of extracellular components like collagen into the cuticle to mediate body size regulation.

2024-07-01 | GSE266398 | GEO

Quantitative proteomics of the SMAD transcription factor family reveals IPO5 as a BMP Receptor-SMAD specific importin

Project description:Gene-specific transcription factors (GSTFs) control of gene transcription by DNA binding and specific protein complex recruitment, which regulates promoter accessibility for transcription initiation by RNA polymerase II. GSTFs that are frequently mutated in colon and rectal carcinomas are Suppressor of Mothers Against Decapentaplegic 2 (SMAD2) and SMAD4, which play an important role in the TGF-β signaling pathways controlling cell fate and proliferation (ref.). The SMAD protein family is a diverse and it can be divided into three subclasses: receptor activated SMADs, inhibitory SMADs and the common SMAD4 co-activator. To study protein interactors of the SMAD protein family we generated a quantitative proteomics pipeline that allows for inducible expression of GFP-tagged SMAD proteins followed by affinity purification and MS analysis. The nuclear importin IPO5 was identified as a novel interacting protein of SMAD1. Overexpression of IPO5 shows forced BMP R-SMAD nuclear localization confirming a functional relationship between BMP but not TGF-β R-SMADs and IPO5. Finally we provide evidence that the length of the lysine stretch in the NLS is involved in importin selection.

2016-10-10 | PXD004529 | Pride

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification

| PRJNA674869 | ENA

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [HiChIP]

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [HiChIP]

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Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [ChIPSeq7221]

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [ChIPSeq7221]

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Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [BulkRNAseq7221]

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [BulkRNAseq7221]

| PRJNA744930 | ENA

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [ChIP-seq]

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [ChIP-seq]

| PRJNA674872 | ENA

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [bulk RNA-seq]

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [bulk RNA-seq]

| PRJNA674871 | ENA

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [single-cell RNA-seq]

Project description:Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [single-cell RNA-seq]

| PRJNA674885 | ENA

Oct1 cooperates with Smad transcription factors to promote mesodermal lineage specification [HiChIP]

Project description:The pathways used by cells to transition between pluripotent and tissue-specific states are incompletely understood. Here we show that the widely-expressed transcription factor Oct1/Pou2f1 activates silent, developmental lineage-appropriate genes to “canalize” developmental progression. Using Oct1 inducible knockout embryonic stem cells, we show that that Oct1 deficiency impairs mesodermal and terminal muscle differentiation in a manner that can be rescued by Oct1 retroviral expression. We show that mesoderm-specific genes are not correctly induced early in the differentiation timecourse. Oct1-deficient cells lose temporal coherence in the induction of lineage-specific genes and show inappropriate developmental lineage branching, resulting in poorly differentiated cells states retaining epithelial characteristics. In embryonic stem cells, Oct1 co-binds with Oct4 to genes critical for mesoderm induction, and continues to bind these genes during differentiation. Oct1 binding events are enriched at the termini of chromatin loops, including loops gained with differentiation. The Utx/Kdm6a histone lysine demethylase also binds to many of these genes, and using a prototypic Pax3 gene we show that Oct1 recruits Utx to remove inhibitory H3K27me3 marks and activate expression. The specificity of the ubiquitous Oct1 protein for mesodermal genes can be explained by cooperative interactions with lineage-driving Smad transcription factors, as we show that Smad and Oct binding sites frequently coexist mesoderm-specific genes, and that Oct1 and Smad3 act cooperatively at the Myog enhancer. Overall, these results identify Oct1 as a key mediator of the induction of mesoderm lineage-specific genes.

2022-11-26 | GSE207828 | GEO

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