Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA396916 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5890620.fastq.gz | Fastqsanger.gz | |||
| SRR5890630.fastq.gz | Fastqsanger.gz | |||
| SRR5890621.fastq.gz | Fastqsanger.gz | |||
| SRR5890631.fastq.gz | Fastqsanger.gz | |||
| SRR5890612.fastq.gz | Fastqsanger.gz |
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Project description:Argonaute (Ago) proteins, which act in post-transcriptional gene regulation directed by small RNAs, are vital for normal stem cell biology. Here we report the genomic characterization of stable Ago-deficient mouse embryonic stem cells (mESC) and determine the direct and system level response to loss of Ago-mediated regulation. We find mESCs lacking all four Ago proteins are viable, do not repress microRNA (miRNA)-targeted cellular RNAs, and show distinctive gene network signatures. Profiling of RNA expression and epigenetic activity in an Ago mutant genetic series indicates that early responses to Ago loss are driven by transcriptional regulatory networks, in particular the Tgf-ß/Smad transcriptional network. This finding is confirmed using a time course analysis of Ago depletion and Ago rescue experiments. Detailed analysis places Tgf-ß/Smad activation upstream of cell cycle regulator activation, such as Cdkn1a, and repression of the c-Myc transcriptional network. The Tgf-ß/Smad pathway is directly controlled by multiple low-affinity miRNA interactions with Tgf-ß/Activin receptor mRNAs and receptor-mediated activation is required for Tgf-ß/Smad target induction with Ago loss. Our characterization reveals the interplay of post-transcriptional regulatory pathways with transcriptional networks in maintaining cell state and likely coordinating cell state transitions.
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Project description:Transforming growth factor (TGF)-β plays crucial roles in embryonic development and adult tissue homeostasis by eliciting various cellular responses in target cells. TGF-β signaling is principally mediated through receptor-activated Smad proteins, which regulate expression of target genes in cooperation with other DNA-binding transcriptionfactors (Smad cofactors). In this study, we found that the basic helix-loop-helix transcription factor Olig1 is a Smad cofactor involved in TGF-b-induced cell motility. Knockdown of Olig1 attenuated TGF-β-induced cell motility in chamber migration and wound healing assays. In contrast, Olig1 knockdown had no effect on bone morphogenetic protein-induced cell motility, TGF-β-induced cytostasis or epithelial-mesenchymal transition. Furthermore, we observed that cooperation of Smad2/3 with Olig1 is regulated by a peptidyl-prolyl cis/trans isomerase, Pin1. TGF-b-induced cell motility, induction of Olig1-regulated genes, and physical interaction between Smad2/3 and Olig1 were all inhibited after knockdown of Pin1, indicating a novel mode of regulation of Smad signaling. We also found that Olig1 interacts with the L3 loop of Smad3. Using a synthetic peptide corresponding to the L3 loop of Smad3, we succeeded in selectively inhibiting TGF-b-induced cell motility. These findings may lead to a new strategy for selective regulation of TGF-b-induced cellular responses. NMuMG cells were transfected with siRNAs (siControl, siOlig1 or siPin1) and treated with or without TGF-b for 1h. We compared genes affected by knockdown of Olig1 and that of Pin1.
2013-07-01 | E-GEOD-46405 | biostudies-arrayexpress
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