Lin28/let-7 axis regulates the timig of cession of nephrogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA482367 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7551580_1.fastq.gz | Fastqsanger.gz | |||
| SRR7551580_2.fastq.gz | Fastqsanger.gz | |||
| SRR7551590_1.fastq.gz | Fastqsanger.gz | |||
| SRR7551590_2.fastq.gz | Fastqsanger.gz | |||
| SRR7551600_1.fastq.gz | Fastqsanger.gz |
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Project description:To study role of Lin28/let-7 axis on nephrogenesis, we profiled kidney transcriptom of LIN28 OE, let-7 KO, and their wild-type littermate control mice.
2019-01-14 | GSE117510 | GEO
Project description:The Lin28/let-7 pathway regulates the mammalian caudal body axis elongation program
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Project description:This SuperSeries is composed of the following subset Series: GSE39855: LIN28 binds messenger RNAs at GGAGA motifs and regulates splicing factor abundance (splicing array) GSE39872: LIN28 binds messenger RNAs at GGAGA motifs and regulates splicing factor abundance (HTS) Refer to individual Series
2012-09-10 | E-GEOD-39873 | biostudies-arrayexpress
Project description:The heterochronic genes Lin28a/b and let-7 are well-established regulators of invertebrate development, however their functions in patterning the mammalian body plan remain unexplored. In this study, we discovered a novel function of Lin28/let-7 in controlling caudal vertebrae number during body axis formation. We found that FoxD1-driven overexpression of Lin28a or LIN28B led to a striking increase in caudal vertebrae number, whereas loss of Lin28a stunted tail formation. Accordingly, perturbation of the let-7 microRNA family led to the opposite phenotypes. We further show that overexpressing Lin28a in embryos resulted in increased tail bud cell proliferation, whereas Lin28a KO decreased cellular proliferation. This was accompanied by a transcriptional shift, including down-regulation of the neural marker Sox2, and resulted in a pro-mesodermal phenotype with decreased proportions of neural tissue relative to mesoderm in Lin28a-overexpressing embryos. Strikingly, Lin28a KO and let-7 over-expression demonstrated opposite effects, suggesting that the Lin28/let-7 pathway acts upstream of the signaling pathways controlling the self-renewal and cell fate commitment of neuro-mesodermal progenitors. We propose that Lin28a/b activity controls the pool of caudal progenitors during tail development, promotes their self-renewal potential, is involved in controlling the balance of neural versus mesodermal cell fate decisions, and that progressive down-regulation of Lin28a allows for species-specific vertebral formula to be achieved. These findings suggest that Lin28/let-7 play a role in the regulation of tail length through heterochrony of the body plan.
2019-05-01 | GSE123193 | GEO
Project description:LIN28 is a conserved RNA binding protein implicated in pluripotency, reprogramming and oncogenesis. Previously shown to act primarily by blocking let-7 microRNA (miRNA) biogenesis, here we elucidate distinct roles of LIN28 regulation via its direct messenger RNA (mRNA) targets. Through cross-linking and immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells and somatic cells expressing exogenous LIN28, we have defined discrete LIN28 binding sites in a quarter of human transcripts. These sites revealed that LIN28 binds to GGAGA sequences enriched within loop structures in mRNAs, reminiscent of its interaction with let-7 miRNA precursors. Among LIN28 mRNA targets, we found evidence for LIN28 autoregulation and also direct but differing effects on the protein abundance of splicing regulators in somatic and pluripotent stem cells. Splicing-sensitive microarrays demonstrated that exogenous LIN28 expression causes widespread downstream alternative splicing changes. These findings identify important regulatory functions of LIN28 via direct mRNA interactions.
2012-09-10 | GSE39872 | GEO
Project description:LIN28 is a conserved RNA binding protein implicated in pluripotency, reprogramming and oncogenesis. Previously shown to act primarily by blocking let-7 microRNA (miRNA) biogenesis, here we elucidate distinct roles of LIN28 regulation via its direct messenger RNA (mRNA) targets. Through cross-linking and immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells and somatic cells expressing exogenous LIN28, we have defined discrete LIN28 binding sites in a quarter of human transcripts. These sites revealed that LIN28 binds to GGAGA sequences enriched within loop structures in mRNAs, reminiscent of its interaction with let-7 miRNA precursors. Among LIN28 mRNA targets, we found evidence for LIN28 autoregulation and also direct but differing effects on the protein abundance of splicing regulators in somatic and pluripotent stem cells. Splicing-sensitive microarrays demonstrated that exogenous LIN28 expression causes widespread downstream alternative splicing changes. These findings identify important regulatory functions of LIN28 via direct mRNA interactions.
2012-09-10 | GSE39855 | GEO
Project description:LIN28 is a conserved RNA binding protein implicated in pluripotency, reprogramming and oncogenesis. Previously shown to act primarily by blocking let-7 microRNA (miRNA) biogenesis, here we elucidate distinct roles of LIN28 regulation via its direct messenger RNA (mRNA) targets. Through cross-linking and immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells and somatic cells expressing exogenous LIN28, we have defined discrete LIN28 binding sites in a quarter of human transcripts. These sites revealed that LIN28 binds to GGAGA sequences enriched within loop structures in mRNAs, reminiscent of its interaction with let-7 miRNA precursors. Among LIN28 mRNA targets, we found evidence for LIN28 autoregulation and also direct but differing effects on the protein abundance of splicing regulators in somatic and pluripotent stem cells. Splicing-sensitive microarrays demonstrated that exogenous LIN28 expression causes widespread downstream alternative splicing changes. These findings identify important regulatory functions of LIN28 via direct mRNA interactions. CLIP-seq for LIN28-V5 in stable human Flp-In-293 cells, and LIN28 in hES cells; strand-specific mRNA-seq for uninfected, control KD, and LIN28 KD human H9 ES cells; and strand-specific smallRNA-seq for uninfected, control KD, and LIN28 KD human H9 ES cells.
2012-09-10 | E-GEOD-39872 | biostudies-arrayexpress
Project description:LIN28 is a conserved RNA binding protein implicated in pluripotency, reprogramming and oncogenesis. Previously shown to act primarily by blocking let-7 microRNA (miRNA) biogenesis, here we elucidate distinct roles of LIN28 regulation via its direct messenger RNA (mRNA) targets. Through cross-linking and immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells and somatic cells expressing exogenous LIN28, we have defined discrete LIN28 binding sites in a quarter of human transcripts. These sites revealed that LIN28 binds to GGAGA sequences enriched within loop structures in mRNAs, reminiscent of its interaction with let-7 miRNA precursors. Among LIN28 mRNA targets, we found evidence for LIN28 autoregulation and also direct but differing effects on the protein abundance of splicing regulators in somatic and pluripotent stem cells. Splicing-sensitive microarrays demonstrated that exogenous LIN28 expression causes widespread downstream alternative splicing changes. These findings identify important regulatory functions of LIN28 via direct mRNA interactions. In triplicate, polyA-selected RNA was extracted from untreated Flp-In-293 cells, stable LIN28V5 293 cells, TDP-43 over-expressed Flp-In-293 cells, control over-expressed Flp-In-293 cells, LIN28 depleted hES cells, and control depleted hES cells, and hybridized to custom human splicing sensitive microarrays
2012-09-10 | E-GEOD-39855 | biostudies-arrayexpress
Project description:We used immunoprecipitation to pulldown Lin28 associated RNA targets and used genome-wide high throughput deep sequencing to identified those Lin28-associated RNAs. Keywords: Lin28 IP-RNAseq
2011-01-18 | GSE23109 | GEO
Project description:The let-7 tumor suppressor microRNAs are known for their regulation of oncogenes, while the RNA-binding proteins Lin28a/b promote malignancy by inhibiting let-7 biogenesis. We have uncovered unexpected roles for the Lin28/let-7 pathway in regulating metabolism. When overexpressed in mice, both Lin28a and LIN28B promote an insulin-sensitized state that resists high-fat-diet induced diabetes. Conversely, muscle-specific loss of Lin28a or overexpression of let-7 results in insulin resistance and impaired glucose tolerance. These phenomena occur, in part, through the let-7-mediated repression of multiple components of the insulin-PI3K-mTOR pathway, including IGF1R, INSR, and IRS2. In addition, the mTOR inhibitor, rapamycin, abrogates Lin28a-mediated insulin sensitivity and enhanced glucose uptake. Moreover, let-7 targets are enriched for genes containing SNPs associated with type 2 diabetes and control of fasting glucose in human genome-wide association studies. These data establish the Lin28/let-7 pathway as a central regulator of mammalian glucose metabolism.
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