RNA sequencing of RipmiR-141~200c and RipmiR-141~200c Zeb1200M islets
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB45958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6133630.fastq.gz | Fastqsanger.gz | |||
| ERR6133631.fastq.gz | Fastqsanger.gz | |||
| ERR6133632.fastq.gz | Fastqsanger.gz | |||
| ERR6133633.fastq.gz | Fastqsanger.gz | |||
| ERR6133634.fastq.gz | Fastqsanger.gz |
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Project description:We performed RNA sequencing of islets of Langerhans isolated from RipmiR-141~200c and RipmiR-141~200c Zeb1200M mice to determine the transcriptomic effects of mutating miR-200 binding sites in the endogenous Zeb1 3'UTR of mice in which miR-141~200c is overexpressed under the rat insulin promoter (RIP).
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Project description:We used transcription activator-like effector nucleases (TALENs) to generate knockout cells for two related microRNAs (miRNAs), mir-141 and mir-200c, which belong to the deeply conserved mir-200 family. By carrying out deep sequencing, we identified the target genes of each miRNA. Interestingly, miR-141 and miR-200c, despite their overall similarity, suppressed largely non-overlapping groups of targets. Analysis of global mRNA level change in mir-141 and mir-200c knockout compared to wild type cells
2013-09-27 | E-GEOD-51217 | biostudies-arrayexpress
Project description:ERα is one of the most important transcription factors and therapeutic targets in breast cancer. The patterns of ERα expression in normal breast tissue and cancerous lesions are strikingly different. What drives the change of ERα pattern during lesions formation remains unclear. Here, we describe a novel regulatory mechanism through which miR-200c/141 regulates the level as well as the distribution of ERα in the mammary gland. miR-200c/141 is specifically expressed in luminal cells. Luminal-deletion of miR-200c/141 (miR-cKO) leads to a drastic expansion of ERα+ cell proportion. Single cell RNAseq reveals that miR-cKO generates aberrant luminal subpopulations with increased proliferative and anti-apoptotic features. In vivo lineage tracing of ER- luminal cells demonstrates that miR-200c/141 deletion can convert ER- cells into ER+ cells, which contribute partly to the increase of ERα+ luminal cells. Mechanistic study identifies Ccnd1 as a novel target of miR-200c/141 . Upon miR-200c/141deletion, elevated Ccnd1 level corroborates ERα transcriptional activation, leads to enhanced ERα signaling activity, consequently increased transcription of ERα coding gene Esr1 through self-activation at promoter E1. Our findings reveal a new miR-200c/141-Ccnd1-ERα axis, and provide new molecular insights into how miR-200c/141-Ccnd1 enforces the lineage barrier between ER- and ER+ luminal cells, and what drives the change of ERα expression pattern.
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Project description:ES cells express the miR-200 family which becomes down-regulated during the course of differentiation in serum. We generated an ES cell line which expresses miR-200c and miR-141 upon addition of doxycycline. Microarrays were used to gain a global picture of differentiation when miR-200c and miR-141 expression were maintained throughout differentiation through the addition of doxycycline. A2.miR200c ES cells, which express miR-200c/miR-141 upon addition of doxycycline, were differentiated as embryoid bodies in six petri dishes. Half of the samples were treated with doxycycline on days 2 and 4 of differentiation, and RNA was collected from all samples on days 3, 4, and 5.
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