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| Status |
Public on Jun 15, 2014 |
| Title |
Dicer-microRNA-Myc circuit promotes transcription of hundreds of long noncoding RNAs |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Non-coding RNA profiling by high throughput sequencing
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| Summary |
Long noncoding RNAs (lncRNAs) are important regulators of cell fate, and their mis-expression has been implicated in many diseases. While distinct polymerases generate messenger vs. noncoding ribosomal or tRNAs3, little is known about distinct mechanisms controlling lncRNA expression. Here we show that transcription of lncRNAs is quantitatively different from that of messenger RNAs (mRNAs)--as revealed by deficiency of Dicer (Dcr), a key ribonuclease that generates microRNAs (miRNAs). Loss of Dcr in mouse embryonic stem cells (mESCs) led surprisingly to decreased level of the majority of lncRNAs. The canonical Dgcr8-Dcr-miRNA pathway is required for robust lncRNA expression, at the level of transcriptional initiation and elongation of lncRNA genes rather than at the level of their stability. cMyc, an oncogenic transcription factor, whose expression is indirectly regulated by Dcr-miRNA in mESCs, is partly responsible for lncRNA transcription. Loss of cMyc led to a more dramatic decrease of lncRNAs than mRNAs, and cMyc overexpression rescues lncRNA expression in Dcr KO cells. A quantitative metric of “mRNA-lncRNA decoupling” revealed that Dcr and cMyc differentially regulate lncRNAs vs. mRNAs in diverse cell types and in vivo, as evidenced by hundreds of microarray experiments. Thus, Dcr and cMyc may allow numerous lncRNAs to be activated or deactivated as a class, implicating lncRNAs to potential regulatory roles in development and disease states where Dcr and cMyc have been associated with.
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| Overall design |
RNA was sequenced from WT and Dcr KO mESCs and the expression of lncRNAs and mRNAs are compared between WT and Dcr KO mESCs.
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| Contributor(s) |
Zheng GX, Do B, Webster D, Khavari P, Chang H |
| Citation(s) |
24929436 |
| Submission date |
Feb 25, 2014 |
| Last update date |
May 15, 2019 |
| Contact name |
Kun Qu |
| E-mail(s) |
kqu@stanford.edu
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| Organization name |
Stanford University
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| Department |
Dermatology
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| Lab |
Howard Chang
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| Street address |
269 Campus Dr. CCSR 2150
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| City |
Stanford |
| State/province |
CA |
| ZIP/Postal code |
94305 |
| Country |
USA |
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| Platforms (2) |
| GPL9250 |
Illumina Genome Analyzer II (Mus musculus) |
| GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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| Samples (11)
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| Relations |
| BioProject |
PRJNA239352 |
| SRA |
SRP038929 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE55338_RAW.tar |
691.1 Mb |
(http)(custom) |
TAR (of BEDGRAPH) |
| GSE55338_cMycPlusMinus.exp.txt.gz |
337.7 Kb |
(ftp)(http) |
TXT |
| GSE55338_dcrWTKO.exp.txt.gz |
1.4 Mb |
(ftp)(http) |
TXT |
SRA Run Selector |
| Raw data are available in SRA |
| Processed data provided as supplementary file |
| Processed data are available on Series record |
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