Transcription levels of a long noncoding RNA shape a cell fate regulatory circuit (mRNA-seq)
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ABSTRACT:
PROVIDER: PRJNA577696 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10283164.fastq.gz | Fastqsanger.gz | |||
| SRR10283165.fastq.gz | Fastqsanger.gz | |||
| SRR10283166.fastq.gz | Fastqsanger.gz | |||
| SRR10283167.fastq.gz | Fastqsanger.gz | |||
| SRR10283168.fastq.gz | Fastqsanger.gz |
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Project description:Transcription levels of a long noncoding RNA shape a cell fate regulatory circuit (TES-seq)
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Project description:Long noncoding RNAs (lncRNA) play diverse roles in gene regulation controlling key cellular processes, most notably, cell-fate programming {Anderson, 2016 #20;Flynn, 2014 #16;Guttman, 2011 #35;Wang, 2011 #18}. Many long noncoding RNAs (lncRNAs) act in cis through transcription-coupled chromatin alterations that drive changes in local gene expression { Martens, 2004 #47; Kim, 2012 #74;van Werven, 2012 #57;Hainer, 2011 #73;Kim, 2016 #41;Ard, 2016 #21;Latos, 2012 #7}. How transcription of some lncRNAs leads to activation of gene expression, while others inhibit and repress gene expression remains poorly understood {Kornienko, 2013 #17}. Here we investigated in S. cerevisiae the function of the lncRNA IRT2, which is expressed upstream in the promoter of the master regulator for entry into meiosis, IME1. We report the surprising finding that distinct levels of IRT2 transcription regulates opposing chromatin and transcription states in order to ensure that only diploids, and not haploids, enter meiosis and form gametes. In haploid cells, IRT2 transcription at very low levels is required for the correct induction of the adjacent lncRNA IRT1, which in turn represses the IME1 promoter and prevents meiotic entry {van Werven, 2012 #57}. Low levels of IRT2 transcription stimulates histone exchange delivering acetylated histone H3 lysine 56 (H3K56ac) to chromatin, thereby facilitating chromatin disassembly and recruitment of the transcriptional activator of IRT1, Rme1. Inhibiting IRT2 transcription, or mutations that resulted in cells lacking H3K56ac impairs Rme1 recruitment and IRT1 induction, and consequently haploid cells induce IME1 and undergo a lethal meiosis. In contrast to its function at low levels, increasing IRT2 transcription enhances transcription-coupled chromatin assembly and interferes with IRT1 expression, promoting IME1 expression and meiotic entry in diploid cells {Moretto, 2018 #10}. Thus, transcription of lncRNAs, even at very low levels, can play an important role in regulating gene expression, and changes in lncRNA transcription levels can confer distinct regulatory and cell fate outcomes.
2020-12-15 | GSE138897 | GEO
Project description:Long noncoding RNAs (lncRNA) play diverse roles in gene regulation controlling key cellular processes, most notably, cell-fate programming {Anderson, 2016 #20;Flynn, 2014 #16;Guttman, 2011 #35;Wang, 2011 #18}. Many long noncoding RNAs (lncRNAs) act in cis through transcription-coupled chromatin alterations that drive changes in local gene expression { Martens, 2004 #47; Kim, 2012 #74;van Werven, 2012 #57;Hainer, 2011 #73;Kim, 2016 #41;Ard, 2016 #21;Latos, 2012 #7}. How transcription of some lncRNAs leads to activation of gene expression, while others inhibit and repress gene expression remains poorly understood {Kornienko, 2013 #17}. Here we investigated in S. cerevisiae the function of the lncRNA IRT2, which is expressed upstream in the promoter of the master regulator for entry into meiosis, IME1. We report the surprising finding that distinct levels of IRT2 transcription regulates opposing chromatin and transcription states in order to ensure that only diploids, and not haploids, enter meiosis and form gametes. In haploid cells, IRT2 transcription at very low levels is required for the correct induction of the adjacent lncRNA IRT1, which in turn represses the IME1 promoter and prevents meiotic entry {van Werven, 2012 #57}. Low levels of IRT2 transcription stimulates histone exchange delivering acetylated histone H3 lysine 56 (H3K56ac) to chromatin, thereby facilitating chromatin disassembly and recruitment of the transcriptional activator of IRT1, Rme1. Inhibiting IRT2 transcription, or mutations that resulted in cells lacking H3K56ac impairs Rme1 recruitment and IRT1 induction, and consequently haploid cells induce IME1 and undergo a lethal meiosis. In contrast to its function at low levels, increasing IRT2 transcription enhances transcription-coupled chromatin assembly and interferes with IRT1 expression, promoting IME1 expression and meiotic entry in diploid cells {Moretto, 2018 #10}. Thus, transcription of lncRNAs, even at very low levels, can play an important role in regulating gene expression, and changes in lncRNA transcription levels can confer distinct regulatory and cell fate outcomes.
2020-12-15 | GSE138896 | GEO
Project description:Long noncoding RNAs (lncRNA) play diverse roles in gene regulation controlling key cellular processes, most notably, cell-fate programming {Anderson, 2016 #20;Flynn, 2014 #16;Guttman, 2011 #35;Wang, 2011 #18}. Many long noncoding RNAs (lncRNAs) act in cis through transcription-coupled chromatin alterations that drive changes in local gene expression { Martens, 2004 #47; Kim, 2012 #74;van Werven, 2012 #57;Hainer, 2011 #73;Kim, 2016 #41;Ard, 2016 #21;Latos, 2012 #7}. How transcription of some lncRNAs leads to activation of gene expression, while others inhibit and repress gene expression remains poorly understood {Kornienko, 2013 #17}. Here we investigated in S. cerevisiae the function of the lncRNA IRT2, which is expressed upstream in the promoter of the master regulator for entry into meiosis, IME1. We report the surprising finding that distinct levels of IRT2 transcription regulates opposing chromatin and transcription states in order to ensure that only diploids, and not haploids, enter meiosis and form gametes. In haploid cells, IRT2 transcription at very low levels is required for the correct induction of the adjacent lncRNA IRT1, which in turn represses the IME1 promoter and prevents meiotic entry {van Werven, 2012 #57}. Low levels of IRT2 transcription stimulates histone exchange delivering acetylated histone H3 lysine 56 (H3K56ac) to chromatin, thereby facilitating chromatin disassembly and recruitment of the transcriptional activator of IRT1, Rme1. Inhibiting IRT2 transcription, or mutations that resulted in cells lacking H3K56ac impairs Rme1 recruitment and IRT1 induction, and consequently haploid cells induce IME1 and undergo a lethal meiosis. In contrast to its function at low levels, increasing IRT2 transcription enhances transcription-coupled chromatin assembly and interferes with IRT1 expression, promoting IME1 expression and meiotic entry in diploid cells {Moretto, 2018 #10}. Thus, transcription of lncRNAs, even at very low levels, can play an important role in regulating gene expression, and changes in lncRNA transcription levels can confer distinct regulatory and cell fate outcomes.
2020-12-15 | GSE138893 | GEO
Project description:Long noncoding RNAs (lncRNA) play diverse roles in gene regulation controlling key cellular processes, most notably, cell-fate programming {Anderson, 2016 #20;Flynn, 2014 #16;Guttman, 2011 #35;Wang, 2011 #18}. Many long noncoding RNAs (lncRNAs) act in cis through transcription-coupled chromatin alterations that drive changes in local gene expression { Martens, 2004 #47; Kim, 2012 #74;van Werven, 2012 #57;Hainer, 2011 #73;Kim, 2016 #41;Ard, 2016 #21;Latos, 2012 #7}. How transcription of some lncRNAs leads to activation of gene expression, while others inhibit and repress gene expression remains poorly understood {Kornienko, 2013 #17}. Here we investigated in S. cerevisiae the function of the lncRNA IRT2, which is expressed upstream in the promoter of the master regulator for entry into meiosis, IME1. We report the surprising finding that distinct levels of IRT2 transcription regulates opposing chromatin and transcription states in order to ensure that only diploids, and not haploids, enter meiosis and form gametes. In haploid cells, IRT2 transcription at very low levels is required for the correct induction of the adjacent lncRNA IRT1, which in turn represses the IME1 promoter and prevents meiotic entry {van Werven, 2012 #57}. Low levels of IRT2 transcription stimulates histone exchange delivering acetylated histone H3 lysine 56 (H3K56ac) to chromatin, thereby facilitating chromatin disassembly and recruitment of the transcriptional activator of IRT1, Rme1. Inhibiting IRT2 transcription, or mutations that resulted in cells lacking H3K56ac impairs Rme1 recruitment and IRT1 induction, and consequently haploid cells induce IME1 and undergo a lethal meiosis. In contrast to its function at low levels, increasing IRT2 transcription enhances transcription-coupled chromatin assembly and interferes with IRT1 expression, promoting IME1 expression and meiotic entry in diploid cells {Moretto, 2018 #10}. Thus, transcription of lncRNAs, even at very low levels, can play an important role in regulating gene expression, and changes in lncRNA transcription levels can confer distinct regulatory and cell fate outcomes.
2020-12-15 | GSE138895 | GEO
Project description:Transcription levels of a noncoding RNA orchestrate opposing regulatory and cell fate outcomes in yeast
| PRJNA577695 | ENA
Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
| 2330122 | ecrin-mdr-crc
Project description: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. RNA was sequenced from WT and Dcr KO mESCs and the expression of lncRNAs and mRNAs are compared between WT and Dcr KO mESCs.
2014-06-15 | E-GEOD-55338 | biostudies-arrayexpress