Published in Advance December 21, 2009,
doi: 10.1261/rna.1441510
RNA vol. 16: no. 2, pp. 324-337 (February, 2010).
http://rnajournal.cshlp.org/content/16/2/324.abstract?


"Conserved long noncoding RNAs transcriptionally regulated by Oct4 and Nanog modulate pluripotency in mouse embryonic stem cells".

Jameelah S. Mohamed 1, Philip M. Gaughwin 2, Bing Lim 1, 3, Paul Robson 1, 4 and Leonard Lipovich 5, @

1 Stem Cell and Developmental Biology, Genome Institute of Singapore, 138672 Singapore
2 Neuronal Survival Unit, Lund University, 221-84 Lund, Sweden
3 Harvard Institutes of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
4 Department of Biological Sciences, National University of Singapore, 117543 Singapore
5 Center for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan 48201 USA

@ Center for Molecular Medicine and Genetics, Wayne State University, 3228 Scott Hall, 540 E. Canfield Street, Detroit, MI 48201 USA;
e-mail:    llipovich@med.wayne.edu                 fax: (313) 577-5218.


Abstract:

The genetic networks controlling stem cell identity are the focus of intense interest, due to their obvious therapeutic potential as well as exceptional relevance to models of early development. Genome-wide mapping of transcriptional networks in mouse embryonic stem cells (mESCs) reveals that many endogenous noncoding RNA molecules, including long noncoding RNAs (lncRNAs), may play a role in controlling the pluripotent state. We performed a genome-wide screen that combined full-length mESC transcriptome genomic mapping data with chromatin immunoprecipitation genomic location maps of the key mESC transcription factors Oct4 and Nanog. We henceforth identified four mESC-expressed, conserved lncRNA-encoding genes residing proximally to active genomic binding sites of Oct4 and Nanog. Accordingly, these four genes have potential roles in pluripotency. We show that two of these lncRNAs, AK028326 (Oct4-activated) and AK141205 (Nanog-repressed), are direct targets of Oct4 and Nanog. Most importantly, we demonstrate that these lncRNAs are not merely controlled by mESC transcription factors, but that they themselves regulate developmental state: knockdown and overexpression of these transcripts lead to robust changes in Oct4 and Nanog mRNA levels, in addition to alterations in cellular lineage-specific gene expression and in the pluripotency of mESCs. We further characterize AK028326 as a co-activator of Oct4 in a regulatory feedback loop. These results for the first time implicate lncRNAs in the modulation of mESC pluripotency and expand the established mESC regulatory network model to include functional lncRNAs directly controlled by key mESC transcription factors.



Additional References:

1. Li S-D, Chono S, and Huang L,
"Efficient Oncogene Silencing and Metastasis Inhibition via Systemic Delivery of siRNA",
Molecular Therapy vol. 16, no.  5, pp. 942–946 (May, 2008).)

2. Guttman M, Amit I, Garber M, French C, Lin MF, Feldser D, Huarte M, Zuk O, Carey BW, Cassady JP, Cabili MN, Jaenisch R, Mikkelsen TS, Jacks T, Hacohen N, Bernstein BE, Kellis M, Regev A, Rinn JL, Lander ES. ( March, 2009 ).
"Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals".

3. Khalil AM, Guttman M, Huarte M, Garber M, Raj A, Rivea Morales D, Thomas K, Presser A, Bernstein BE, van Oudenaarden A, Regev A, Lander ES, Rinn JL. ( July 14, 2009 ).
"Many human large intergenic noncoding RNAs associate with chromatin-modifying complexes and affect gene expression".

4. Frenster JH, and Hovsepian JA,  (Dec. 2008a)
"Models of successive levels of resolution during individual gene transcription".

5. Whitehead J, Pandey GK, Kanduri C., (Sept. 2009).
"Regulation of the mammalian epigenome by long noncoding RNAs".
Biochim Biophys A009 Sep;1790(9):936-47.

6. Eminli S, Foudi A, Stadtfeld M, Maherali N, Ahfeldt T, Mostoslavsky G, Hock H, Hochedlinger K.
"Differentiation stage determines potential of hematopoietic cells for reprogramming into induced pluripotent stem cells".

7. Mishra PJ,  and Merlino G,
"MicroRNA reexpression as differentiation therapy in cancer".

8. Taulli R, Bersani F, Foglizzo V, Linari A, Vigna E, Ladanyi M, Tuschl T, and Ponzetto C,
"The muscle-specific microRNA miR-206 blocks human rhabdomyosarcoma growth in xenotransplanted mice by promoting myogenic differentiation".

9. Li L, Feng T, Lian Y, Zhang G, Garen A, and Song X, (2009).
"Role of human noncoding RNAs in the control of tumorigenesis".

10. Kim HH, Kuwano Y, Srikantan S, Lee EK, Martindale JL, and Gorospe M, (2009).
"HuR recruits let-7/RISC to repress c-Myc expression".



Conclusions from Embryoma Genomics:

1. Each cell retains all of its embryonic genes for a lifetime.

2. Controls for embryonic genes are often absent in adults.

3. Uncontrolled embryonic genes can replicate wildly.

4.  Replicating genes participate in  intra-cellular competition.

5.  The basis for gene competition is selective transcription.

6.  MicroRNAs can reprogram embryomic transcription.

7.  Gene reprogramming can produce normal phenotypes.

8.  Normal phenotypes can by-pass chromosomal lesions.

9.  MicroRNA therapy may need to be permanent.

10. Transplantation of microRNAs could be preferred.

http://www.embryomas.net/




Conclusions from Euchromatin Thermodynamic Pathways.

1. Pathways within cell genomes involve a flow of information.

2. Information can flow by direct contact or by third parties.

3. Direct contact within whole genomes is difficult to regulate.

4. DNA-DNA direct contects are influenced by agents.

5. Nuclear agents include hydrophilic ionic and hydrophobic conforming ligands.

6. Third parties within genomes involve RNAs and proteins.

7.  RNAs and proteins are easy to regulate or reverse.

8.  Information can be shared, lost, or transformed.

9. System information can be hidden during system isolation.

10.  Local information can be permanently lost during system entropy.

http://www.embryomas.net/




Further Topics in:  Euchromatin,  active DNA, and  RNA  ribo-regulators:

Links to Current Research in Euchromatin:
Links to Euchromatin Activator RNA Reviews:
Links to Euchromatin Activator RNA Research:
Links to Ultrastructural Probes of DNase I-Sensitive Sites:
Links to RNA as a Therapeutic Agent:
Links to Hodgkin Lymphoma Immuno-Pathology:
Links to Activated T-Lymphocyte Immunotherapy:
Links to Medical Systems Biology:
Links to Selective Gene Transcription:
Links to RNA-Induced Epigenetics:
Links to RNA-Induced Embryogenesis:
Links to RNA and Biological Causality:
Links to Reprogramming and Neoplasia:

A Brief History of Activator RNA:

"Ultrastructural Probes of Active DNA Sites, and the RNA Activators of DNA".
(PowerPoint Presentation).


Top of Page - Euchromatin NetworkEuchromatin ResearchResearch in Quantitative Radiology


For Further Information and Feedback:

Jeannette A. Hovsepian, M.D.
E-mail: frensasc@ix.netcom.com
Phone:  +1 650 367 6483



euchromatin: "the most active portion of the genome within the cell nucleus".
embryoma:  "adult neoplasm expressing one or more embryo-exclusive genes".
entropy:  "maximum entropy defines the isolated reaction steady-state equilibrium".