 |
 |
GEO help: Mouse over screen elements for information. |
|
| Status |
Public on Sep 01, 2008 |
| Title |
Sall4 ChIP-chip in mouse ES cell line W4 using NimbleGen MM8 RefSeq Promoter array (2.5kb) |
| Organism |
Mus musculus |
| Experiment type |
Genome binding/occupancy profiling by genome tiling array
|
| Summary |
Embryonic stem cells have potential utility in regenerative medicine due to their pluripotent characteristics. Sall4, a zinc-finger transcription factor, is expressed very early in embryonic development with Oct4 and Nanog, two well characterized pluripotency regulators. Sall4 plays an important role in governing the fate of stem cells through transcriptional regulation of both Oct4 and Nanog. Using chromatin immunoprecipitation coupled to microarray hybridization (ChIP on Chip), we have mapped global gene targets of Sall4 unveiling possible regulation of broad ES cell functions. Approximately 5,000 genes were identified that were bound by the Sall4 protein and many of these have major functions in developmental and regulatory pathways. Sall4 bound more than six times as many annotated genes within promoter regions as Oct4 and twice as many as Nanog. Immunoprecipitation revealed a heterotrimeric protein complex between Sall4, Oct4, and Nanog, consistent with binding site co-occupancies. Further, Sall4 bound many genes that are regulated in part by the chromatin-based epigenetic events mediated by polycomb-repressive complexes and bivalent domains. This suggests that Sall4 plays a central and diverse role in regulating stem cell pluripotency during early embryonic development that involves integration of transcriptional and epigenetic control processes.
Keywords: ChIP-chip
|
| |
|
| Overall design |
We used ChIP-chip to map global promoter bound by Sall4, a zinc finger transcription factor. Growing evidence has suggested that Sall4 plays a vital role in ES cell pluripotency maintenance. Evidence for this includes its recent use as a marker for somatic cell reprogramming, in a genetic signature for ES cells, and evidence that Sall4 enhances reprogramming. These recent findings and two previously described interactions with Oct4 and Nanog strongly support the role of Sall4 in ES cells. This hypothesis was furthered here as we show that Sall4 plays important roles through transcriptional regulation of vital ES cell genes.
|
| |
|
| Contributor(s) |
Yang J, Chai L, Fowles TC, Alipio Z, Xu D, Fink LM, Ward DC, Ma Y |
| Citation(s) |
19060217 |
| |
| Submission date |
Apr 30, 2008 |
| Last update date |
Mar 19, 2012 |
| Contact name |
Yupo Ma |
| E-mail(s) |
[email protected]
|
| URL |
http://www.nevadacancerinstitute.org
|
| Organization name |
Nevada Cancer Institute
|
| Lab |
4
|
| Street address |
1 Breakthrough Way
|
| City |
Las Vegas |
| State/province |
NV |
| ZIP/Postal code |
89135 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL6797 |
Nevada Cancer Institute MM8 RefSeq Promoter tiling array 386K |
|
| Samples (2) |
| GSM285607 |
SALL4 ChIP-chip in W4 mouse ES cells |
| GSM285642 |
Replicate Sall4 ChIP-chip in W4 ES cells |
|
| Relations |
| BioProject |
PRJNA106613 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE11305_RAW.tar |
23.8 Mb |
(http)(custom) |
TAR (of TXT) |
| Processed data included within Sample table |
|
|
|
|
 |
