The Long Noncoding RNA RMST Interacts with SOX2 to Regulate Neurogenesis

Ng, Shi‐Yan; Bogu, Gireesh K.; Soh, Boon Seng; Stanton, Lawrence W.

doi:10.1016/j.molcel.2013.07.017

Cited by 397 publications

(349 citation statements)

References 41 publications

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“…Another group who conducted SOX2 ChIP-seq in hNPCs using the same antibody obtained a similar result of 55 771 peaks; in contrast, a small number of altered genes upon SOX2 KD were detected in hNPCs [55]. This could be due to the functional redundancy of SoxB1 family members.…”

Section: Discussionmentioning

confidence: 80%

Comprehensive profiling reveals mechanisms of SOX2-mediated cell fate specification in human ESCs and NPCs

et al. 2016

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SOX2 is a key regulator of multiple types of stem cells, especially embryonic stem cells (ESCs) and neural progenitor cells (NPCs).Understanding the mechanism underlying the function of SOX2 is of great importance for realizing the full potential of ESCs and NPCs. Here, through genome-wide comparative studies, we show that SOX2 executes its distinct functions in human ESCs (hESCs) and hESC-derived NPCs (hNPCs) through cell type-and stage-dependent transcription programs. Importantly, SOX2 suppresses non-neural lineages in hESCs and regulates neurogenesis from hNPCs by inhibiting canonical Wnt signaling. In hESCs, SOX2 achieves such inhibition by direct transcriptional regulation of important Wnt signaling modulators, WLS and SFRP2. Moreover, SOX2 ensures pluripotent epigenetic landscapes via interacting with histone variant H2A.Z and recruiting polycomb repressor complex 2 to poise developmental genes in hESCs. Together, our results advance our understanding of the mechanism by which cell type-specific transcription factors control lineage-specific gene expression programs and specify cell fate.

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Section: Discussionmentioning

confidence: 80%

Comprehensive profiling reveals mechanisms of SOX2-mediated cell fate specification in human ESCs and NPCs

et al. 2016

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“…Interestingly, it was reported by others that binding to a noncoding RNA allows SOX2 recruitment to promoter regions of neurogenic TFs (50). It is tempting to speculate that a similar role for RNA exists at pluripotency genes regulated by SOX2 in ESCs.…”

Section: Discussionmentioning

confidence: 93%

Functional and mechanistic studies of XPC DNA-repair complex as transcriptional coactivator in embryonic stem cells

Cattoglio

Zhang

Grubisic

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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The embryonic stem cell (ESC) state is transcriptionally controlled by OCT4, SOX2, and NANOG with cofactors, chromatin regulators, noncoding RNAs, and other effectors of signaling pathways. Uncovering components of these regulatory circuits and their interplay provides the knowledge base to deploy ESCs and induced pluripotent stem cells. We recently identified the DNA-repair complex xeroderma pigmentosum C (XPC)-RAD23B-CETN2 as a stem cell coactivator (SCC) required for OCT4/SOX2 transcriptional activation. Here we investigate the role of SCC genome-wide in murine ESCs by mapping regions bound by RAD23B and analyzing transcriptional profiles of SCC-depleted ESCs. We establish OCT4 and SOX2 as the primary transcription factors recruiting SCC to regulatory regions of pluripotency genes and identify the XPC subunit as essential for interaction with the two proteins. The present study reveals new mechanistic and functional aspects of SCC transcriptional activity, and thus underscores the diversified functions of this regulatory complex.transcription | pluripotency | protein-protein interactions | ChIP-seq | RNA-seq

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“…Likewise, the number of genes regulated by Hnrnpk knockdown in reprogramming exceeds those regulated by lincRNA-p21 knockdown. In this regard, HNRNPK and other members of the hnRNP family interact with multiple lincRNAs [29,30]. This makes it tempting to speculate that hnRNP proteins are widespread mediators of lincRNA function in reprogramming, which act by facilitating the assembly of various chromatin complexes (activating or repressive) at specific loci.…”

Section: Discussionmentioning

confidence: 99%

The p53-induced lincRNA-p21 derails somatic cell reprogramming by sustaining H3K9me3 and CpG methylation at pluripotency gene promoters

et al. 2014

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Recent studies have boosted our understanding of long noncoding RNAs (lncRNAs) in numerous biological processes, but few have examined their roles in somatic cell reprogramming. Through expression profiling and functional screening, we have identified that the large intergenic noncoding RNA p21 (lincRNA-p21) impairs reprogramming. Notably, lincRNA-p21 is induced by p53 but does not promote apoptosis or cell senescence in reprogramming. Instead, lincRNA-p21 associates with the H3K9 methyltransferase SETDB1 and the maintenance DNA methyltransferase DNMT1, which is facilitated by the RNA-binding protein HNRNPK. Consequently, lincRNA-p21 prevents reprogramming by sustaining H3K9me3 and/or CpG methylation at pluripotency gene promoters. Our results provide insight into the role of lncRNAs in reprogramming and establish a novel link between p53 and heterochromatin regulation.

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The Long Noncoding RNA RMST Interacts with SOX2 to Regulate Neurogenesis

Cited by 397 publications

References 41 publications

Comprehensive profiling reveals mechanisms of SOX2-mediated cell fate specification in human ESCs and NPCs

Comprehensive profiling reveals mechanisms of SOX2-mediated cell fate specification in human ESCs and NPCs

Functional and mechanistic studies of XPC DNA-repair complex as transcriptional coactivator in embryonic stem cells

The p53-induced lincRNA-p21 derails somatic cell reprogramming by sustaining H3K9me3 and CpG methylation at pluripotency gene promoters

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