ArticlePloS one2012
Dynamic status of REST in the mouse ESC pluripotency network.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- REST in the Road Map of Brain Development.Cellular and molecular neurobiology · 2023Review
- Roles of the Neuron-Restrictive Silencer Factor in the Pathophysiological Process of the Central Nervous System.Frontiers in cell and developmental biology · 2022Review
- REST represses miR-124 and miR-203 to regulate distinct oncogenic properties of glioblastoma stem cells.Neuro-oncology · 2017Article
- REST is a crucial regulator for acquiring EMT-like and stemness phenotypes in hormone-refractory prostate cancer.Scientific reports · 2017Article
- The Importance of REST for Development and Function of Beta Cells.Frontiers in cell and developmental biology · 2017Review
- Mir-21-Sox2 Axis Delineates Glioblastoma Subtypes with Prognostic Impact.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- REST-miR-21-SOX2 axis maintains pluripotency in E14Tg2a.4 embryonic stem cells.Stem cell research · 2015Article
- NRSF: an angel or a devil in neurogenesis and neurological diseases.Journal of molecular neuroscience : MN · 2015Review
- A comparison of the rest complex binding patterns in embryonic stem cells and epiblast stem cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundREST is abundantly expressed in mouse embryonic stem cells (ESCs). Many genome-wide analyses have found REST to be an integral part of the ESC pluripotency network. However, experimental systems have produced contradictory findings: (1) REST is required for the maintenance of ESC pluripotency and loss of REST causes increased expression of differentiation markers, (2) REST is not required for the maintenance of ESC pluripotency and loss of REST does not change expression of differentiation markers, and (3) REST is not required for the maintenance of ESC pluripotency but loss of REST causes decreased expression of differentiation markers. These reports highlight gaps in our knowledge of the ESC network.
methodsEmploying biochemical and genome-wide analyses of various culture conditions and ESC lines, we have attempted to resolve some of the discrepancies in the literature.
resultsWe show that Rest+/- and Rest-/- AB-1 mutant ESCs, which did not exhibit a role of REST in ESC pluripotency when cultured in the presence of feeder cells, did show impaired self-renewal when compared with the parental cells under feeder-free culture conditions, but only in early passage cells. In late passage cells, both Rest+/- and Rest-/- AB-1 ESCs restored pluripotency, suggesting a passage and culture condition-dependent response. Genome-wide analysis followed by biochemical validation supported this response and further indicated that the restoration of pluripotency was associated by increased expression of the ESC pluripotency factors. E14Tg2a.4 ESCs with REST-knockdown, which earlier showed a REST-dependent pluripotency when cultured under feeder-free conditions, as well as Rest-/- AB-1 ESCs, showed no REST-dependent pluripotency when cultured in the presence of either feeder cells or laminin, indicating that extracellular matrix components can rescue REST's role in ESC pluripotency.
conclusionsREST regulates ESC pluripotency in culture condition- and ESC line-dependent fashion and ESC pluripotency needs to be evaluated in a context dependent manner.
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Registered trials
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