2015
DOI: 10.15252/embj.201490649
|View full text |Cite
|
Sign up to set email alerts
|

Reprogramming of cell fate: epigenetic memory and the erasure of memories past

Abstract: Cell identity is a reflection of a cell type-specific gene expression profile, and consequently, cell type-specific transcription factor networks are considered to be at the heart of a given cellular phenotype. Although generally stable, cell identity can be reprogrammed in vitro by forced changes to the transcriptional network, the most dramatic example of which was shown by the induction of pluripotency in somatic cells by the ectopic expression of defined transcription factors alone. Although changes to cel… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

1
121
0

Year Published

2015
2015
2020
2020

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 153 publications
(122 citation statements)
references
References 128 publications
(198 reference statements)
1
121
0
Order By: Relevance
“…In particular, its efficiency remains low (Mikkelsen et al, 2008;Pasque et al, 2012;Gaspar-Maia et al, 2013;Sridharan et al, 2013;Nashun et al, 2015), the extreme stability of adult somatic cell epigenetic signature makes iPSCs prone to errors (Plath and Lowry, 2011), and the use of DNA constructs and the subsequent possibility of exogenous sequence integration preclude their clinical use for safety concerns (Stadtfeld et al, 2008;Kim et al, 2009;Zhou and Freed, 2009;Seki et al, 2010). In order to circumvent these limits, smallmolecule compounds have been used to modulate the epigenetic state by inhibiting and/or activating, in a reversible way, specific signaling pathways (Huangfu et al, 2008;Ichida et al, 2009;Li et al, 2011;Hou et al, 2013).…”
Section: Erasing Of "Epigenetic Memory"mentioning
confidence: 99%
“…In particular, its efficiency remains low (Mikkelsen et al, 2008;Pasque et al, 2012;Gaspar-Maia et al, 2013;Sridharan et al, 2013;Nashun et al, 2015), the extreme stability of adult somatic cell epigenetic signature makes iPSCs prone to errors (Plath and Lowry, 2011), and the use of DNA constructs and the subsequent possibility of exogenous sequence integration preclude their clinical use for safety concerns (Stadtfeld et al, 2008;Kim et al, 2009;Zhou and Freed, 2009;Seki et al, 2010). In order to circumvent these limits, smallmolecule compounds have been used to modulate the epigenetic state by inhibiting and/or activating, in a reversible way, specific signaling pathways (Huangfu et al, 2008;Ichida et al, 2009;Li et al, 2011;Hou et al, 2013).…”
Section: Erasing Of "Epigenetic Memory"mentioning
confidence: 99%
“…Maintenance of a specific cellular phenotype depends on the continued transcription of cell-type-specific genes, largely through open chromatin architecture (3,4) maintained by a small group of lineage-restricted DNA-binding transcription factors (TFs) (5,6) that establish a unique transcriptional regulatory network (7). Many physiologic or pathophysiologic perturbations can affect the differentiated state of a cell quantitatively, but fewer affect the state of differentiation qualitatively.…”
mentioning
confidence: 99%
“…The sequence of biochemical changes required to establish a new stable chromatin environment at active enhancers remains poorly defined. In some systems, changing the chromatin environment requires passage through DNA replication, hence stripping of chromatin to re-establish a new chromatin environment (MacAlpine and Almouzni 2013; Nashun et al 2015). It is an open question whether passage through DNA replication is needed for all pioneers (Iwafuchi-Doi and Zaret 2014), but for Pax7, the activation of target genes that require pioneering is far slower than for transcriptional activation of enhancers/genes that are already in an open active chromatin conformation.…”
Section: The Essence Of Pioneeringmentioning
confidence: 99%