CoChat
Sign Up
Cited by 155

The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.

Molecular features of cellular reprogramming and development

Smith, Zachary D., Sindhu, Camille, Meissner, Alexander·2016·Nature Reviews Molecular Cell Biology
DOI 10.1038/nrm.2016.6
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nrm.2016.6

Cites

26 of 26 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • MYC is considered one of the most potent amplifiers of reprogramming.

    “it is considered one of the most potent amplifiers of reprogramming 58 .”

    From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [58]

    The section “Transcriptional changes during early reprogramming” (page unavailable) says MYC enhances transcription of responsive cell-cycle genes after OSKM induction, supporting a role in early reprogramming. It does not rank MYC among the most potent amplifiers of reprogramming; the amplification described is of transcription, not reprogramming itself. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • The earliest phenotypic and transcriptional changes following OSKM expression begin with an immediate increase in cell proliferation induced by MYC.

    “The earliest phenotypic and transcriptional changes following OSKM expression begin with an immediate increase in cell proliferation induced by MYC 58 .”

    From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [58]

  • Cells switch from oxidative phosphorylation to glycolysis during the early reprogramming phase.

    “Interestingly, cells switch from oxidative phosphorylation to glycolysis during this early reprogramming phase 58 .”

    From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [58]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 195

  1. Takahashi, K. & Yamanaka, S. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell 126, 663–676 (2006). · DOI · Paper page
  2. Davis, R. L., Weintraub, H. & Lassar, A. B. Expression of a single transfected cDNA converts fibroblasts to myoblasts. Cell 51, 987–1000 (1987). · DOI
  3. Su, A. I. et al. Large-scale analysis of the human and mouse transcriptomes. Proc. Natl Acad. Sci. USA 99, 4465–4470 (2002). · DOI · Paper page
  4. Graf, T. & Enver, T. Forcing cells to change lineages. Nature 462, 587–594 (2009). · DOI · Paper page
  5. Kondoh, H. & Kamachi, Y. SOX-partner code for cell specification: regulatory target selection and underlying molecular mechanisms. Int. J. Biochem. Cell Biol. 42, 391–399 (2010). · DOI
  6. Masui, S. et al. Pluripotency governed by Sox2 via regulation of Oct3/4 expression in mouse embryonic stem cells. Nat. Cell Biol. 9, 625–635 (2007). · DOI
  7. Miyagi, S. et al. Consequence of the loss of Sox2 in the developing brain of the mouse. FEBS Lett. 582, 2811–2815 (2008). · DOI
  8. Sarkar, A. & Hochedlinger, K. The Sox family of transcription factors: versatile regulators of stem and progenitor cell fate. Cell Stem Cell 12, 15–30 (2013). · DOI
  9. Lodato, M. A. et al. SOX2 co-occupies distal enhancer elements with distinct POU factors in ESCs and NPCs to specify cell state. PLoS Genet. 9, e1003288 (2013). · DOI
  10. Ieda, M. et al. Direct reprogramming of fibroblasts into functional cardiomyocytes by defined factors. Cell 142, 375–386 (2010). · DOI · Paper page
  11. D'Alessio, A. C. et al. A systematic approach to identify candidate transcription factors that control cell identity. Stem Cell Rep. 5, 763–775 (2015). · DOI · Paper page
  12. Lupien, M. et al. FoxA1 translates epigenetic signatures into enhancer-driven lineage-specific transcription. Cell 132, 958–970 (2008). · DOI · Paper page
  13. Arvey, A., Agius, P., Noble, W. S. & Leslie, C. Sequence and chromatin determinants of cell-type-specific transcription factor binding. Genome Res. 22, 1723–1734 (2012). · DOI
  14. ENCODE Project Consortium. An integrated encyclopedia of DNA elements in the human genome. Nature 489, 57–74 (2012). · DOI · Paper page
  15. Mikkelsen, T. S. et al. Dissecting direct reprogramming through integrative genomic analysis. Nature 454, 49–55 (2008). · DOI
  16. Zunder, E. R., Lujan, E., Goltsev, Y., Wernig, M. & Nolan, G. P. A continuous molecular roadmap to iPSC reprogramming through progression analysis of single-cell mass cytometry. Cell Stem Cell 16, 323–337 (2015). · DOI
  17. Hansson, J. et al. Highly coordinated proteome dynamics during reprogramming of somatic cells to pluripotency. Cell Rep. 2, 1579–1592 (2012). · DOI · Paper page
  18. Guo, S. et al. Nonstochastic reprogramming from a privileged somatic cell state. Cell 156, 649–662 (2014). · DOI
  19. Smith, Z. D., Nachman, I., Regev, A. & Meissner, A. Dynamic single-cell imaging of direct reprogramming reveals an early specifying event. Nat. Biotechnol. 28, 521–526 (2010). · DOI
  20. Brambrink, T. et al. Sequential expression of pluripotency markers during direct reprogramming of mouse somatic cells. Cell Stem Cell 2, 151–159 (2008). · DOI
  21. Samavarchi-Tehrani, P. et al. Functional genomics reveals a BMP-driven mesenchymal-to-epithelial transition in the initiation of somatic cell reprogramming. Cell Stem Cell 7, 64–77 (2010). · DOI · Paper page
  22. Hussein, S. M. et al. Genome-wide characterization of the routes to pluripotency. Nature 516, 198–206 (2014). · DOI · Paper page
  23. Koche, R. P. et al. Reprogramming factor expression initiates widespread targeted chromatin remodeling. Cell Stem Cell 8, 96–105 (2011). · DOI · Paper page
  24. Sridharan, R. et al. Role of the murine reprogramming factors in the induction of pluripotency. Cell 136, 364–377 (2009). · DOI
  25. Lee, D. S. et al. An epigenomic roadmap to induced pluripotency reveals DNA methylation as a reprogramming modulator. Nat. Commun. 5, 5619 (2014). · DOI · Paper page
  26. Onder, T. T. et al. Chromatin-modifying enzymes as modulators of reprogramming. Nature 483, 598–602 (2012). · DOI
  27. Liang, G., He, J. & Zhang, Y. Kdm2b promotes induced pluripotent stem cell generation by facilitating gene activation early in reprogramming. Nat. Cell Biol. 14, 457–466 (2012). References 31 and 32 identify the H3K79 methyltransferase DOT1L and the H3K36 demethylase KDM2B as participating in the early disassembly of epigenetic modifications associated with transcription elongation at somatically active genes. · DOI
  28. Mansour, A. A. et al. The H3K27 demethylase Utx regulates somatic and germ cell epigenetic reprogramming. Nature 488, 409–413 (2012). This work reveals that the H3K27 demethylase UTX participates in the activation of pluripotency-associated genes by removing differentiation-associated repressive modifications at CpG island-containing promoters. · DOI
  29. Ramirez-Carrozzi, V. R. et al. A unifying model for the selective regulation of inducible transcription by CpG islands and nucleosome remodeling. Cell 138, 114–128 (2009). · DOI
  30. Kim, J. et al. A Myc network accounts for similarities between embryonic stem and cancer cell transcription programs. Cell 143, 313–324 (2010). Kim et al . demonstrate that transcriptional signatures shared between ES cells and hyperproliferative cancer cell models reflect a discrete MYC-driven genetic module that is separate from that of OCT4 and SOX2 in pluripotent cells and uniquely present in proliferating, OSKM-dependent intermediates. · DOI
  31. Nie, Z. et al. c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells. Cell 151, 68–79 (2012). · DOI
  32. Rahl, P. B. et al. c-Myc regulates transcriptional pause release. Cell 141, 432–445 (2010). Rahl et al . demonstrate that MYC stabilizes transcription elongation, which explains its contribution to the early phenotypic response to direct reprogramming and its more universal binding to the promoters of cell cycle genes at this stage. · DOI · Paper page
  33. Mathieu, J. et al. Hypoxia-inducible factors have distinct and stage-specific roles during reprogramming of human cells to pluripotency. Cell Stem Cell 14, 592–605 (2014). · DOI
  34. Panopoulos, A. D. et al. The metabolome of induced pluripotent stem cells reveals metabolic changes occurring in somatic cell reprogramming. Cell Res. 22, 168–177 (2012). · DOI
  35. Folmes, C. D. et al. Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming. Cell Metab. 14, 264–271 (2011). · DOI
  36. Cao, Y. et al. miR-290/371-Mbd2-Myc circuit regulates glycolytic metabolism to promote pluripotency. EMBO J. 34, 609–623 (2015). · DOI
  37. Zhang, J., Nuebel, E., Daley, G. Q., Koehler, C. M. & Teitell, M. A. Metabolic regulation in pluripotent stem cells during reprogramming and self-renewal. Cell Stem Cell 11, 589–595 (2012). · DOI
  38. Li, R. et al. A mesenchymal-to-epithelial transition initiates and is required for the nuclear reprogramming of mouse fibroblasts. Cell Stem Cell 7, 51–63 (2010). · DOI · Paper page
  39. Thiery, J. P., Acloque, H., Huang, R. Y. & Nieto, M. A. Epithelial-mesenchymal transitions in development and disease. Cell 139, 871–890 (2009). · DOI · Paper page
  40. Wang, G. et al. Critical regulation of miR-200/ZEB2 pathway in Oct4/Sox2-induced mesenchymal-to-epithelial transition and induced pluripotent stem cell generation. Proc. Natl Acad. Sci. USA 110, 2858–2863 (2013). · DOI · Paper page
  41. Ichida, J. K. et al. A small-molecule inhibitor of Tgf-β signaling replaces Sox2 in reprogramming by inducing Nanog. Cell Stem Cell 5, 491–503 (2009). · DOI · Paper page
  42. Maherali, N. & Hochedlinger, K. Tgfβ signal inhibition cooperates in the induction of iPSCs and replaces Sox2 and cMyc. Curr. Biol. 19, 1718–1723 (2009). · DOI · Paper page
  43. Lujan, E. et al. Early reprogramming regulators identified by prospective isolation and mass cytometry. Nature 521, 352–356 (2015). Lujan et al . identified transcriptional activators that are associated with the induction of pluripotency but are not necessary for the maintenance of self-renewal. · DOI
  44. Jaenisch, R. & Young, R. Stem cells, the molecular circuitry of pluripotency and nuclear reprogramming. Cell 132, 567–582 (2008). · DOI
  45. Buganim, Y. et al. Single-cell expression analyses during cellular reprogramming reveal an early stochastic and a late hierarchic phase. Cell 150, 1209–1222 (2012). This study demonstrates that the consolidation of pluripotency proceeds deterministically following the induction of endogenous SOX2 expression. · DOI · Paper page
  46. Golipour, A. et al. A late transition in somatic cell reprogramming requires regulators distinct from the pluripotency network. Cell Stem Cell 11, 769–782 (2012). This paper demonstrates that the terminal steps of reprogramming require withdrawal of exogenous OSKM factors to consolidate autonomous self-renewal and reactivate the endogenous pluripotency network. · DOI
  47. Hanna, J. et al. Direct cell reprogramming is a stochastic process amenable to acceleration. Nature 462, 595–601 (2009). This work demonstrates that all perpetually dividing reprogramming cell lineages will eventually generate iPSCs, supporting a single switch-like transition into deterministic reprogramming. · DOI · Paper page
  48. Araki, R. et al. Conversion of ancestral fibroblasts to induced pluripotent stem cells. Stem Cells 28, 213–220 (2010). Araki et al . characterize the morphological, proliferative and molecular properties of iPSC-forming cell lineages from the time of OSKM induction using continuous live-cell imaging. · DOI
  49. O'Malley, J. et al. High-resolution analysis with novel cell-surface markers identifies routes to iPS cells. Nature 499, 88–91 (2013). · DOI
  50. Maherali, N. et al. Global epigenetic remodeling in directly reprogrammed fibroblasts. Cell Stem Cell 1, 55–70 (2007). · DOI · Paper page
  51. Wernig, M. et al. In vitro reprogramming of fibroblasts into a pluripotent ES-cell-like state. Nature 448, 318–324 (2007). · DOI
  52. Polo, J. M. et al. Cell type of origin influences the molecular and functional properties of mouse induced pluripotent stem cells. Nat. Biotechnol. 28, 848–855 (2010). · DOI
  53. Tonge, P. D. et al. Divergent reprogramming routes lead to alternative stem-cell states. Nature 516, 192–197 (2014). · DOI
  54. Pasque, V. et al. X chromosome reactivation dynamics reveal stages of reprogramming to pluripotency. Cell 159, 1681–1697 (2014). · DOI
  55. Maza, I. et al. Transient acquisition of pluripotency during somatic cell transdifferentiation with iPSC reprogramming factors. Nat. Biotechnol. 33, 769–774 (2015). · DOI
  56. Bar-Nur, O. et al. Lineage conversion induced by pluripotency factors involves transient passage through an iPSC stage. Nat. Biotechnol. 33, 761–768 (2015). · DOI
  57. Okita, K., Ichisaka, T. & Yamanaka, S. Generation of germline-competent induced pluripotent stem cells. Nature 448, 313–317 (2007). · DOI
  58. Posfai, E., Tam, O. H. & Rossant, J. Mechanisms of pluripotency in vivo and in vitro. Curr. Top. Dev. Biol. 107, 1–37 (2014). · DOI
  59. Nichols, J. et al. Formation of pluripotent stem cells in the mammalian embryo depends on the POU transcription factor Oct4. Cell 95, 379–391 (1998). · DOI
  60. Chambers, I. et al. Functional expression cloning of Nanog, a pluripotency sustaining factor in embryonic stem cells. Cell 113, 643–655 (2003). · DOI
  61. Mitsui, K. et al. The homeoprotein Nanog is required for maintenance of pluripotency in mouse epiblast and ES cells. Cell 113, 631–642 (2003). · DOI
  62. Chen, X. et al. Integration of external signaling pathways with the core transcriptional network in embryonic stem cells. Cell 133, 1106–1117 (2008). · DOI
  63. Azuara, V. et al. Chromatin signatures of pluripotent cell lines. Nat. Cell Biol. 8, 532–538 (2006). · DOI
  64. Ziller, M. J. et al. Dissecting neural differentiation regulatory networks through epigenetic footprinting. Nature 518, 355–359 (2015). · DOI
  65. Boyer, L. A. et al. Polycomb complexes repress developmental regulators in murine embryonic stem cells. Nature 441, 349–353 (2006). · DOI
  66. Singh, A. M. et al. Cell-cycle control of bivalent epigenetic domains regulates the exit from pluripotency. Stem Cell Rep. 5, 323–336 (2015). · DOI
  67. Creyghton, M. P. et al. Histone H3K27ac separates active from poised enhancers and predicts developmental state. Proc. Natl Acad. Sci. USA 107, 21931–21936 (2010). · DOI · Paper page
  68. Meissner, A. Epigenetic modifications in pluripotent and differentiated cells. Nat. Biotechnol. 28, 1079–1088 (2010). · DOI
  69. Taberlay, P. C. et al. Polycomb-repressed genes have permissive enhancers that initiate reprogramming. Cell 147, 1283–1294 (2011). Taberlay et al . demonstrate that OCT4 binding to the MyoD enhancer results in H3K4 methylation and H3K27 demethylation at the promoter, which is indicative of a transient topological interaction that precedes transcription. · DOI · Paper page
  70. Marks, H. et al. The transcriptional and epigenomic foundations of ground state pluripotency. Cell 149, 590–604 (2012). · DOI
  71. Brinkman, A. B. et al. Sequential ChIP-bisulfite sequencing enables direct genome-scale investigation of chromatin and DNA methylation cross-talk. Genome Res. 22, 1128–1138 (2012). · DOI · Paper page
  72. Chamberlain, S. J., Yee, D. & Magnuson, T. Polycomb repressive complex 2 is dispensable for maintenance of embryonic stem cell pluripotency. Stem Cells 26, 1496–1505 (2008). · DOI
  73. Galonska, C., Ziller, M. J., Karnik, R. & Meissner, A. Ground state conditions induce rapid reorganization of core pluripotency factor binding before global epigenetic reprogramming. Cell Stem Cell 17, 462–470 (2015). · DOI
  74. Geula, S. et al. m6A mRNA methylation facilitates resolution of naive pluripotency toward differentiation. Science 347, 1002–1006 (2015). Geula et al . identified a requirement for DNA, H3K27 and mRNA methylation for self-renewal in mouse epiblast stem cells but not for stem cells cultured in 2i/LIF. · DOI
  75. Chan, Y. S. et al. A PRC2-dependent repressive role of PRDM14 in human embryonic stem cells and induced pluripotent stem cell reprogramming. Stem Cells 31, 682–692 (2013). · DOI
  76. Liao, J. et al. Targeted disruption of DNMT1, DNMT3A and DNMT3B in human embryonic stem cells. Nat. Genet. 47, 469–478 (2015). · DOI
  77. Voigt, P., Tee, W. W. & Reinberg, D. A double take on bivalent promoters. Genes Dev. 27, 1318–1338 (2013). · DOI
  78. Landeira, D. et al. Jarid2 is a PRC2 component in embryonic stem cells required for multi-lineage differentiation and recruitment of PRC1 and RNA polymerase II to developmental regulators. Nat. Cell Biol. 12, 618–624 (2010). · DOI
  79. Jia, J. et al. Regulation of pluripotency and self- renewal of ESCs through epigenetic-threshold modulation and mRNA pruning. Cell 151, 576–589 (2012). · DOI
  80. Pasini, D. et al. Regulation of stem cell differentiation by histone methyltransferases and demethylases. Cold Spring Harb. Symp. Quant. Biol. 73, 253–263 (2008). · DOI
  81. Joshi, O. et al. Dynamic reorganization of extremely long-range promoter-promoter interactions between two states of pluripotency. Cell Stem Cell 17, 748–757 (2015). · DOI
  82. Deaton, A. M. & Bird, A. CpG islands and the regulation of transcription. Genes Dev. 25, 1010–1022 (2011). · DOI · Paper page
  83. Mendenhall, E. M. et al. GC-rich sequence elements recruit PRC2 in mammalian ES cells. PLoS Genet. 6, e1001244 (2010). · DOI
  84. Simon, J. A. & Kingston, R. E. Mechanisms of Polycomb gene silencing: knowns and unknowns. Nat. Rev. Mol. Cell Biol. 10, 697–708 (2009). · DOI
  85. He, J. et al. Kdm2b maintains murine embryonic stem cell status by recruiting PRC1 complex to CpG islands of developmental genes. Nat. Cell Biol. 15, 373–384 (2013). · DOI
  86. Farcas, A. M. et al. KDM2B links the Polycomb Repressive Complex 1 (PRC1) to recognition of CpG islands. eLife 1, e00205 (2012). · DOI
  87. Wu, X., Johansen, J. V. & Helin, K. Fbxl10/Kdm2b recruits Polycomb repressive complex 1 to CpG islands and regulates H2A ubiquitylation. Mol. Cell 49, 1134–1146 (2013). · DOI
  88. Blackledge, N. P. et al. Variant PRC1 complex-dependent H2A ubiquitylation drives PRC2 recruitment and polycomb domain formation. Cell 157, 1445–1459 (2014). This study identified a specific complex, normally recruited to CpG islands by the H3K36 demethylase KDM2B, that is sufficient to recruit PRC2 and establish H3K27me3 downstream of PRC1. · DOI
  89. Li, E. Chromatin modification and epigenetic reprogramming in mammalian development. Nat. Rev. Genet. 3, 662–673 (2002). · DOI · Paper page
  90. Weinberger, L., Ayyash, M., Novershtern, N. & Hanna, J. H. Dynamic stem cell states: naive to primed pluripotency in rodents and humans. Nat. Rev. Mol. Cell Biol. http://dx.doi.org/10.1038/nrm.2015.28 (2016). · DOI · Paper page
  91. Tesar, P. J. et al. New cell lines from mouse epiblast share defining features with human embryonic stem cells. Nature 448, 196–199 (2007). · DOI
  92. Brons, I. G. et al. Derivation of pluripotent epiblast stem cells from mammalian embryos. Nature 448, 191–195 (2007). · DOI
  93. Huangfu, D. et al. Induction of pluripotent stem cells by defined factors is greatly improved by small-molecule compounds. Nat. Biotechnol. 26, 795–797 (2008). · DOI
  94. Fouse, S. et al. Promoter CpG methylation contributes to ES cell gene regulation in parallel with Oct4/Nanog, PcG complex, and histone H3 K4/K27 trimethylation. Cell Stem Cell 2, 1–10 (2008). · DOI
  95. Tsumura, A. et al. Maintenance of self-renewal ability of mouse embryonic stem cells in the absence of DNA methyltransferases Dnmt1, Dnmt3a and Dnmt3b. Genes Cells 11, 805–814 (2006). · DOI
  96. Jackson, M. et al. Severe global DNA hypomethylation blocks differentiation and induces histone hyperacetylation in embryonic stem cells. Mol. Cell. Biol. 24, 8862–8871 (2004). · DOI
  97. Leeb, M. et al. Polycomb complexes act redundantly to repress genomic repeats and genes. Genes Dev. 24, 265–276 (2010). · DOI · Paper page
  98. Pasini, D. et al. Coordinated regulation of transcriptional repression by the RBP2 H3K4 demethylase and Polycomb-Repressive Complex 2. Genes Dev. 22, 1345–1355 (2008). · DOI
  99. Dovey, O. M., Foster, C. T. & Cowley, S. M. Histone deacetylase 1 (HDAC1), but not HDAC2, controls embryonic stem cell differentiation. Proc. Natl Acad. Sci. USA 107, 8242–8247 (2010). · DOI
  100. Ng, R. K. et al. Epigenetic restriction of embryonic cell lineage fate by methylation of Elf5. Nat. Cell Biol. 10, 1280–1290 (2008). · DOI
  101. Yuan, P. et al. Eset partners with Oct4 to restrict extraembryonic trophoblast lineage potential in embryonic stem cells. Genes Dev. 23, 2507–2520 (2009). · DOI
  102. Bilodeau, S., Kagey, M. H., Frampton, G. M., Rahl, P. B. & Young, R. A. SetDB1 contributes to repression of genes encoding developmental regulators and maintenance of ES cell state. Genes Dev. 23, 2484–2489 (2009). · DOI
  103. Fei, Q. et al. SETDB1 modulates PRC2 activity at developmental genes independently of H3K9 trimethylation in mouse ES cells. Genome Res. 25, 1325–1335 (2015). · DOI
  104. Ficz, G. et al. FGF signaling inhibition in ESCs drives rapid genome-wide demethylation to the epigenetic ground state of pluripotency. Cell Stem Cell 13, 351–359 (2013). · DOI
  105. Habibi, E. et al. Whole-genome bisulfite sequencing of two distinct interconvertible DNA methylomes of mouse embryonic stem cells. Cell Stem Cell 13, 360–369 (2013). · DOI
  106. Hackett, J. A. et al. Synergistic mechanisms of DNA demethylation during transition to ground-state pluripotency. Stem Cell Rep. 1, 518–531 (2013). · DOI
  107. Leitch, H. G. et al. Naive pluripotency is associated with global DNA hypomethylation. Nat. Struct. Mol. Biol. 20, 311–316 (2013). · DOI · Paper page
  108. Theunissen, T. W. et al. Nanog overcomes reprogramming barriers and induces pluripotency in minimal conditions. Curr. Biol. 21, 65–71 (2011). · DOI
  109. Tran, K. A. et al. Collaborative rewiring of the pluripotency network by chromatin and signalling modulating pathways. Nat. Commun. 6, 6188 (2015). · DOI
  110. Bar-Nur, O. et al. Small molecules facilitate rapid and synchronous iPSC generation. Nat. Methods 11, 1170–1176 (2014). · DOI
  111. Jahner, D. et al. De novo methylation and expression of retroviral genomes during mouse embryogenesis. Nature 298, 623–628 (1982). · DOI
  112. Gifford, W. D., Pfaff, S. L. & Macfarlan, T. S. Transposable elements as genetic regulatory substrates in early development. Trends Cell Biol. 23, 218–226 (2013). · DOI
  113. Lander, E. S. et al. Initial sequencing and analysis of the human genome. Nature 409, 860–921 (2001). · DOI · Paper page
  114. Smith, Z. D. et al. DNA methylation dynamics of the human preimplantation embryo. Nature 511, 611–615 (2014). · DOI
  115. Thomas, J. H. & Schneider, S. Coevolution of retroelements and tandem zinc finger genes. Genome Res. 21, 1800–1812 (2011). · DOI
  116. Friedli, M. et al. Loss of transcriptional control over endogenous retroelements during reprogramming to pluripotency. Genome Res. 24, 1251–1259 (2014). · DOI
  117. Ohnuki, M. et al. Dynamic regulation of human endogenous retroviruses mediates factor-induced reprogramming and differentiation potential. Proc. Natl Acad. Sci. USA 111, 12426–12431 (2014). · DOI
  118. Bourque, G. et al. Evolution of the mammalian transcription factor binding repertoire via transposable elements. Genome Res. 18, 1752–1762 (2008). · DOI
  119. Kunarso, G. et al. Transposable elements have rewired the core regulatory network of human embryonic stem cells. Nat. Genet. 42, 631–634 (2010). Genomic analysis of OCT4 and NANOG binding in mouse and human ES cells revealed substantial divergence that can be partially explained by the species-specific radiation of repetitive elements with OCT4- and NANOG-binding motifs that function as enhancers. · DOI
  120. Loewer, S. et al. Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells. Nat. Genet. 42, 1113–1117 (2010). · DOI
  121. Lu, X. et al. The retrovirus HERVH is a long noncoding RNA required for human embryonic stem cell identity. Nat. Struct. Mol. Biol. 21, 423–425 (2014). References 135 and 139 demonstrate that endogenous retroviruses of the LTR7 subfamily are specifically bound by OCT4, SOX2 and KLF4 in humans, and that their transcription supports generation of iPSCs. · DOI
  122. Durruthy-Durruthy, J. et al. The primate-specific noncoding RNA HPAT5 regulates pluripotency during human preimplantation development and nuclear reprogramming. Nat. Genet. 48, 44–52 (2015). · DOI
  123. Macfarlan, T. S. et al. Embryonic stem cell potency fluctuates with endogenous retrovirus activity. Nature 487, 57–63 (2012). Macfarlan et al . find that specific retrotransposons are dynamically expressed in a small population of mouse ES cells that globally resemble early cleavage stage embryos and have an unusual extra-embryonic potential. · DOI
  124. Toyooka, Y., Shimosato, D., Murakami, K., Takahashi, K. & Niwa, H. Identification and characterization of subpopulations in undifferentiated ES cell culture. Development 135, 909–918 (2008). · DOI
  125. Singh, A. M., Hamazaki, T., Hankowski, K. E. & Terada, N. A heterogeneous expression pattern for Nanog in embryonic stem cells. Stem Cells 25, 2534–2542 (2007). · DOI
  126. Singer, Z. S. et al. Dynamic heterogeneity and DNA methylation in embryonic stem cells. Mol. Cell 55, 319–331 (2014). · DOI
  127. Hayashi, K., Lopes, S. M., Tang, F. & Surani, M. A. Dynamic equilibrium and heterogeneity of mouse pluripotent stem cells with distinct functional and epigenetic states. Cell Stem Cell 3, 391–401 (2008). · DOI
  128. Papatsenko, D. et al. Single-cell analyses of ESCs reveal alternative pluripotent cell states and molecular mechanisms that control self-renewal. Stem Cell Rep. 5, 207–220 (2015). · DOI
  129. Ishiuchi, T. et al. Early embryonic-like cells are induced by downregulating replication-dependent chromatin assembly. Nat. Struct. Mol. Biol. 22, 662–671 (2015). · DOI
  130. Elsasser, S. J., Noh, K. M., Diaz, N., Allis, C. D. & Banaszynski, L. A. Histone H3.3 is required for endogenous retroviral element silencing in embryonic stem cells. Nature 522, 240–244 (2015). · DOI
  131. Sadic, D. et al. Atrx promotes heterochromatin formation at retrotransposons. EMBO Rep. 16, 836–850 (2015). · DOI
  132. Yang, B. X. et al. Systematic identification of factors for provirus silencing in embryonic stem cells. Cell 163, 230–245 (2015). · DOI
  133. Feldman, N. et al. G9a-mediated irreversible epigenetic inactivation of Oct-3/4 during early embryogenesis. Nat. Cell Biol. 8, 188–194 (2006). · DOI · Paper page
  134. You, J. S. et al. OCT4 establishes and maintains nucleosome-depleted regions that provide additional layers of epigenetic regulation of its target genes. Proc. Natl Acad. Sci. USA 108, 14497–14502 (2011). You et al . demonstrate that OCT4 can bind to nucleosomal DNA at DNA-hypomethylated enhancers in somatic cells to initiate a preliminary nucleosome-free region. · DOI · Paper page
  135. MacArthur, B. D. et al. Nanog-dependent feedback loops regulate murine embryonic stem cell heterogeneity. Nat. Cell Biol. 14, 1139–1147 (2012). · DOI
  136. Epsztejn-Litman, S. et al. De novo DNA methylation promoted by G9a prevents reprogramming of embryonically silenced genes. Nat. Struct. Mol. Biol. 15, 1176–1183 (2008). · DOI
  137. Hochedlinger, K., Yamada, Y., Beard, C. & Jaenisch, R. Ectopic expression of Oct-4 blocks progenitor-cell differentiation and causes dysplasia in epithelial tissues. Cell 121, 465–477 (2005). · DOI · Paper page
  138. Shields, J. M., Christy, R. J. & Yang, V. W. Identification and characterization of a gene encoding a gut-enriched Kruppel-like factor expressed during growth arrest. J. Biol. Chem. 271, 20009–20017 (1996). · DOI
  139. Garrett-Sinha, L. A., Eberspaecher, H., Seldin, M. F. & de Crombrugghe, B. A gene for a novel zinc-finger protein expressed in differentiated epithelial cells and transiently in certain mesenchymal cells. J. Biol. Chem. 271, 31384–31390 (1996). · DOI
  140. Stadler, M. B. et al. DNA-binding factors shape the mouse methylome at distal regulatory regions. Nature 480, 490–495 (2011). · DOI · Paper page
  141. Meshorer, E. & Misteli, T. Chromatin in pluripotent embryonic stem cells and differentiation. Nat. Rev. Mol. Cell Biol. 7, 540–546 (2006). · DOI
  142. Whyte, W. A. et al. Master transcription factors and mediator establish super-enhancers at key cell identity genes. Cell 153, 307–319 (2013). · DOI · Paper page
  143. Whyte, W. A. et al. Enhancer decommissioning by LSD1 during embryonic stem cell differentiation. Nature 482, 221–225 (2012). References 160–162 demonstrate that super-enhancers regulate cell-type specific genes. The H3K4 demethylase LSD1 interacts with these enhancers in mouseES cells and controls differentiation by removing epigenetic modifications associated with their activity. · DOI · Paper page
  144. Wang, Y. et al. LSD1 is a subunit of the NuRD complex and targets the metastasis programs in breast cancer. Cell 138, 660–672 (2009). · DOI
  145. Foster, C. T. et al. Lysine-specific demethylase 1 regulates the embryonic transcriptome and CoREST stability. Mol. Cell. Biol. 30, 4851–4863 (2010). · DOI
  146. Shi, Y. et al. Histone demethylation mediated by the nuclear amine oxidase homolog LSD1. Cell 119, 941–953 (2004). · DOI · Paper page
  147. Macfarlan, T. S. et al. Endogenous retroviruses and neighboring genes are coordinately repressed by LSD1/KDM1A. Genes Dev. 25, 594–607 (2011). · DOI
  148. Rudolph, T. et al. Heterochromatin formation in Drosophila is initiated through active removal of H3K4 methylation by the LSD1 homolog SU(VAR)3-3. Mol. Cell 26, 103–115 (2007). · DOI
  149. Lessard, J. A. & Crabtree, G. R. Chromatin regulatory mechanisms in pluripotency. Annu. Rev. Cell Dev. Biol. 26, 503–532 (2010). · DOI
  150. dos Santos, R. L. et al. MBD3/NuRD facilitates induction of pluripotency in a context-dependent manner. Cell Stem Cell 15, 102–110 (2014). · DOI
  151. Luo, M. et al. NuRD blocks reprogramming of mouse somatic cells into pluripotent stem cells. Stem Cells 31, 1278–1286 (2013). · DOI · Paper page
  152. Cacchiarelli, D. et al. Integrative analyses of human reprogramming reveal dynamic nature of induced pluripotency. Cell 162, 412–424 (2015). · DOI
  153. Jin, C. et al. H3.3/H2A. Z double variant-containing nucleosomes mark 'nucleosome-free regions' of active promoters and other regulatory regions. Nat. Genet. 41, 941–945 (2009). · DOI
  154. Mito, Y., Henikoff, J. G. & Henikoff, S. Histone replacement marks the boundaries of cis-regulatory domains. Science 315, 1408–1411 (2007). · DOI
  155. He, H. H. et al. Nucleosome dynamics define transcriptional enhancers. Nat. Genet. 42, 343–347 (2010). · DOI
  156. Sherwood, R. I. et al. Discovery of directional and nondirectional pioneer transcription factors by modeling DNase profile magnitude and shape. Nat. Biotechnol. 32, 171–178 (2014). · DOI
  157. Soufi, A., Donahue, G. & Zaret, K. S. Facilitators and impediments of the pluripotency reprogramming factors' initial engagement with the genome. Cell 151, 994–1004 (2012). · DOI · Paper page
  158. Heng, J. C. et al. The nuclear receptor Nr5a2 can replace Oct4 in the reprogramming of murine somatic cells to pluripotent cells. Cell Stem Cell 6, 167–174 (2010). · DOI
  159. Hutchins, A. P. et al. Co-motif discovery identifies an Esrrb-Sox2-DNA ternary complex as a mediator of transcriptional differences between mouse embryonic and epiblast stem cells. Stem Cells 31, 269–281 (2013). · DOI
  160. Maekawa, M. et al. Direct reprogramming of somatic cells is promoted by maternal transcription factor Glis1. Nature 474, 225–229 (2011). · DOI
  161. Wang, W. et al. Rapid and efficient reprogramming of somatic cells to induced pluripotent stem cells by retinoic acid receptor gamma and liver receptor homolog 1. Proc. Natl Acad. Sci. USA 108, 18283–18288 (2011). · DOI
  162. Jolma, A. et al. DNA-binding specificities of human transcription factors. Cell 152, 327–339 (2013). · DOI
  163. Nakagawa, M. et al. Generation of induced pluripotent stem cells without Myc from mouse and human fibroblasts. Nat. Biotechnol. 26, 101–106 (2008). · DOI · Paper page
  164. Kingston, R. E. & Narlikar, G. J. ATP-dependent remodeling and acetylation as regulators of chromatin fluidity. Genes Dev. 13, 2339–2352 (1999). · DOI
  165. Ho, L. et al. An embryonic stem cell chromatin remodeling complex, esBAF, is essential for embryonic stem cell self-renewal and pluripotency. Proc. Natl Acad. Sci. USA 106, 5181–5186 (2009). · DOI
  166. Pardo, M. et al. An expanded Oct4 interaction network: implications for stem cell biology, development, and disease. Cell Stem Cell 6, 382–395 (2010). · DOI · Paper page
  167. Floer, M. et al. A RSC/nucleosome complex determines chromatin architecture and facilitates activator binding. Cell 141, 407–418 (2010). · DOI
  168. Cheloufi, S. The histone chaperone CAF-1 safeguards somatic cell identity. Nature 528, 218–224 (2015). · DOI
  169. Ang, Y. S. et al. Wdr5 mediates self-renewal and reprogramming via the embryonic stem cell core transcriptional network. Cell 145, 183–197 (2011). · DOI
  170. Apostolou, E. et al. Genome-wide chromatin interactions of the Nanog locus in pluripotency, differentiation, and reprogramming. Cell Stem Cell 12, 699–712 (2013). · DOI
  171. Yang, P., Wu, W. & Macfarlan, T. S. Maternal histone variants and their chaperones promote paternal genome activation and boost somatic cell reprogramming. Bioessays 37, 52–59 (2015). · DOI
  172. Lin, C. J., Koh, F. M., Wong, P., Conti, M. & Ramalho-Santos, M. Hira-mediated H3.3 incorporation is required for DNA replication and ribosomal RNA transcription in the mouse zygote. Dev. Cell 30, 268–279 (2014). · DOI
  173. Inoue, A. & Zhang, Y. Nucleosome assembly is required for nuclear pore complex assembly in mouse zygotes. Nature Struct. Mol. Biol. 21, 609–616 (2014). · DOI
  174. Boskovic, A. et al. Higher chromatin mobility supports totipotency and precedes pluripotency in vivo. Genes Dev. 28, 1042–1047 (2014). · DOI
  175. Oback, B. & Wells, D. N. Donor cell differentiation, reprogramming, and cloning efficiency: elusive or illusive correlation? Mol. Reprod. Dev. 74, 646–654 (2007). · DOI
  176. Gonzalez-Munoz, E., Arboleda-Estudillo, Y., Otu, H. H. & Cibelli, J. B. Histone chaperone ASF1A is required for maintenance of pluripotency and cellular reprogramming. Science 345, 822–825 (2014). · DOI
  177. Shinagawa, T. et al. Histone variants enriched in oocytes enhance reprogramming to induced pluripotent stem cells. Cell Stem Cell 14, 217–227 (2014). · DOI
  178. Miyamoto, K. et al. Nuclear Wave1 is required for reprogramming transcription in oocytes and for normal development. Science 341, 1002–1005 (2013). · DOI · Paper page
  179. Nashun, B., Akiyama, T., Suzuki, M. G. & Aoki, F. Dramatic replacement of histone variants during genome remodeling in nuclear-transferred embryos. Epigenetics 6, 1489–1497 (2011). · DOI
  180. Wen, D. et al. Histone variant H3.3 is an essential maternal factor for oocyte reprogramming. Proc. Natl Acad. Sci. USA 111, 7325–7330 (2014). · DOI
  181. Gao, S. et al. Rapid H1 linker histone transitions following fertilization or somatic cell nuclear transfer: evidence for a uniform developmental program in mice. Dev. Biol. 266, 62–75 (2004). · DOI
  182. Burton, A. & Torres-Padilla, M. E. Chromatin dynamics in the regulation of cell fate allocation during early embryogenesis. Nat. Rev. Mol. Cell Biol. 15, 723–734 (2014). · DOI
  183. Nakamura, T. et al. PGC7 binds histone H3K9me2 to protect against conversion of 5mC to 5hmC in early embryos. Nature 486, 415–419 (2012). · DOI
  184. Eggan, K. et al. X-chromosome inactivation in cloned mouse embryos. Science 290, 1578–1581 (2000). · DOI
  185. Pasque, V., Gillich, A., Garrett, N. & Gurdon, J. B. Histone variant macroH2A confers resistance to nuclear reprogramming. EMBO J. 30, 2373–2387 (2011). · DOI
  186. Inoue, K. et al. Impeding Xist expression from the active X chromosome improves mouse somatic cell nuclear transfer. Science 330, 496–499 (2010). · DOI
  187. Chan, M. M., Smith, Z. D., Egli, D., Regev, A. & Meissner, A. Mouse ooplasm confers context-specific reprogramming capacity. Nat. Genet. 44, 978–980 (2012). · DOI
  188. Matoba, S. et al. Embryonic development following somatic cell nuclear transfer impeded by persisting histone methylation. Cell 159, 884–895 (2014). This work identified H3K9 methylation as a significant epigenetic impediment to successful zygotic genome activation and progression of embryonic development during SCNT. · DOI
  189. Blelloch, R. et al. Reprogramming efficiency following somatic cell nuclear transfer is influenced by the differentiation and methylation state of the donor nucleus. Stem Cells 24, 2007–2013 (2006). · DOI
  190. Pereira, C. F. et al. ESCs require PRC2 to direct the successful reprogramming of differentiated cells toward pluripotency. Cell Stem Cell 6, 547–556 (2010). · DOI
  191. Piccolo, F. M. et al. Different roles for Tet1 and Tet2 proteins in reprogramming-mediated erasure of imprints induced by EGC fusion. Mol. Cell 49, 1023–1033 (2013). · DOI
  192. Foshay, K. M. et al. Embryonic stem cells induce pluripotency in somatic cell fusion through biphasic reprogramming. Mol. Cell 46, 159–170 (2012). · DOI
  193. Han, D. W. et al. Pluripotential reprogramming of the somatic genome in hybrid cells occurs with the first cell cycle. Stem Cells 26, 445–454 (2008). · DOI
  194. Looney, T. J. et al. Systematic mapping of occluded genes by cell fusion reveals prevalence and stability of cis-mediated silencing in somatic cells. Genome Res. 24, 267–280 (2014). · DOI
  195. Weintraub, H. et al. Activation of muscle-specific genes in pigment, nerve, fat, liver, and fibroblast cell lines by forced expression of MyoD. Proc. Natl Acad. Sci. USA 86, 5434–5438 (1989). · DOI

Cited by

Sorted by citations

Metadata

Authors
Smith, Z. D., Sindhu, C., & Meissner, A.
Venue
Nature Reviews Molecular Cell Biology
Publisher
Springer Science and Business Media LLC
Published
2016-02-17
Volume
17
Issue
3
Pages
139-154
ISSN
  • 1471-0072
  • 1471-0080
DOI
10.1038/nrm.2016.6
Cited by
155
References
26
Language
en
Licence
www.springer.com/tdm (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review