Epigenomics is the systematic analysis of the global state of gene expression not attributable to mutational changes in the underlying DNA genome. An organism has multiple, cell type-specific, epigenomes comprising epigenetic marks such as DNA methylation, histone modification and specifically positioned nucleosomes.

Latest Research and Reviews

  • Research |

    Ernesto Guccione and colleagues report that the transcription factor PRDM15 regulates naive pluripotency in mouse embryos and embryonic stem cells and in derivation of mouse and human iPSCs. They further show that PRDM15 promotes WNT signaling and inhibits MAPK–ERK signaling by directly regulating the expression of R-spondin1 and Sprouty1, respectively.

    • Slim Mzoughi
    • , Jingxian Zhang
    • , Delphine Hequet
    • , Shun Xie Teo
    • , Haitong Fang
    • , Qiao Rui Xing
    • , Marco Bezzi
    • , Michelle Kay Yi Seah
    • , Sheena L M Ong
    • , Eun Myoung Shin
    • , Heike Wollmann
    • , Esther S M Wong
    • , Muthafar Al-Haddawi
    • , Colin L Stewart
    • , Vinay Tergaonkar
    • , Yuin-Han Loh
    • , N Ray Dunn
    • , Daniel M Messerschmidt
    •  & Ernesto Guccione
  • Research |

    A low-input Hi-C method is used to show that chromatin organization is markedly relaxed in pre-implantation mouse embryos after fertilization and that the subsequent maturation of 3D chromatin architecture is surprisingly slow.

    • Zhenhai Du
    • , Hui Zheng
    • , Bo Huang
    • , Rui Ma
    • , Jingyi Wu
    • , Xianglin Zhang
    • , Jing He
    • , Yunlong Xiang
    • , Qiujun Wang
    • , Yuanyuan Li
    • , Jing Ma
    • , Xu Zhang
    • , Ke Zhang
    • , Yang Wang
    • , Michael Q. Zhang
    • , Juntao Gao
    • , Jesse R. Dixon
    • , Xiaowo Wang
    • , Jianyang Zeng
    •  & Wei Xie
    Nature 547, 232–235

News and Comment

  • Editorial |

    This month's research articles span the range of scales of gene-regulatory mechanisms, from a deceptively simple gene therapy vector, via synthetic gene expression circuits, to extremely intricate epigenetic switches. We encourage investigation of synthetic circuits exploring the functions of the 3D genome.

  • Comments and Opinion |

    The emerging field of omics has the potential to advance and strengthen research into endocrine-disrupting chemicals (EDCs). In this Opinion article, Andrea Baccarelli and colleagues discuss the potential of using omics technologies — both established and developing — to characterize present and past EDC exposures and predict risk of developing EDC-related diseases.

    • Carmen Messerlian
    • , Rosie M. Martinez
    • , Russ Hauser
    •  & Andrea A. Baccarelli
  • News and Views |

    Promoters and enhancers have long been regarded as distinct elements, a notion that has been challenged more recently. Two new studies now identify promoters that function as long-range enhancers in vivo to regulate the transcription of distal genes.

    • Rui R Catarino
    • , Christoph Neumayr
    •  & Alexander Stark
    Nature Genetics 49, 972–973
  • Editorial |

    Understanding of how epigenetic information is acquired, processed and transmitted through cell division, and potentially across generations, remains limited. Mechanistic studies aiming to elucidate the molecular underpinnings of these phenomena may provide insights into development, disease susceptibility and evolution.

  • News and Views |

    Mammalian SWI/SNF complexes have critical roles in development and differentiation, and are implicated in the pathogenesis of several diseases; however, the mechanisms underpinning disease manifestation and the specificity of the subunits mutated are incompletely understood. Newly identified loss-of-function mutations in the SMARCD2 gene (part of the SMARCD1, SMARCD2 and SMARCD3 paralog family) reveal an evolutionarily conserved role specifically for the SMARCD2 subunit in granulopoiesis, and further investigation implicates the CEBPɛ transcription factor as a key effector of this specific function.

    • Brittany C Michel
    •  & Cigall Kadoch
    Nature Genetics 49, 655–657