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Curr Opin Genet Dev. 2015 Oct;34:17-23. doi: 10.1016/j.gde.2015.06.003. Epub 2015 Jul 13.

Unwind and transcribe: chromatin reprogramming in the early mammalian embryo.

Author information

1
Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, 35 Medical Center Way, University of California, San Francisco, CA 94143, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, 35 Medical Center Way, University of California, San Francisco, CA 94143, USA.
2
Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, 35 Medical Center Way, University of California, San Francisco, CA 94143, USA.
3
Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, 35 Medical Center Way, University of California, San Francisco, CA 94143, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, 35 Medical Center Way, University of California, San Francisco, CA 94143, USA. Electronic address: mrsantos@ucsf.edu.

Abstract

Within the first few days of life, the unipotent gametic genomes are rapidly reprogrammed to support emergence of pluripotent cells in the early mammalian embryo. It is now appreciated that this crucial stage of development involves dramatic changes to chromatin at multiple levels, such as DNA methylation, histone modifications, histone mobility, and higher-order chromatin organization. Technological advances are beginning to allow genome-wide views of this chromatin reprogramming, and provide new approaches to functionally dissect its regulation. Here we review recent insights into the dynamic chromatin environment of the early mouse embryo. New data challenge long-held assumptions, for example, with regards to the asymmetry of DNA methylation of the parental genomes or the onset of functional zygotic genome activation. We discuss how impaired chromatin reprogramming can lead to early embryonic lethality, but might also have delayed effects that only manifest later in embryogenesis or postnatally, potentially influencing the propensity for adult-onset diseases.

PMID:
26183187
PMCID:
PMC4674342
DOI:
10.1016/j.gde.2015.06.003
[Indexed for MEDLINE]
Free PMC Article

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