Friend or Foe: Epigenetic Regulation of Retrotransposons in Mammalian Oogenesis and Early Development.

Yale J Biol Med

Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL.

Published: December 2016

Epigenetics is the study of phenotypic variation arising from developmental and environmental factors regulating gene transcription at molecular, cellular, and physiological levels. A naturally occurring biological process driven by epigenetics is the egg-to-embryo developmental transition when two fully differentiated adult cells - egg and sperm - revert to an early stem cell type with totipotency but subsequently differentiates into pluripotent embryonic stem cells that give rise to any cell type. Transposable elements (TEs) are active in mammalian oocytes and early embryos, and this activity, albeit counterintuitive because TEs can lead to genomic instability in somatic cells, correlates to successful development. TEs bridge genetic and epigenetic landscapes because TEs are genetic elements whose silencing and de-repression are regulated by epigenetic mechanisms that are sensitive to environmental factors. Ultimately, transposition events can change size, content, and function of mammalian genomes. Thus, TEs act beyond mutagenic agents reshuffling the genomes, and epigenetic regulation of TEs may act as a proximate mechanism by which evolutionary forces increase a species' hidden reserve of epigenetic and phenotypic variability facilitating the adaptation of genomes to their environment.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5168827PMC

Publication Analysis

Top Keywords

epigenetic regulation
8
environmental factors
8
cell type
8
tes
6
epigenetic
5
friend foe
4
foe epigenetic
4
regulation retrotransposons
4
retrotransposons mammalian
4
mammalian oogenesis
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!