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Ex vivo Culture of Human Placental Explants for the Study of Viral Transmission Across the Maternal-Fetal Interface

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Published on: December 30, 2025

Endogenous retroviruses function as species-specific enhancer elements in the placenta.

Edward B Chuong¹, M A Karim Rumi, Michael J Soares

¹Department of Genetics, Stanford University School of Medicine, Stanford, California, USA. echuong@stanford.edu

Nature Genetics

|February 12, 2013

Summary

Species-specific placental enhancers are enriched for endogenous retroviruses (ERVs). These ERVs, particularly the RLTR13D5 family, drive gene expression in placental cells, highlighting their role in mammalian placental evolution.

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Amplification, Next-generation Sequencing, and Genomic DNA Mapping of Retroviral Integration Sites

Amplification, Next-generation Sequencing, and Genomic DNA Mapping of Retroviral Integration Sites

Published on: March 22, 2016

Area of Science:

Evolutionary Biology
Developmental Biology
Genomics

Background:

Mammalian placenta exhibits significant interspecies diversity, indicating rapid evolutionary changes.
Understanding the molecular basis of placental evolution is crucial for deciphering developmental diversification.

Purpose of the Study:

To investigate the molecular drivers behind the evolutionary diversification of the mammalian placenta.
To identify the role of endogenous retroviruses (ERVs) in shaping placental regulatory elements.

Main Methods:

Comparative analysis of biochemically predicted enhancers in mouse and rat trophoblast stem cells (TSCs).
Genome-wide identification and characterization of species-specific enhancers.
Functional assays to assess the regulatory activity of ERV-derived enhancers in placental cells.

Main Results:

Species-specific enhancers are significantly enriched for endogenous retroviruses (ERVs) across the genome.
The RLTR13D5 ERV family provides hundreds of mouse-specific enhancers, marked by H3K4me1 and H3K27ac.
These ERV enhancers bind key TSC regulatory factors (Cdx2, Eomes, Elf5) and can drive gene expression in rat placental cells.
ERV enhancer activity is largely restricted to hypomethylated tissues, suggesting access to a reservoir of regulatory variation.

Conclusions:

Endogenous retroviral (ERV) enhancer co-option is a significant mechanism driving the evolutionary diversification of mammalian placental development.
ERVs represent a substantial source of novel regulatory elements that can be repurposed during evolution.
Tissue-specific hypomethylation may facilitate the activation of ERV-derived regulatory elements in specific cell types.