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Related Experiment Video

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Mouse In Vivo Placental Targeted CRISPR Manipulation

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Atypical E2F repressors and activators coordinate placental development.

Madhu M Ouseph¹, Jing Li, Hui-Zi Chen

¹Solid Tumor Biology Program, Department of Molecular Virology, Immunology and Medical Genetics, Human Cancer Genetics Program, Comprehensive Cancer Center, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43210, USA.

Developmental Cell

|April 21, 2012

Summary

The E2F7/E2F8 transcription factors are crucial for placental development and fetal survival. Their function is antagonized by E2F3a, and removing E2F3a rescues E2F7/E2F8-deficient embryos.

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Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

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Area of Science:

Developmental biology
Molecular genetics
Genomics

Background:

The E2F transcription factor family plays vital roles in cell cycle regulation and development.
The atypical E2F7 and E2F8 members are essential for embryonic development, but their specific roles are unclear.
Understanding E2F7/E2F8 function is critical for deciphering developmental pathways.

Purpose of the Study:

To identify the critical tissues and molecular pathways regulated by E2F7/E2F8 during murine embryonic development.
To investigate the interaction between E2F7/E2F8 and other E2F family members.
To determine the necessity and sufficiency of E2F7/E2F8 function in extraembryonic lineages.

Main Methods:

Utilized fetal and placental lineage-specific cre mouse models.
Performed expression profiling to analyze gene expression changes.
Employed biochemical approaches to study protein interactions.

Main Results:

Demonstrated that E2F7/E2F8 function in extraembryonic trophoblast lineages is essential for fetal survival.
Identified E2F3a as a canonical activator that antagonizes E2F7/E2F8.
Showed that loss of E2F3a rescues E2F7/E2F8-deficient embryos by normalizing placental development.

Conclusions:

Established a placental transcriptional network regulated by distinct E2F family arms (activation and repression).
Highlighted the critical role of E2F7/E2F8 in extraembryonic cell proliferation and placental development.
Confirmed the essentiality of this network for fetal viability.