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Rapid and Efficient Spatiotemporal Monitoring of Normal and Aberrant Cytosine Methylation within Intact Zebrafish Embryos

Rapid and Efficient Spatiotemporal Monitoring of Normal and Aberrant Cytosine Methylation within Intact Zebrafish Embryos

Published on: August 18, 2022

Developmental genome-wide DNA methylation asymmetry between mouse placenta and embryo.

L M Legault^1,2, K Doiron¹, A Lemieux^1,2

¹Research Center of the CHU Sainte-Justine , Montreal, Canada.

|February 15, 2020

Summary

DNA methylation patterns differ between embryonic and placental cells early in development. This asymmetry is driven by DNMT3B and persists throughout prenatal development, impacting gene regulation.

Keywords:

DNA methylation early development embryo placenta

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Published on: June 12, 2018

Area of Science:

Developmental Biology
Epigenetics
Genomics

Background:

DNA methylation is crucial for embryonic development, but its unequal distribution between embryonic and placental lineages is poorly understood.
Understanding this asymmetry is key to deciphering developmental programming.

Purpose of the Study:

To investigate the origins and long-term consequences of DNA methylation asymmetry between embryonic and placental cells.
To identify the key enzymes responsible for establishing and maintaining these differential methylation patterns.

Main Methods:

Generation of high-resolution DNA methylation maps in mouse embryos and placentas at mid-gestation (E10.5).
Analysis of differentially methylated regions (DMRs) to uncover developmental asymmetry.
Investigation of the roles of DNA methyltransferases DNMT3A and DNMT3B in establishing methylation patterns at peri-implantation stages (E3.5-E6.5).

Main Results:

Discovery of specific DMR subtypes contributing to methylation asymmetry between embryonic and placental cells.
Demonstration that this asymmetry arises rapidly (E3.5-E6.5) and is maintained throughout prenatal development and in somatic tissues.
Identification of DNMT3B as the primary driver of asymmetric methylation at peri-implantation stages, with DNMT3A showing limited compensatory function in its absence.

Conclusions:

Early-acting DNA methylation asymmetry between embryo and placenta is established rapidly and has lasting effects.
DNMT3B plays a critical role in establishing asymmetric methylation patterns, with DNMT3A exhibiting partial compensatory capacity.
The roles of DNMT3A and DNMT3B in methylation asymmetry shift as development progresses.