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In-vitro Mutagenesis

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

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Updated: Nov 28, 2025

Mouse In Vivo Placental Targeted CRISPR Manipulation

Mouse In Vivo Placental Targeted CRISPR Manipulation

Published on: April 14, 2023

Maternal DOT1L is dispensable for mouse development.

Ji Liao¹, Piroska E Szabó²

¹Center for Epigenetics, Van Andel Research Institute, Grand Rapids, MI, 49503, USA.

Scientific Reports

|November 27, 2020

Summary

This summary is machine-generated.

Maternally deposited DOT1L (disruptor of telomeric silencing 1-like) is not essential for mouse embryo development. The paternally inherited copy of Dot1l is sufficient, and DOT1L is dispensable for genomic imprinting.

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Quantitative Analysis of Protein Expression to Study Lineage Specification in Mouse Preimplantation Embryos

Quantitative Analysis of Protein Expression to Study Lineage Specification in Mouse Preimplantation Embryos

Published on: February 22, 2016

Area of Science:

Epigenetics
Developmental Biology
Genetics

Background:

Chromatin modifying enzymes are crucial for epigenome remodeling in early embryos.
Maternal factors play a significant role when the embryonic genome is not yet active.
DOT1L methylates histone H3 lysine 79 (H3K79), and its homozygous null mutation is embryonic lethal.

Purpose of the Study:

To determine if maternally deposited DOT1L is required for mouse embryonic development.
To investigate DOT1L's role in genomic imprinting establishment and protection.

Main Methods:

Conditional knockout of Dot1l in growing oocytes using Zp3-Cre transgenic mice.
Analysis of development and fertility in maternal mutant Dot1l offspring.
Assessment of imprinted gene expression in zygotes derived from maternal mutant oocytes.

Main Results:

Maternal deletion of Dot1l (Dot1l^mat-/+) resulted in offspring with normal development and fertility.
The paternally inherited copy of Dot1l was sufficient to support normal embryonic development.
Maternal DOT1L deletion did not impact parental allele-specific expression of imprinted genes.

Conclusions:

Maternal DOT1L and H3K79 methylation are dispensable for zygotic and preimplantation mouse development.
Unlike other histone methyltransferases, maternal DOT1L is not required for imprint establishment or protection.
Embryonic development relies on the paternally inherited Dot1l copy when maternal contribution is absent.