Related Experiment Video

Updated: Aug 16, 2026

Generation of Maternal Mutants Using zpc:cas9 Knock-in Zebrafish
09:17

Generation of Maternal Mutants Using zpc:cas9 Knock-in Zebrafish

Published on: July 22, 2025

The targeted disruption of the MYPT1 gene results in embryonic lethality

Ryuji Okamoto1, Masaaki Ito, Noboru Suzuki

  • 1The First Department of Internal Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.

Transgenic Research
|September 9, 2005
PubMed

Insights

Myosin phosphatase (MP) deficiency causes embryonic lethality in mice. MYPT1, essential for MP regulation, is crucial for mouse embryogenesis, with its absence leading to death before 7.5 days post-coitum.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Biochemistry

Background:

  • Myosin phosphatase (MP) dephosphorylates the regulatory light chain of myosin II, a critical process in cellular function.
  • MYPT1 is a key regulatory subunit of smooth and nonmuscle MP, controlling its activation and function.

Purpose of the Study:

  • To investigate the physiological roles of MYPT1 in mouse development.
  • To determine the consequences of MYPT1 gene disruption on embryogenesis.

Main Methods:

  • Gene targeting was used to generate MYPT1-deficient mice.
  • Phenotypic analysis of heterozygous and homozygous MYPT1 knockout mice was performed.
  • Embryonic development was monitored to identify the stage of lethality.

Main Results:

  • Heterozygous MYPT1-deficient mice exhibited normal MYPT1 expression and no distinct phenotype.
  • No homozygous MYPT1-deficient mice were observed in F2 generation, indicating embryonic lethality.
  • Embryonic lethality occurred before 7.5 days post-coitum (dpc) in MYPT1-deficient embryos.

Conclusions:

  • MYPT1 is essential for successful mouse embryogenesis.
  • The absence of MYPT1 leads to early embryonic lethality, highlighting its critical role in developmental processes.

More Related Videos

Loss-of-Function Approach in the Embryonic Chick Retina by Using Tol2 Transposon-Mediated Transgenic Expression of Artificial microRNAs06:58

Loss-of-Function Approach in the Embryonic Chick Retina by Using Tol2 Transposon-Mediated Transgenic Expression of Artificial microRNAs

Published on: May 18, 2022

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein05:48

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein

Published on: March 16, 2022

Related Concept Videos

In-vitro Mutagenesis01:16

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.
Lethal Alleles02:41

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...