Early Embryonic Lethality Caused by Targeted Disruption of the Mouse Thioredoxin Gene
Open accessAbstract
Thioredoxins belong to a widely distributed group of small proteins with strong reducing activities mediated by a consensus redox-active dithiol (Cys-Gly-Pro-Cys). Thioredoxin was first isolated as a hydrogen donor for enzymatic synthesis of deoxyribonucleotides by ribonucleotide reductase in Escherichia coli. Recent studies have revealed a variety of roles that thioredoxin plays in transcription, growth control, and immune function. In this report, we describe the phenotype of mice carrying a targeted disruption of the thioredoxin gene (Txn). Heterozygotes are viable, fertile, and appear normal. In contrast, homozygous mutants die shortly after implantation, and the concepti were resorbed prior to gastrulation. When preimplantation embryos were placed in culture, the inner cell mass cells of the homozygous embryos failed to proliferate. These results indicate that Txn expression is essential for early differentiation and morphogenesis of the mouse embryo.
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Both Trx1 and Trx2 appear to be essential, as complete deficiency of either subtype causes early embryonic lethality in mice.
“Both Trx1 and Trx2 appear to be essential, as complete deficiency of either subtype causes early embryonic lethality in mice (280, 317).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [280]
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“[363] Txn1 Thioredoxin 1 (C) Embryonic lethal Reducing substrate to Msr and peroxiredoxns [364] Txn2 Thioredoxin 2 (M) Embryonic lethal Same as above [365] Txnrd1 Thioredoxin reductase 1 (C) Embryonic lethal Reduces thioredoxin by NADPH [366] Txnrd2 Thioredoxin reductase 2 (M) Embryonic lethal Same as above [367] Ttpa…”
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“In addition, both are absolutely essential for mammalian life as evidenced by embryonic lethality in GCL and Trx-1 knockout mice (Dalton et al., 2000; Matsui et al., 1996).”
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Redox Control in Mammalian Embryo Development
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“5) owing to reduced proliferation of the inner cell mass (251).”
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Background
- Authors
- Matsui, M., Oshima, M., Oshima, H., Takaku, K., Maruyama, T., Yodoi, J., & Taketo, M. M.
- Affiliations
- Kyoto University (JP)
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 1996-08
- Volume
- 178
- Issue
- 1
- Pages
- 179-185
- ISSN
- 0012-1606 (ISSN-L)
- OpenAlex
- W1991387227
- Cited by
- 546
- References
- 0
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 7 · 2023: 15 · 2022: 16 · 2021: 12 · 2020: 10 · 2019: 18 · 2018: 13 · 2017: 22 · 2016: 14 · 2015: 24 · 2014: 26 · 2013: 18 · 2012: 25
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Keywords
- thioredoxin, targeted gene disruption, mouse embryo, early embryonic lethality, preimplantation embryo, inner cell mass, embryo resorption, gastrulation, embryonic morphogenesis, embryonic differentiation
- MeSH terms
- Animals, Blastocyst, Cell Division, Decidua, Female, Embryonic and Fetal Development, Genes, Homozygote, Organ Culture Techniques, Phenotype, Thioredoxins, Mice, Knockout, Gene Targeting, Mice
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