ARNT-Deficient Mice and Placental Differentiation
Open accessAbstract
We used homologous recombination in embryonic stem cells to generate mice heterozygous for an aryl hydrocarbon nuclear translocator (ARNT) null mutation. These mice were intercrossed, but no live homozygous Arnt-/- knockout mice were produced among 64 newborns. Homozygotes die in utero between 9.5 and 10.5 days of gestation. Abnormalities included neural tube closure defects, forebrain hypoplasia, delayed rotation of the embryo, placental hemorrhaging, and visceral arch abnormalities. However, the primary cause of lethality appears to be failure of the embryonic component of the placenta to vascularize and form the labyrinthine spongiotrophoblast. This may be related to ARNT's known role in hypoxic induction of angiogenesis. We found no defects in yolk sac circulation.
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One Arnt null model disrupted the bHLH domain by inserting a NeoPGK cassette; another removed the bHLH exon by homologous recombination.
“One model was developed through a gene targeting approach that created a disruption of the bHLH domain with the insertion of a NeoPGK cassette (Maltepe et al., 1997). In another, homologous recombination was used to remove the bHLH exon (Kozak et al., 1997).”
From Rodent Genetic Models of Ah Receptor Signaling (2021) · cites this paper as Kozak et al., 1997
The Abstract and “Generation of Mice Heterozygous for an Arnt Null” section support the use of homologous recombination. But the Fig. 1 targeting-strategy description reports insertion into the targeted allele, not removal of the bHLH exon; the paper mentions loss of the bHLH domain only as a possible consequence of exon skipping. The Maltepe model is not attributed to Kozak et al. in the citing sentence. (LLM, conf=0.88)
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References 33 · Cited by 328
Research works printed but not linked: 5
- and are at the site of closest contact of maternal and embry- Copyright ᭧ 1997 by Academic Press. All rights of reproduction in any form reserved.
- Bradley, A. (1987). Production and analysis of chimeric mice. In insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r). Cell 75, 59-72. ''Teratocarcinomas and Embryonic Stem Cells: A Practical Ap- Maglione, D., Guerriero, V., Viglietto, G., Delli-Bovi, P., and Per- proach'' (E. J. Robertson, Ed.), pp. 113-151. IRL Press, Oxford/
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- Authors
- Kozak, K. R., Abbott, B., & Hankinson, O.
- Affiliations
- University of California, Los Angeles (US)
- Environmental Protection Agency (US)
- Corresponding author
- Hankinson, Oliver
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 1997-11
- Volume
- 191
- Issue
- 2
- Pages
- 297-305
- ISSN
- 0012-1606 (ISSN-L)
- OpenAlex
- W2004986960
- Cited by
- 328
- References
- 33
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 10 · 2022: 4 · 2021: 6 · 2020: 6 · 2019: 8 · 2018: 6 · 2017: 11 · 2016: 5 · 2015: 7 · 2014: 8 · 2013: 14 · 2012: 11
- FWCI
- 6.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Jonsson Comprehensive Cancer Center
- National Institutes of Health (ES06439)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Keywords
- ARNT, placental differentiation, placental hemorrhage, spongiotrophoblast, embryonic lethality, neural tube defects, hypoxia-induced angiogenesis
- MeSH terms
- Animals, Cell Differentiation, DNA-Binding Proteins, Embryonic and Fetal Development, Genotype, Heterozygote, Mice, Inbred Strains, Phenotype, Placenta, Recombination, Genetic, Transcription Factors, Blotting, Southern, Blotting, Western, Polymerase Chain Reaction, Receptors, Aryl Hydrocarbon, Mice, Knockout, Gene Targeting, Gene Expression Regulation, Developmental, Mice, Aryl Hydrocarbon Receptor Nuclear Translocator
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