The AxinTg1 transgenic insertional allele has the ~600 kb human epsilon-globin gene inserted between exon 1 and exon 3 (deleting exon 2) of the Axin1 locus. The transgene directs expression of truncated Axin1 mRNA product (still containing exons 3-10) that results in a recessive loss-of-function allele.
Frank Costantini, Columbia University Medical Center
The AxinTg1 transgenic insertional allele (previously called FuTg1 or Hε46) has a tandem array of the human epsilon-globin gene (~600 kb in total) inserted between exon 1 and exon 3 (deleting exon 2) of the Axin1 locus. The transgene directs expression of a truncated Axin1 mRNA product (still containing exons 3-10) that results in a recessive loss-of-function allele. Homozygous AxinTg1 mice die between embryonic day (E)8-E10 with abnormalities in developmental patterning (duplication of embryonic axis and parts of the embryo) and nervous system development (truncated headfolds, severely underdeveloped/absent forebrain, and kinked neural tube). Some incidence of cardia bifida and enlarged pericardium are reported in severely affected homozygotes. These AxinTg1 mutant mice may be useful for studying developmental patterning, axis duplication, forebrain development, negative regulation of canonical Wnt signaling pathway, β-catenin/cadherin function, and apoptosis.
An 8.1 kb transgene harboring a tandem array of the human epsilon-globin gene (~600 kb in total) was microinjected into (CBA/J x C57BL/6J)F2 zygotes, and founder mice were bred to (CBA/J x C57BL/6J)F1 mice. Transgenic founder line 46 (Hε46) was established on a CBA/J;C57BL/6J hybrid background and found to have the transgene inserted between exon 1 and exon 3 of the Axin1 locus; also resulting in deletion of exon 2 and parts of the two flanking introns. Mice heterozygous for this AxinTg1 transgenic insertional allele (previously called FuTg1 or Hε46), were backcrossed to C57BL/6J inbred mice for approximately 20 generations by the laboratory of Dr. Frank Costantini (Columbia University Medical Center). Heterozygous embryos were then cryopreserved. Aliquots of these frozen embryos were sent to Mutant Mouse Regional Resource Center node at The Jackson Laboratory (Mmjax) and used to establish a live mutant colony.
Allele Name | fused transgenic 1 |
---|---|
Allele Type | Transgenic |
Allele Synonym(s) | AxinTg1; H epsilon 46 |
Gene Symbol and Name | Axin1, axin 1 |
Gene Synonym(s) | |
Strain of Origin | (CBA/J x C57BL/6J)F2 |
Chromosome | 17 |
Molecular Note | In this mutation, an ~600 kb transgene is inserted between exons 1 and 3, and exon 2 and 20 kb from the two flanking introns are deleted. This disruption results in the absence of the major wild-type 3.9 kb mRNA in homozygotes. |
Mutations Made By | Frank Costantini, Columbia University Medical Center |
When maintaining a live colony, hemizygous mice may be bred to wildtype siblings or to C57BL/6J inbred mice (Stock No. 000664). Homozygous mice die in utero.
When using the B6.Cg-Axin1Fu-Tg1/CosMmjax mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #32035 in your Materials and Methods section.
Facility Barrier Level Descriptions
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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