Hoxb4-ENE-GFPCre transgenic mice have expression of a GFP/Cre fusion protein directed primarily to developing spinal cord and hindbrain by the mouse homeobox B4 early neuronal enhancer (ENE) region and heat shock protein 1B minimal promoter. These Hoxb4-ENE-GFPCre transgenic mice may be useful as a Cre-lox or fluorescent tool for the fate-mapping/lineage-tracing of Hoxb4-expressing neurons in the developing neural tube.
Sabine P Cordes, Samuel Lunenfeld Research Institute
Genetic Background | Generation |
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Allele Type |
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Transgenic (Recombinase-expressing) |
Hoxb4-ENE-GFPCre transgenic mice are viable and fertile, with expression of a GFP/Cre fusion protein directed primarily to developing spinal cord and hindbrain by the mouse homeobox B4 early neuronal enhancer (ENE) region and heat shock protein 1B minimal promoter. Cre recombinase activity is observed from embryonic day (E)9.0-13.5 throughout the neural tube in the hindbrain, the dorsal root ganglia, motor neurons, and the Xth cranial ganglia (vagus); with a sharp anterior boundary at rhombomeres 6 and 7 (r6/r7). Ectopic cre activity is reported in the Vth cranial nerve (trigeminal) of E10.5-11.5 embryos. GFP fluorescence is first detectable at E9.0, strongest at E10.5, and absent by ~E12.0. GFP fluorescence is localized to the neural tube and the hindbrain with a sharp anterior limit between rhombomeres 7 and 8 (r7/r8) at E9.5. GFP expression at the anterior r7/r8 boundary was maintained through E11.5, while the posterior boundary expanded caudally from E9.5-E11.5. When bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Hoxb4-expressing cells of the offspring. These Hoxb4-ENE-GFPCre transgenic mice may be useful as a Cre-lox or fluorescent tool for the fate-mapping/lineage-tracing of Hoxb4-expressing neurons in the developing neural tube.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
The ~3.2 kb Hoxb4-ENE-GFP-Cre (or Hoxb4-ENE-hsp68-GFPCre) transgene was designed with (from 5' to 3') an 880 bp fragment containing the early neuronal enhancer (ENE) region located downstream of the mouse homeobox B4 gene (Hoxb4), a 600 bp minimal promoter sequence from the mouse heat shock protein 1B gene (Hspa1b or hsp68), a Green Fluorescent Protein/Cre Recombinase (EGFP/Cre) fusion protein coding sequence followed by an SV40-IVS-polyA signal. The donating investigator reports that this transgene was injected into the pronuclei of FVB/NJ fertilized eggs. The resulting transgenic offspring were bred to ICR outbred mice to establish the founder line. These Hoxb4-ENE-GFPCre transgenic mice were bred to ICR for at least 8-10 generations. These mice were then bred to C57BL/6J mice at least once. Transgenic mice on this mixed genetic background (approximately 50% C57BL/6J and 50% ICR) were sent to The Jackson Laboratory. Upon arrival, mice were bred with C57BL/6J inbred mice (Stock No. 000664) for at least one generation to establish the colony.
Expressed Gene | GFP, Green Fluorescent Protein, |
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Expressed Gene | cre, cre recombinase, bacteriophage P1 |
Site of Expression | Expression of a GFP/Cre fusion protein is directed primarily to developing spinal cord and hindbrain. |
Allele Name | transgene insertion 1, Sabine P Cordes |
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Allele Type | Transgenic (Recombinase-expressing) |
Allele Synonym(s) | Hoxb4-ENE-GFP-Cre; Tg(Hoxb4-GFP/cre)1Sapc |
Gene Symbol and Name | Tg(Rr5-GFP/cre)1Sapc, transgene insertion 1, Sabine P Cordes |
Gene Synonym(s) | |
Promoter | Rr5, regulatory region 5, mouse, laboratory |
Expressed Gene | GFP, Green Fluorescent Protein, |
Expressed Gene | cre, cre recombinase, bacteriophage P1 |
Site of Expression | Expression of a GFP/Cre fusion protein is directed primarily to developing spinal cord and hindbrain. |
Strain of Origin | FVB/NJ |
Chromosome | UN |
Molecular Note | The early neuronal Hoxb4 enhancers with an Hspa1b minimal promoter were used to drive expression of a GFP/cre fusion gene in neural tissue including the neural tube up to the r6/r7 boundary, the dorsal root ganglia, the trigeminal (Vth) cranial nerve, and Xth cranial nerve. No line information was given. |
Mutations Made By | Sabine Cordes, Samuel Lunenfeld Research Institute |
When maintaining a live colony, transgenic carrier mice may be bred to wildtype (noncarrier) mice from the colony.
When using the STOCK Tg(Rr5-GFP/cre)1Sapc/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #012452 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Hemizygous or non carrier for Tg(Rr5-GFP/cre)1Sapc |
Frozen Mouse Embryo | STOCK Tg(Rr5-GFP/cre)1Sapc/J | $2595.00 |
Frozen Mouse Embryo | STOCK Tg(Rr5-GFP/cre)1Sapc/J | $2595.00 |
Frozen Mouse Embryo | STOCK Tg(Rr5-GFP/cre)1Sapc/J | $3373.50 |
Frozen Mouse Embryo | STOCK Tg(Rr5-GFP/cre)1Sapc/J | $3373.50 |
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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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