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Updated: Jun 4, 2026
Whole-mount Imaging of Mouse Embryo Sensory Axon Projections
Published on: December 9, 2014
Generation of Axin1 conditional mutant mice
Rong Xie1, Rulang Jiang, Di Chen
1Department of Orthopaedics, Center for Musculoskeletal Research, Rochester, New York, USA.
Abstract:
Axin1 is a critical negative regulator of the canonical Wnt-signaling pathway. It is a concentration-limiting factor in the β-catenin degradation complex. Axin1 null mutant mouse embryos died at embryonic day 9.5, precluding direct genetic analysis of the roles of Axin1 in many developmental and physiological processes using these mutant mice. In this study, we have generated mice carrying two directly repeated loxP sites flanking the exon 2 region of the Axin1 gene. We show that floxed-allele-carrying mice (Axin1( fx/fx) ) mice appear normal and fertile. Upon crossing the Axin1( fx/fx) mice to the CMV-Cre transgenic mice, the loxP-flanked exon 2 region that encodes the N-terminus and the conserved regulation of G-protein signaling domain was efficiently deleted by Cre-mediated excision in vivo. Moreover, we show that mouse embryos homozygous for the Cre/loxP-mediated deletion of exon 2 of the Axin1 gene display embryonic lethality and developmental defects similar to those reported for Axin1(-/-) mice. Thus, this Axin1(fx/fx) mouse model will be valuable for systematic tissue-specific dissection of the roles of Axin1 in embryonic and postnatal development and diseases.
Insights
Researchers developed a new Axin1(fx/fx) mouse model to study the Wnt-signaling pathway. This model enables detailed analysis of Axin1
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- Axin1 is a key negative regulator of the Wnt-signaling pathway, crucial for embryonic development.
- Axin1 acts as a concentration-limiting factor in the beta-catenin degradation complex.
- Previous Axin1 null mutant mice exhibited early embryonic lethality, hindering detailed study.
Purpose of the Study:
- To generate a conditional knockout mouse model for Axin1 to overcome limitations of null mutants.
- To enable systematic, tissue-specific analysis of Axin1 functions in development and disease.
Main Methods:
- Generation of Axin1(fx/fx) mice with loxP sites flanking exon 2.
- Cre-mediated excision of the floxed exon 2 in vivo using CMV-Cre transgenic mice.
- Analysis of resulting homozygous deletion mutants for developmental phenotypes.
Main Results:
- Axin1(fx/fx) mice are phenotypically normal and fertile.
- Cre/loxP-mediated deletion of Axin1 exon 2 resulted in embryonic lethality.
- Homozygous deletion embryos exhibited developmental defects comparable to Axin1(-/-) mice.
Conclusions:
- The Axin1(fx/fx) mouse model provides a valuable tool for studying Axin1's roles.
- This model facilitates tissue-specific investigations into Axin1's functions during embryonic and postnatal development.
- The model is applicable for dissecting Axin1's involvement in various diseases.
