Related Experiment Video
Updated: Aug 5, 2026
07:26
Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
Published on: January 31, 2025
Fucci-G1 insertion partially disrupts Shh expression
Yuka Morikawa1,2, Ann Bromley1,2, Jeffrey D Steimle2
1Cardiomyocyte Renewal Lab, Texas Heart Institute at Baylor College of Medicine, Houston, TX 77030, USA.
Biology Open
|August 4, 2026
Summary
The Fucci-G1 mouse transgene insertion site was identified near the Shh lung gut enhancer (SLGE). Homozygous Fucci-G1 embryos show developmental defects and reduced Shh signaling, impacting craniofacial and foregut development.
Area of Science:
- Genetics
- Developmental Biology
- Molecular Biology
Background:
- Fucci mouse lines are essential for cell cycle research.
- The genomic locations of Fucci transgene insertions are largely unknown.
- Understanding insertion sites is crucial for interpreting experimental results.
Purpose of the Study:
- To identify the genomic insertion sites of Fucci-G1 and Fucci-S/G2/M transgenes.
- To investigate the developmental consequences of the Fucci-G1 insertion.
- To assess potential interactions between the Fucci-G1 transgene and the Shh pathway.
Main Methods:
- Whole-genome sequencing to determine transgene insertion loci.
- Phenotypic analysis of homozygous Fucci-G1 embryos.
- Gene expression analysis (Shh and targets) using in situ hybridization.
Main Results:
- The Fucci-G1 transgene is inserted near the Shh lung gut enhancer (SLGE) on chromosome 5.
- Homozygous Fucci-G1 embryos exhibit perinatal lethality with craniofacial and foregut defects.
- Shh expression and its targets are downregulated in homozygous Fucci-G1 embryos, suggesting SLGE disruption.
Conclusions:
- Heterozygous Fucci-G1 mice are suitable for cell cycle studies.
- The Fucci-G1 insertion can interfere with studies involving the SHH signaling pathway.
- Genomic context is critical for interpreting results from genetically engineered mouse models.
