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Related Experiment Video

Updated: Jan 13, 2026

Removal of an Internal Translational Start Site from mRNA While Retaining Expression of the Full-Length Protein
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Generation of Mice Harboring Bicc1 Conditional Null Alleles.

Chia-Feng Liu1, Steven Leon1, Isabella Herrig1

  • 1Department of Heart, Blood and Kidney Research, Cleveland Clinic Research, Cleveland Clinic, Cleveland, Ohio, USA.

Genesis (New York, N.Y. : 2000)
|January 9, 2026
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Summary

Researchers developed two new mouse models to study the Bicaudal C1 (Bicc1) gene, crucial for organ development and preventing polycystic kidney disease (PKD). These models allow for targeted gene deletion to understand Bicc1

Keywords:
Bicc1Cre‐loxPPKDRNA‐binding proteingene targeting

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Bicaudal C1 (Bicc1) is an RNA-binding protein essential for organ development and maintaining epithelial tissue homeostasis.
  • Bicc1 null mutations result in polycystic kidney disease (PKD) and early prenatal lethality.
  • Understanding tissue-specific functions of Bicc1 is crucial for elucidating PKD pathogenesis.

Purpose of the Study:

  • To engineer and validate novel conditional knockout (cKO) mouse models for Bicc1.
  • To create tools for dissecting the tissue-specific roles of Bicc1 during development.
  • To establish a platform for investigating Bicc1-related pathologies, including PKD.

Main Methods:

  • Generation of two independent Bicc1 cKO mouse lines using distinct genetic engineering strategies.
  • ES cell-based approach with loxP sites flanking exon 4 (E4) for Cre-mediated deletion.
  • CRISPR/Cas9 genome editing to introduce loxP sites around exons 4 and 5 (E4-5).
  • Validation of alleles via PCR genotyping, sequencing, and functional recombination confirmation with Cre drivers.

Main Results:

  • Successfully generated two independent Bicc1 cKO mouse lines targeting essential coding regions.
  • Validated the genetic integrity and functional recombination of both engineered alleles.
  • Established robust models for conditional Bicc1 gene inactivation in specific tissues.

Conclusions:

  • The developed Bicc1 cKO mouse models offer a powerful resource for studying gene function in a tissue-specific manner.
  • These models will facilitate research into the mechanistic basis of PKD and other Bicc1-associated diseases.
  • Further investigation using these models will advance understanding of Bicc1's role in development and homeostasis.