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PLoS One. 2014 Mar 3;9(3):e88816. doi: 10.1371/journal.pone.0088816. eCollection 2014.

Loss of polycystin-1 inhibits Bicc1 expression during mouse development.

Author information

  • 1Division of Translational Cancer Research and Therapy, State Key Laboratory of Molecular Oncology, Cancer Hospital and Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; Department of Medicine, Vanderbilt University, Nashville, Tennessee, United States of America.
  • 2Division of Translational Cancer Research and Therapy, State Key Laboratory of Molecular Oncology, Cancer Hospital and Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • 3Department of Medicine, Vanderbilt University, Nashville, Tennessee, United States of America.
  • 4Department of Biochemistry, Vanderbilt University, Nashville, Tennessee, United States of America.
  • 5Department of Medicine, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
  • 6Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
  • 7Department of Pathology, Moffitt Cancer Center, Tampa, Florida, United States of America.
  • 8Division of Translational Cancer Research and Therapy, State Key Laboratory of Molecular Oncology, Cancer Hospital and Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; Department of Medicine, Vanderbilt University, Nashville, Tennessee, United States of America; Department of Cell & Developmental Biology, Vanderbilt University, Nashville, Tennessee, United States of America.

Abstract

Bicc1 is a mouse homologue of Drosophila Bicaudal-C (dBic-C), which encodes an RNA-binding protein. Orthologs of dBic-C have been identified in many species, from C. elegans to humans. Bicc1-mutant mice exhibit a cystic phenotype in the kidney that is very similar to human polycystic kidney disease. Even though many studies have explored the gene characteristics and its functions in multiple species, the developmental profile of the Bicc1 gene product (Bicc1) in mammal has not yet been completely characterized. To this end, we generated a polyclonal antibody against Bicc1 and examined its spatial and temporal expression patterns during mouse embryogenesis and organogenesis. Our results demonstrated that Bicc1 starts to be expressed in the neural tube as early as embryonic day (E) 8.5 and is widely expressed in epithelial derivatives including the gut and hepatic cells at E10.5, and the pulmonary bronchi at E11.5. In mouse kidney development, Bicc1 appears in the early ureteric bud and mesonephric tubules at E11.5 and is also expressed in the metanephros at the same stage. During postnatal kidney development, Bicc1 expression gradually expands from the cortical to the medullary and papillary regions, and it is highly expressed in the proximal tubules. In addition, we discovered that loss of the Pkd1 gene product, polycystin-1 (PC1), whose mutation causes human autosomal dominant polycystic kidney disease (ADPKD), downregulates Bicc1 expression in vitro and in vivo. Our findings demonstrate that Bicc1 is developmentally regulated and reveal a new molecular link between Bicc1 and Pkd1.

PMID:
24594709
[PubMed - indexed for MEDLINE]
PMCID:
PMC3940423
Free PMC Article
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