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A Conditional Knockout Mouse Model Reveals That Calponin-3 Is Dispensable for Early B Cell Development
Alexandra Flemming1, Qi-Quan Huang2, Jian-Ping Jin3
1Department of Molecular Immunology, Max-Planck-Institut of Immunobiology and Epigenetics, Freiburg, Germany; Biology III, Faculty of Biology, Albert-Ludwigs-University Freiburg, Freiburg, Germany.
Plos One
|June 6, 2015
Summary
Calponin-3 is a novel protein potentially involved in B cell receptor signaling. Despite its expression during B cell development, its deletion did not cause major developmental defects, suggesting compensatory mechanisms.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Calponins are conserved actin-associated proteins.
- Calponin-3's physiological role is largely unknown due to lack of models.
- Precursor B cell receptor (pre-BCR) signaling is crucial for B cell development.
Purpose of the Study:
- Identify novel proteins in pre-BCR signaling.
- Investigate the role of calponin-3 in B cell development and signaling.
- Develop a tool for studying calponin-3 in vivo.
Main Methods:
- Unbiased screening to identify signaling proteins.
- Generation of a calponin-3-GFP knock-in mouse model.
- Conditional deletion of calponin-3 (Cnn3) in mice.
- Analysis of B cell development and signaling.
Main Results:
- Calponin-3 is expressed in developing B cells, localizes to the plasma membrane, and is phosphorylated in a Syk-dependent manner.
- Calponin-3 expression increases during B cell maturation.
- Conditional deletion of calponin-3 did not result in significant B cell developmental defects.
- A calponin-3-GFP knock-in mouse model was successfully generated.
Conclusions:
- Calponin-3 is a putative novel mediator downstream of the pre-BCR.
- Lymphocytes may possess compensatory mechanisms for calponin-3 loss.
- The generated mouse model will facilitate further research on calponin-3 in various cell types.
