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Generation and characterization of dickkopf3 mutant mice
Ivan del Barco Barrantes1, Ana Montero-Pedrazuela, Ana Guadaño-Ferraz
1Division of Molecular Embryology, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.
Molecular and Cellular Biology
|March 2, 2006
Summary
Dickkopf-3 (Dkk3) deficiency in mice did not affect thyroid hormone metabolism but altered NK cell frequency, immunoglobulin M, and hemoglobin levels, leading to hyperactivity.
Area of Science:
- Molecular Biology
- Genetics
- Immunology
Background:
- Dickkopf (DKK) genes are secreted Wnt antagonists.
- DKK3 is a divergent member with an unclear function.
- Previous hypotheses suggested DKK3 acts as a thyroid hormone-binding protein.
Purpose of the Study:
- To generate and characterize Dkk3 mutant mice.
- To investigate the function of Dkk3, particularly its potential role in thyroid hormone metabolism.
- To identify potential phenotypic alterations in Dkk3-deficient mice.
Main Methods:
- Generation of Dkk3 mutant mice.
- Comprehensive phenotypic analysis, including organ morphology, physiology, and clinical chemistry.
- Assessment of deiodinase activities and thyroid hormone levels.
- Analysis of immune cell populations (NK cells), immunoglobulin M, hemoglobin, hematocrit, and lung ventilation.
Main Results:
- Dkk3-deficient mice are viable and fertile with no major changes in organ morphology, physiology, or most clinical chemistry parameters.
- The data do not support a role for Dkk3 in thyroid hormone metabolism; mutant mice are euthyroid.
- Significant alterations observed include changes in Natural Killer (NK) cell frequency, immunoglobulin M, hemoglobin, and hematocrit levels, along with altered lung ventilation.
- Dkk3-deficient mice exhibit hyperactivity.
Conclusions:
- Dkk3 is not essential for thyroid hormone metabolism.
- Dkk3 plays a role in regulating NK cell frequency, hematological parameters, and lung ventilation.
- Dkk3 deficiency leads to hyperactivity in mice, suggesting a broader physiological role beyond Wnt antagonism.
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