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Progressive kidney degeneration in mice lacking tensin
1Department of Molecular Genetics and Cell Biology, The University of Chicago, Illinois 60637, USA.
The Journal of Cell Biology
|March 24, 1997
Summary
Tensin deficiency leads to kidney abnormalities and cyst formation in mice, suggesting its crucial role in renal focal adhesion. Other tissues compensate for tensin loss, indicating functional redundancy.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Tensin is a focal adhesion phosphoprotein involved in cell-matrix interactions.
- Its precise biological functions and redundancy in different tissues are not fully understood.
Purpose of the Study:
- To investigate the biological functions of tensin.
- To generate and characterize tensin-deficient mice to understand its role in vivo.
Main Methods:
- Cloning of the mouse tensin gene.
- Gene targeting to create tensin knockout mice (-/-).
- Phenotypic analysis of knockout mice, including histological and ultrastructural examination of kidneys.
Main Results:
- Tensin null mice developed normally initially but showed progressive kidney abnormalities, including renal failure and proximal tubule cysts.
- Ultrastructural analysis revealed disrupted cell-matrix junctions and loss of polarity in abnormal kidney regions.
- Other tissues compensated for tensin deficiency, with no apparent abnormalities observed.
Conclusions:
- Tensin plays a critical role in maintaining kidney focal adhesion integrity and normal tubule structure.
- Loss of tensin in the kidney leads to a weakening of focal adhesions, resulting in cystogenesis.
- Tensin's functions are largely redundant in most tissues, with compensation by other focal adhesion proteins.