The p53 gene is a tumor suppressor whose absence or silence contributes to cancer formation. Vanderbilt-Ingram Cancer Center investigators recently defined the role of a family member – p73.
Using a p73-deficient mouse model developed in the laboratory of Jennifer Pietenpol, Ph.D., investigators led by Clayton Marshall found that p73 regulates at least 100 genes linked to the generation of cilia – hair-like projections on cells whose coordinated movement pushes molecules and fluid in various organs of the body.
In a cover story for Cell Reports, they reported that all of the tissues requiring motile cilia for their function in the p73-deficient mice were lacking multi-ciliated cells. The mice developed inflammatory and infectious illnesses caused by loss of cilia in the sinus, ears and airways, and were sterile due to loss of cilia to move eggs and sperm.
The findings were also confirmed in human lung tissues.
The team further characterized the regulation of Foxj1 by p73 as necessary for the formation of cilia. The findings may have implications for the study of lung diseases and sterility.
The research was supported by grants from the National Institutes of Health (CA105436, CA070856, CA068485 and DA022873).
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