Negative regulation of Caenorhabditis elegans epidermal damage responses by death-associated protein kinase
Abstract
Wounding of epidermal layers triggers multiple coordinated responses to damage. We show here that the Caenorhabditis elegans ortholog of the tumor suppressor death-associated protein kinase, dapk-1, acts as a previously undescribed negative regulator of barrier repair and innate immune responses to wounding. Loss of DAPK-1 function results in constitutive formation of scar-like structures in the cuticle, and up-regulation of innate immune responses to damage. Overexpression of DAPK-1 represses innate immune responses to needle wounding. Up-regulation of innate immune responses in dapk-1 requires the TIR-1/p38 signal transduction pathway; loss of function in this pathway synergizes with dapk-1 to drastically reduce adult lifespan. Our results reveal a previously undescribed function for the DAPK tumor suppressor family in regulation of epithelial damage responses.
- Publication:
-
Proceedings of the National Academy of Science
- Pub Date:
- February 2009
- DOI:
- 10.1073/pnas.0809339106
- Bibcode:
- 2009PNAS..106.1457T
- Keywords:
-
- antimicrobial peptide;
- epidermis;
- innate immunity;
- wound repair;
- cuticle;
- Biological Sciences:Developmental Biology