The DAF-16/FOXO transcription factor functions as a regulator of epidermal innate immunity.
PLoS Pathog
; 9(10): e1003660, 2013.
Article
en En
| MEDLINE
| ID: mdl-24146615
ABSTRACT
The Caenorhabditis elegans DAF-16 transcription factor is critical for diverse biological processes, particularly longevity and stress resistance. Disruption of the DAF-2 signaling cascade promotes DAF-16 activation, and confers resistance to killing by pathogenic bacteria, such as Pseudomonas aeruginosa, Staphylococcus aureus, and Enterococcus faecalis. However, daf-16 mutants exhibit similar sensitivity to these bacteria as wild-type animals, suggesting that DAF-16 is not normally activated by these bacterial pathogens. In this report, we demonstrate that DAF-16 can be directly activated by fungal infection and wounding in wild-type animals, which is independent of the DAF-2 pathway. Fungal infection and wounding initiate the Gαq signaling cascade, leading to Ca(2+) release. Ca(2+) mediates the activation of BLI-3, a dual-oxidase, resulting in the production of reactive oxygen species (ROS). ROS then activate DAF-16 through a Ste20-like kinase-1/CST-1. Our results indicate that DAF-16 in the epidermis is required for survival after fungal infection and wounding. Thus, the EGL-30-Ca(2+)-BLI-3-CST-1-DAF-16 signaling represents a previously unknown pathway to regulate epidermal damage response.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Factores de Transcripción
/
Infecciones por Bacterias Grampositivas
/
Enfermedades Cutáneas Bacterianas
/
Caenorhabditis elegans
/
Proteínas de Caenorhabditis elegans
/
Dermatomicosis
/
Epidermis
/
Inmunidad Innata
Límite:
Animals
Idioma:
En
Año:
2013
Tipo del documento:
Article