CaMK-II is a PKD2 target that promotes pronephric kidney development and stabilizes cilia.
Development
; 138(16): 3387-97, 2011 Aug.
Article
en En
| MEDLINE
| ID: mdl-21752935
ABSTRACT
Intracellular Ca²âº signals influence gastrulation, neurogenesis and organogenesis through pathways that are still being defined. One potential Ca²âº mediator of many of these morphogenic processes is CaMK-II, a conserved calmodulin-dependent protein kinase. Prolonged Ca²âº stimulation converts CaMK-II into an activated state that, in the zebrafish, is detected in the forebrain, ear and kidney. Autosomal dominant polycystic kidney disease has been linked to mutations in the Ca²âº-conducting TRP family member PKD2, the suppression of which in vertebrate model organisms results in kidney cysts. Both PKD2-deficient and CaMK-II-deficient zebrafish embryos fail to form pronephric ducts properly, and exhibit anterior cysts and destabilized cloacal cilia. PKD2 suppression inactivates CaMK-II in pronephric cells and cilia, whereas constitutively active CaMK-II restores pronephric duct formation in pkd2 morphants. PKD2 and CaMK-II deficiencies are synergistic, supporting their existence in the same genetic pathway. We conclude that CaMK-II is a crucial effector of PKD2 Ca²âº that both promotes morphogenesis of the pronephric kidney and stabilizes primary cloacal cilia.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Pez Cebra
/
Proteínas Portadoras
/
Proteínas de Pez Cebra
/
Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina
/
Enfermedades Renales Poliquísticas
Límite:
Animals
Idioma:
En
Revista:
Development
Asunto de la revista:
BIOLOGIA
/
EMBRIOLOGIA
Año:
2011
Tipo del documento:
Article
País de afiliación:
Estados Unidos