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XB-ART-53092
Dev Biol. April 1, 2017; 424 (1): 28-39.

The CapZ interacting protein Rcsd1 is required for cardiogenesis downstream of Wnt11a in Xenopus laevis.

Hempel A , Kühl SJ , Rothe M , Rao Tata P , Sirbu IO , Vainio SJ , Kühl M .


Abstract
Wnt proteins are critical for embryonic cardiogenesis and cardiomyogenesis by regulating different intracellular signalling pathways. Whereas canonical Wnt/β-catenin signalling is required for mesoderm induction and proliferation of cardiac progenitor cells, β-catenin independent, non-canonical Wnt signalling regulates cardiac specification and terminal differentiation. Although the diverse cardiac malformations associated with the loss of non-canonical Wnt11 in mice such as outflow tract (OFT) defects, reduced ventricular trabeculation, myofibrillar disorganization and reduced cardiac marker gene expression are well described, the underlying molecular mechanisms are still not completely understood. Here we aimed to further characterize Wnt11 mediated signal transduction during vertebrate cardiogenesis. Using Xenopus as a model system, we show by loss of function and corresponding rescue experiments that the non-canonical Wnt signalling mediator Rcsd1 is required downstream of Wnt11 for ventricular trabeculation, terminal differentiation of cardiomyocytes and cardiac morphogenesis. We here place Rcsd1 downstream of Wnt11 during cardiac development thereby providing a novel mechanism for how non-canonical Wnt signalling regulates vertebrate cardiogenesis.

PubMed ID: 28237811
Article link: Dev Biol.

Genes referenced: actc1 alcam capza1 gapdh isl1 myh6 nkx2-5 pes1 ppan rcsd1 tbx20 tnni3 tnnt2 wnt11 wnt11b

Morpholinos referenced: rcsd1 MO rcsd1 MO2 rcsd1 MO3


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