PAPC couples the segmentation clock to somite morphogenesis by regulating N-cadherin dependent adhesion
2017
Vertebrate segmentation is characterized by the periodic formation of epithelial
somites from the mesenchymal presomitic mesoderm (PSM). How the rhythmic
signaling pulse delivered by the Segmentation Clock is translated into the
periodic morphogenesis of somites remains poorly understood. Here, we focused
on the role of Paraxial protocadherin (PAPC/Pcdh8) in this process. We showed
that in chicken and mouse embryos, PAPC expression is tightly regulated by the
Clock and Wavefront system in the posterior PSM. We observed that PAPC
exhibits a striking complementary pattern to N-Cadherin (CDH2), marking the
interface of the future somite boundary in the anterior PSM. Gain and loss of
function of PAPC in chicken embryos disrupt somite segmentation by altering the
CDH2-dependent epithelialization of PSM cells. Our data suggest that clathrin mediated
endocytosis is increased in PAPC expressing cells, subsequently
affecting CDH2 internalization in the anterior compartment of the future somite.
This in turn generates a differential adhesion interface, allowing formation of the
acellular fissure that defines the somite boundary. Thus periodic expression of
PAPC in the anterior PSM triggers rhythmic endocytosis of CDH2, allowing for
segmental de-adhesion and individualization of somites.
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