A model of the action of components of the heterotrimeric Gs complex in wing maturation.

<p>The neurohormone bursicon acts on the Gs-coupled GPCR <i>rickets</i> expressed in wing cells. The GPCR activity leads to dissociation of the heterotrimeric Gs complex into GTP-loaded Gαs and free Gβγ-heterodimer. Gαs[GTP] activates the cAMP-PKA pathway to promote apoptosis. Gβγ, on the other hand, acts to induce the epithelial-mesenchymal transition. These two processes, acting in coordination, lead to post-eclosion wing expansion and solidification. Expression of the constitutively active Gαs or cholera toxin stimulates the Gαs-dependent branch in this signaling. Expression of Gαo inhibits this signaling through sequestration of the Gβγ-subunits.