  Growing experimental evidence indicates that topological defects could serve
as organizing centers in the morphogenesis of tissues. Here, we provide a
quantitative explanation for this phenomenon, rooted in the buckling theory of
deformable active polar liquid crystals. Using a combination of linear
stability analysis and computational fluid dynamics, we demonstrate that active
layers, such as confined cell monolayers, are unstable to the formation of
protrusions in the presence of disclinations. The instability originates from
an interplay between the focusing of the elastic forces, mediated by defects,
and the renormalization of the system's surface tension by the active flow. The
posttransitional regime is also characterized by several complex
morphodynamical processes, such as oscillatory deformations, droplet
nucleation, and active turbulence. Our findings offer an explanation of recent
observations on tissue morphogenesis and shed light on the dynamics of active
surfaces in general.
