Abstract: Vinculin is a highly conserved protein involved in cell adhesion and mechanotransduction, and both gain and loss of its activity causes defective cell behaviour. Here, we examine how altering vinculin activity perturbs integrin function within the context of $\textit{Drosophila}$ development. Whereas loss of vinculin produced relatively minor phenotypes, gain of vinculin activity, via a loss of head-tail autoinhibition, caused lethality. The minimal domain capable of inducing lethality is the talin-binding D1 domain, and this appears to require...
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