During development, adhesion between distinct cell types is crucial for tissue assembly. Now, on p.785, Eliezer Gilsohn and Talila Volk show that the novel tendon-derived protein Slowdown (Slow) promotes muscle integrity in Drosophila embryos by ensuring that myotendinous junctions (MTJs) form correctly between muscle and tendon cells to `glue' them together. MTJs, a type of hemi-adherens junction, consist mainly of muscle-specific integrin receptors and their tendon-derived extracellular matrix ligand thrombospondin. The researchers identified Slow in a microarray screen for target genes of the tendon-specific transcription factor Stripe. They show that muscle and/or tendons rupture upon muscle contraction in slow mutant larvae and that slow mutant flies are unable to fly. These defects, they report, are the result of improper assembly of the embryonic MTJ. Other experiments indicate that Slow normally forms a complex with thrombospondin that can alter the morphology and directionality of muscle ends. Thus, Gilsohn and Volk conclude, Slow promotes muscle integrity by modulating integrin-mediated adhesion at MTJs.