Tiggrin is a novel extracellular matrix ligand for the Drosophila PS2
integrins, We have used flanking P elements to generate a precise dele
tion of tiggrin. Most flies lacking tiggrin die as larvae or pupae, A
few adults do emerge and these appear to be relatively normal, display
ing only misshapen abdomens and a low frequency of wing defects, Exami
nation of larvae shows that muscle connections, function and morpholog
y are defective in tiggrin mutants. Muscle contraction waves that exte
nd the length of the larvae are much slower in tiggrin mutants, Direct
examination of bodywall muscles shows defects in muscle attachment si
tes, where tiggrin is specifically localized, and muscles appear thinn
er. Transgenes expressing tiggrin are capable of rescuing tiggrin muta
nt phenotypes, Transgenes expressing a mutant tiggrin, whose Arg-Gly-A
sp (RGD) integrin recognition sequence has been mutated to Leu-Gly-Ala
(LGA) show much reduced, but significant, rescuing ability. Cell spre
ading assays detect no interactions of this mutant tiggrin with PS2 in
tegrins, Therefore, while the RGD sequence is critical for PS2 interac
tions and full activity in the whole fly, the mutant tiggrin retains s
ome function(s) that are probably mediated by interactions with other
ECM molecules or cell surface receptors.