Abstract
Heterodimeric cell surface receptor integrin is widely expressed in the nervous system, but its specific role during axon development has not been directly tested
in vivo
. We show that the
Drosophila
nervous system expresses low levels of positron-specific (PS) integrin subunits αPS1, αPS2, and βPS during embryonic axogenesis. Furthermore, certain subsets of neurons express higher levels of integrin mRNAs than do the rest. Null mutations in either the αPS1 or αPS2 subunit gene cause widespread axon pathfinding errors that can be rescued by supplying the wild-type integrin subunit to the mutant nervous system. In contrast, misexpressing either the αPS1 or αPS2 integrin subunit in all neurons leads to no obvious axon pathfinding errors. We propose that integrin does not itself serve as either a “clutch” constituting molecule or a specific growth cone “receptor,” as proposed previously, but rather as part of a molecular network that cooperatively guarantees accurate axon guidance.
