Abstract
Drosophila fat body-derived SPARC acts as a chaperone for collagen IV (Col(IV)), enabling their diffusion and incorporation into distal tissue basement membranes (BMs). Disruption of SPARC or Col(IV) production by the fat body is lethal, despite expression by other tissues such as imaginal discs. Wing disc-derived SPARC does not associate with Col(IV) in BMs and is not essential for survival. We show that differential association of fat body- and wing disc-derived SPARC with Col(IV) is not due to differences in SPARC glycosylation nor to the absence of SPARC and Col(IV) co-expression. Further, we demonstrate that SPARC domain II/III produced by the fat body is sufficient for Col(IV) diffusion to both proximal and distal BMs, and rescues lethality associated with loss of SPARC. However, SPARC domain II/III does not diffuse beyond the hemolymph. Thus, the essential Col(IV) chaperone-like activity specific to fat body-derived SPARC is not required beyond the hemolymph.