During development of the Caenorhabditis elegans gonad, the gonadal leader cells, called distal tip cells (DTCs), migrate in a U-shaped pattern to form the U-shaped gonad arms. The ADAMTS (a disintegrin and metalloprotease with thrombospondin motifs) family metalloproteases MIG-17 and GON-1 are required for correct DTC migration. Mutations in
mig-17 result in misshapen gonads due to the misdirected DTC migration, and mutations in
gon-1 result in shortened and swollen gonads due to the premature termination of DTC migration. Although the phenotypes shown by
mig-17 and
gon-1 mutants are very different from one another, mutations that result in amino acid substitutions in the same basement membrane protein genes,
emb-9/collagen IV
a1,
let-2/collagen IV
a2 and
fbl-1/fibulin-1, were identified as genetic suppressors of
mig-17 and
gon-1 mutants. To understand the roles shared by these two proteases, we examined the effects of the
mig-17 suppressors on
gon-1 and the effects of the
gon-1 suppressors and enhancers on
mig-17 gonadal defects. Some of the
emb-9,
let-2 and
fbl-1 mutations suppressed both
mig-17 and
gon-1, whereas others acted only on
mig-17 or
gon-1. These results suggest that
mig-17 and
gon-1 have their specific functions as well as functions commonly shared between them for gonad formation. The levels of collagen IV accumulation in the DTC basement membrane were significantly higher in the
gon-1 mutants as compared with wild type and were reduced to the wild-type levels when combined with suppressor mutations, but not with enhancer mutations, suggesting that the ability to reduce collagen IV levels is important for
gon-1 suppression.