The U-shape of the gonad arms is formed by directional movement of distal tip cells (DTCs), which is regulated by MIG-17, an ADAMTS protease. MIG-17 is secreted from the muscle cells and localizes to the gonadal basement membrane to control DTC migration. To obtain further insights into the molecular mechanisms of DTC migration involving MIG-17, we isolated suppressor mutants of
mig-17 DTC migration defects. One of these,
k185 was a dominant suppressor and mapped between
sma-2 and
unc-32 on LGIII. A genomic fragment containing the
mig-22 gene from
k185 mutant animals could suppress
mig-17 when introduced as a transgene. We previously reported that the MIG-22 protein is chondroitin polymerizing factor, a co-factor for chondroitin synthase whose loss-of-function mutations
(k141 and
tk24) cause abnormal DTC migration similar to that seen in
mig-17 mutants. Double mutants between
mig-17(null) and
mig-22 alleles showed enhanced DTC migration defects, suggesting that these genes do not constitute a single pathway. The MIG-17-Venus fusion protein localized normally to the gonad in
mig-22(
k141) mutants. Because
mig-22(
k185) mutants showed normal DTC migration,
k185 does not appear to be a simple loss-of-function mutation. The expression of the
mig-22(
k185) gene under the control of the
mig-24 promoter, which drives gene expressed in DTCs, rescued DTC migration defects of
mig-17 mutants. Surprisingly, transgenic expression of wild-type
mig-22 under either a DTC or a seam cell-specific promoter also rescued
mig-17. The expression of
sqv-5, a gene for chondroitin synthase, under the
mig-22 promoter failed to rescue
mig-17. To determine whether chondroitin biosynthesis is affected in
mig-22(
k185), we are trying to analyze the levels of chondroitin in
mig-17;
mig-22(
k185) and
mig-17 mutants.