The ADAMTSs are a family of zinc-dependent metalloproteases that play important roles in a variety conditions. Members of ADAMTS family have been implicated in the cleavage of proteoglycan and the control of organ shape during development. The C.elegans
gon-1</I> gene, an ADAMTS family member, was found to be important in gonadal morphogenesis. It was reported that
gon-1</I> is expressed at Distal Tip Cell (DTC) and body wall muscle. DTC does not migrate in
gon-1</I> mutant and that the mutant shows gonad elongation defect. Furthermore, abnormal DTC structure was observed in
gon-1</I> mutants. We investigated which organelles are influenced by
gon-1</I> RNAi. We labeled ER with C31E10.7::Venus (Cytochrome
b5 reporter) under the control of the DTC specific
lag-2</I> promoter, the ER morphology was changed by knock down of
gon-1</I> gene. We performed
gon-1</I> RNAi in the transgenic animals that expressed Venus fused to secretory signal sequence under the control of the
lag-2</I> promoter or
myo-3</I> promoter. Knocking down of the
gon-1</I> gene resulted in an inhibition of fluorescent protein secretion from DTC and muscle. In addition,
gon-1</I> RNAi induced
xbp-1</I> mRNA splicing and up-regulation of the Bip homolog,
hsp-4</I>. These results suggest that
gon-1</I> RNAi induced ER stress. We found that down-regulation of Dipeptidyl peptidase-IV like proteases (dpf</I>s) expression suppress Gon-1 phenotype such as DTC migration defect, secretion defects. Furthermore, down-regulation of dpf</I>s alleviated ER stress induced by
gon-1</I> RNAi. To determine the unfolded protein response pathway that involves dpf</I>s and
gon-1</I>, we performed each RNAi against orthologues of ATF6, PERK, IRE1 and XBP1. We found that inactivation of dpf</I>s function does not suppress Gon-1 phenotype in
ire-1</I> (RNAi) or
xbp-1</I> (RNAi) background. We speculate that
ire-1/xbp-1</I> pathway is playing a main role in the
gon-1/dpf</I> pathway.