A dominant mutation of mig-22 suppresses DTC migration defects of mig-17. Export

@inproceedings{citeulike:3333869, abstract = { 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.}, author = {Sassa, Toshihiro and Toyoda, Hidenao and Ohkura, Kiyotaka and Nishiwaki, Kiyoji}, citeulike-article-id = {3333869}, citeulike-linkout-0 = {http://www.wormbase.org/db/misc/paper?name=WBPaper00030675}, journal = {International Worm Meeting}, keywords = {c28c128, c\_elegans, caenorhabditis\_elegans, celegans, elegans, f57b74, hlh-12, meeting\_abstract, mig-17, mig-22, nematode, par24, sma-2, sqv-5, t24d11, unc-32, wormbase, zk3702, zk6378}, posted-at = {2008-09-24 21:04:41}, priority = {3}, title = {A dominant mutation of mig-22 suppresses DTC migration defects of mig-17.}, url = {http://www.wormbase.org/db/misc/paper?name=WBPaper00030675}, year = {2007} }

TY - CONF ID - citeulike:3333869 L3 - citeulike-article-id:3333869 N2 - 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. JF - International Worm Meeting TI - A dominant mutation of mig-22 suppresses DTC migration defects of mig-17. KW - c28c128 KW - c_elegans KW - caenorhabditis_elegans KW - celegans KW - elegans KW - f57b74 KW - hlh-12 KW - meeting_abstract KW - mig-17 KW - mig-22 KW - nematode KW - par24 KW - sma-2 KW - sqv-5 KW - t24d11 KW - unc-32 KW - wormbase KW - zk3702 KW - zk6378 AU - Sassa, Toshihiro AU - Toyoda, Hidenao AU - Ohkura, Kiyotaka AU - Nishiwaki, Kiyoji PY - 2007/// UR - http://www.wormbase.org/db/misc/paper?name=WBPaper00030675 ER -