TY - JOUR
T1 - Multiple redundant Wnt signaling components function in two processes during C. elegans vulval development
AU - Gleason, Julie E.
AU - Szyleyko, Elizabeth A.
AU - Eisenmann, David M.
N1 - Funding Information:
We thank Rik Korswagen for providing huIs24 and a cwn-1(ok546); egl-20(n585) strain, Mike Herman for providing a lin-44(n1792); egl-20(n585) strain and the C. elegans Gene Knockout Consortium for their invaluable service to the community. We thank Rik Korswagen, Toshia Myers and Iva Greenwald for generously sharing results. We thank Sara Peyrot for beginning the analysis of Wnt redundancy in vulval development, and we thank current and previous members of the Eisenmann laboratory for support and helpful discussions. Some nematode strains used in this work were provided by the Caenorhabditis Genetics Center, which is funded by the National Institutes of Health National Center for Research Resources (NCRR). This work was supported by NSF grant IBN-0131485 and NIH grant GM65424.
PY - 2006/10/15
Y1 - 2006/10/15
N2 - In Caenorhabditis elegans, vulval precursor cell (VPC) fate is specified by the action of RTK/Ras, Notch and Wnt signaling pathways. While the identity of signals for the Ras and Notch pathways is known, the source and identity of the Wnt ligand acting on the VPCs are unknown. Single mutations in any of the five Wnt genes (lin-44, cwn-1, cwn-2, egl-20 and mom-2) do not cause strong defects in VPC fate specification, suggesting that functionally redundant Wnts are required. Surprisingly, we found that all five Wnts influence VPC fate. The strongest defects we observed were in the lin-44; cwn-1; egl-20 triple mutant. Anterior VPCs were more strongly affected by loss of Wnt function than posterior VPCs, and expression from Wnt{proportion}GFP transcriptional reporters showed that the Wnts most strongly affecting VPC fate were expressed predominantly in the posterior, suggesting that some of the redundant Wnt ligands act over a distance to affect the VPCs. In addition to ligand redundancy, we found that at least three Wnt receptors, lin-17, mom-5 and mig-1, function in the VPCs. We also examined ligand and receptor function in another Wnt-mediated vulval process, the orientation of the P7.p lineage. Here, too, we found that four of five Wnt receptors can influence P7.p orientation, suggesting that a surprising amount of functional redundancy exists in Wnt signaling during C. elegans vulval induction.
AB - In Caenorhabditis elegans, vulval precursor cell (VPC) fate is specified by the action of RTK/Ras, Notch and Wnt signaling pathways. While the identity of signals for the Ras and Notch pathways is known, the source and identity of the Wnt ligand acting on the VPCs are unknown. Single mutations in any of the five Wnt genes (lin-44, cwn-1, cwn-2, egl-20 and mom-2) do not cause strong defects in VPC fate specification, suggesting that functionally redundant Wnts are required. Surprisingly, we found that all five Wnts influence VPC fate. The strongest defects we observed were in the lin-44; cwn-1; egl-20 triple mutant. Anterior VPCs were more strongly affected by loss of Wnt function than posterior VPCs, and expression from Wnt{proportion}GFP transcriptional reporters showed that the Wnts most strongly affecting VPC fate were expressed predominantly in the posterior, suggesting that some of the redundant Wnt ligands act over a distance to affect the VPCs. In addition to ligand redundancy, we found that at least three Wnt receptors, lin-17, mom-5 and mig-1, function in the VPCs. We also examined ligand and receptor function in another Wnt-mediated vulval process, the orientation of the P7.p lineage. Here, too, we found that four of five Wnt receptors can influence P7.p orientation, suggesting that a surprising amount of functional redundancy exists in Wnt signaling during C. elegans vulval induction.
KW - C. elegans
KW - CK1
KW - Development
KW - Differentiation
KW - Frizzled
KW - GSK-3
KW - Genetics
KW - Redundancy
KW - Vulva
KW - Wnt
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U2 - 10.1016/j.ydbio.2006.06.050
DO - 10.1016/j.ydbio.2006.06.050
M3 - Article
C2 - 16930586
AN - SCOPUS:33748969657
SN - 0012-1606
VL - 298
SP - 442
EP - 457
JO - Developmental biology
JF - Developmental biology
IS - 2
ER -