Wnt and EGF pathways act together to induce C. elegans male hook development
Abstract
Comparative studies of vulva development between Caenorhabditis elegans and other nematode species have provided some insight into the evolution of patterning networks. However, molecular genetic details are available only in C. elegans and Pristionchus pacificus. To extend our knowledge on the evolution of patterning networks, we studied the C. elegans male hook competence group (HCG), an equivalence group that has similar developmental origins to the vulval precursor cells (VPCs), which generate the vulva in the hermaphrodite. Similar to VPC fate specification, each HCG cell adopts one of three fates (1°, 2°, 3°), and 2° HCG fate specification is mediated by LIN-12/Notch. We show that 2° HCG specification depends on the presence of a cell with the 1° fate. We also provide evidence that Wnt signaling via the Frizzled-like Wnt receptor LIN-17 acts to specify the 1° and 2° HCG fate. A requirement for EGF signaling during 1° fate specification is seen only when LIN-17 activity is compromised. In addition, activation of the EGF pathway decreases dependence on LIN-17 and causes ectopic hook development. Our results suggest that WNT plays a more significant role than EGF signaling in specifying HCG fates, whereas in VPC specification EGF signaling is the major inductive signal. Nonetheless, the overall logic is similar in the VPCs and the HCG: EGF and/or WNT induce a 1° lineage, and LIN-12/NOTCH induces a 2° lineage. Wnt signaling is also required for execution of the 1° and 2° HCG lineages. lin-17 and bar-1/β-catenin are preferentially expressed in the presumptive 1° cell P11.p. The dynamic subcellular localization of BAR-1–GFP in P11.p is concordant with the timing of HCG fate determination.
Additional Information
© 2009 Elsevier. Received 16 July 2008; revised 26 November 2008; accepted 19 December 2008. Available online 30 December 2008. We thank Jennifer Green for the HS::CAM-1 strain, Bhagwati Gupta for the lin-17::GFP construct, David Eisenmann for the BAR-1– GFP strain, Helen Chamberlin for unpublished data the Caenorhabditis Genetic Center for providing some strains used in this study, Raymond Lee for suggesting eat-4::GFP as a neuronal marker and Takao Inoue for the cwn-1::GFP and cwn-2::GFP reporters. We thank Mihoko Kato, Cheryl Van Buskirk, Jennifer Green, Takao Inoue, Weiwei Zhong, Jolene Fernandes, Iva Greenwald, William Fixsen, Victor Ambros and Elissa Hallem for helpful discussions and critical reading of this manuscript. P.W.S. and H.R.H. are Investigators of the Howard Hughes Medical Institute. H.R.H. was supported by NIH grant GM24663. A.S. was supported by a HHMI Pre-Doctoral Fellowship. While at MIT, M.A.H., P.W.S. and E.L.F. were supported by USPHS training grant GM07287. Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.ydbio.2008.12.023.Attached Files
Accepted Version - nihms102170.pdf
Supplemental Material - Yu2009p1028Dev_Biol_supp.doc
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Additional details
- PMCID
- PMC2695933
- Eprint ID
- 14506
- DOI
- 10.1016/j.ydbio.2008.12.023
- Resolver ID
- CaltechAUTHORS:20090707-095026171
- NIH
- GM24663
- Howard Hughes Medical Institute (HHMI)
- NIH
- GM07287
- Created
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2009-08-12Created from EPrint's datestamp field
- Updated
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2021-11-08Created from EPrint's last_modified field