The roles of EGF and Wnt signaling during patterning of the C. elegans Bγ/δ Equivalence Group
- Creators
- Seah, Adeline
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Sternberg, Paul W.
Abstract
Background: During development, different signaling pathways interact to specify cell fate by regulating transcription factors necessary for fate specification and morphogenesis. In Caenorhabditis elegans, the EGF-Ras and Wnt signaling pathways have been shown to interact to specify cell fate in three equivalence groups: the vulval precursor cells (VPCs), the hook competence group (HCG) and P11/12. In the VPCs, HCG and P11/12 pair, EGF and Wnt signaling positively regulate different Hox genes, each of which also functions during fate specification. In the male, EGF-Ras signaling is required to specify the Bγ fate within the Bγ/δ equivalence pair, while Notch signaling is required for Bδ fate specification. In addition, TGF-β signaling by dbl-1/dpp controls ceh-13/labial/Hox1 expression in Bγ. Results: We show that EGF-Ras signaling is required for Bγ expression of ceh-13/labial/Hox1. The transcription factors lin-1/ETS and lin-31/Forkhead, functioning downstream of the EGF pathway, as well as sur-2/MED23 (a component of the Mediator complex) also control ceh-13 expression in Bγ. In addition, our results indicate that lin-44/Wnt, mom-2/Wnt and lin-17/Fz are necessary to maintain the division of Bγ along a longitudinal axis. We also show that dbl-1/dpp acts either in parallel or downstream of EGF pathway to regulate ceh-13/Hox1 expression in Bγ. Lastly, we find that a dbl-1/dpp null mutation did not cause any vulval or P12 defects and did not enhance vulval and P12 defects of reduction-of-function mutations of components of the EGF pathway. Conclusions: ceh-13/labial/Hox1 expression in Bγ is regulated by the EGF pathway and downstream factors lin-1/ETS lin-31/Forkhead and sur-2/MED23. Wnt signaling is required for proper Bγ division, perhaps to orient the Bγ mitotic spindle. Our results suggest that dbl-1/dpp is not required for VPC and P12 specification, highlighting another difference among these EGF-dependent equivalence groups.
Additional Information
© 2009 Seah and Sternberg; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Received: 18 September 2009. Accepted: 31 December 2009. Published: 31 December 2009. We thank Fritz Muller for pMF1, Cheryl Van Buskirk for the HS::EGF strain, Helen Chamberlin for discussions and unpublished data, Erich Schwarz for discussions on motif enrichment, Mihoko Kato and Cheryl Van Buskirk for discussions and helpful comments on the manuscript. PWS is an Investigator of the Howard Hughes Medical Institute, which supported this work. AS was supported by a HHMI Pre-Doctoral Fellowship. Authors' contributions: AS participated in the design of the study, carried out all experimental procedures and drafted the manuscript. PWS conceived of the study and helped to draft the manuscript. Both authors have read and approved the final manuscript.Attached Files
Published - Seah2009p7009BMC_Dev_Biol.pdf
Supplemental Material - 1471-213x-9-74-s1.doc
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Additional details
- PMCID
- PMC2813230
- Eprint ID
- 17703
- Resolver ID
- CaltechAUTHORS:20100309-100907034
- Howard Hughes Medical Institute (HHMI)
- Created
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2010-03-15Created from EPrint's datestamp field
- Updated
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2021-11-08Created from EPrint's last_modified field