The roles of EGF and Wnt signaling during patterning of the C. elegans Bgamma/delta Equivalence Group.
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 Bgamma fate within the Bgamma/delta equivalence pair, while Notch signaling is required for Bdelta fate specification. In addition, TGF-beta signaling by dbl-1/dpp controls ceh-13/labial/Hox1 expression in Bgamma.


RESULTS
We show that EGF-Ras signaling is required for Bgamma 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 Bgamma. In addition, our results indicate that lin-44/Wnt, mom-2/Wnt and lin-17/Fz are necessary to maintain the division of Bgamma 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 Bgamma. 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 Bgamma 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 Bgamma division, perhaps to orient the Bgamma 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.
Seah
Adeline
A
California Institute of Technology, Pasadena, 91125, USA. seah@caltech.edu
Sternberg
Paul W
PW
D000818:Animals; D019521:Body Patterning; D017173:Caenorhabditis elegans / Q000196:embryology* / Q000235:genetics / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000378:metabolism; D004815:Epidermal Growth Factor / Q000378:metabolism*; D005260:Female; D018398:Homeodomain Proteins / Q000378:metabolism; D008297:Male; D015398:Signal Transduction; D014157:Transcription Factors / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014844:Vulva / Q000196:embryology; D051153:Wnt Proteins / Q000378:metabolism*
C118851:CEH-13 protein, C elegans; D029742:Caenorhabditis elegans Proteins; D004268:DNA-Binding Proteins; D018398:Homeodomain Proteins; C097533:Lin-1 protein, C elegans; C095846:Sur-2 protein, C elegans; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D051153:Wnt Proteins; C081464:lin-31 protein, C elegans; D004815:Epidermal Growth Factor