Re-programming of C. elegans male epidermal precursor fates by Wnt, Hox, and LIN-12/Notch activities.
In Caenorhabditiselegans males, different subsets of ventral epidermal precursor (Pn.p) cells adopt distinct fates in a position-specific manner: three posterior cells, P(9-11).p, comprise the hook sensillum competence group (HCG) with three potential fates (1 degrees , 2 degrees , or 3 degrees ), while eight anterior cells, P(1-8).p, fuse with the hyp7 epidermal syncytium. Here we show that activation of the canonical BAR-1 beta-catenin pathway of Wnt signaling alters the competence of P(3-8).p and specifies ectopic HCG-like fates. This fate transformation requires the Hox gene mab-5. In addition, misexpression of mab-5 in P(1-8).p is sufficient to establish HCG competence among these cells, as well as to generate ectopic HCG fates in combination with LIN-12 or EGF signaling. While increased Wnt signaling induces predominantly 1 degrees HCG fates, increased LIN-12 or EGF signaling in combination with MAB-5 overexpression promotes 2 degrees HCG fates in anterior Pn.p cells, suggesting distinctive functions of Wnt, LIN-12, and EGF signaling in specification of HCG fates. Lastly, wild-type mab-5 function is necessary for normal P(9-11).p fate specification, indicating that regulation of ectopic HCG fate formation revealed in anterior Pn.p cells reflect mechanisms of pattern formation during normal hook development.
Yu
Hui
H
HHMI and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. hui.yu@rice.edu
Seah
Adeline
A
Sternberg
Paul W
PW
D000818:Animals; D030801:Animals, Genetically Modified; D019521:Body Patterning / Q000235:genetics / Q000502:physiology*; D017173:Caenorhabditis elegans / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D019070:Cell Lineage; D049109:Cell Proliferation; D000078404:Epidermal Cells; D004815:Epidermal Growth Factor / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D004817:Epidermis / Q000378:metabolism; D005260:Female; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D008856:Microscopy, Fluorescence; D009154:Mutation; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D051880:Receptors, Notch / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D051153:Wnt Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology
D029742:Caenorhabditis elegans Proteins; D018398:Homeodomain Proteins; C101684:LIN-17 protein, C elegans; C082460:Lin-12 protein, C elegans; C081538:Mab-5 protein, C elegans; D008565:Membrane Proteins; D043562:Receptors, G-Protein-Coupled; D051880:Receptors, Notch; D014157:Transcription Factors; D051153:Wnt Proteins; D004815:Epidermal Growth Factor