An HMG1-like protein facilitates Wnt signaling in Caenorhabditis elegans.
We show that during Caenorhabditis elegans male spicule development, the specification of a glial versus neuronal cell fate in a canonical neurogenic sublineage is dependent on Wnt signaling. Inactivation of a Wnt signaling pathway mediated by the Wnt receptor LIN-17 transforms the SPD sheath cell into its sister, the SPD neuron. We discovered a new mutant, son-1, that displays this same cell fate transformation. The son-1 mutation enhances the phenotypes of reduction-of-function lin-17 mutants in several developmental processes, including vulva development, somatic gonad development, and male tail patterning. son-1 encodes an HMG1/2-like DNA-binding protein and is localized in all cell nuclei through development as revealed by a GFP reporter construct. Disruption of son-1 function by RNA-mediated interference results in the same spicule defect as caused by overexpression of POP-1, a TCF/LEF class HMG protein known to act downstream of the Wnt signaling pathway. Our results provide in vivo evidence for the functional involvement of an HMG1/2-like protein, SON-1, in Wnt signaling. The sequence nonspecific HMG protein SON-1 and the sequence specific HMG protein POP-1 might both act in the Wnt responding cells to regulate gene transcription in opposite directions.
Jiang
L I
LI
Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, California 91125 USA.
Sternberg
P W
PW
D000595:Amino Acid Sequence; D000818:Animals; D030801:Animals, Genetically Modified / Q000378:metabolism; D001483:Base Sequence; D017173:Caenorhabditis elegans / Q000166:cytology / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D029742:Caenorhabditis elegans Proteins; D019070:Cell Lineage; D002874:Chromosome Mapping; D004268:DNA-Binding Proteins / Q000378:metabolism; D005838:Genotype; D049452:Green Fluorescent Proteins; D006609:High Mobility Group Proteins / Q000378:metabolism*; D008164:Luminescent Proteins / Q000378:metabolism; D008297:Male; D015778:Minor Histocompatibility Antigens; D008954:Models, Biological; D008957:Models, Genetic; D008969:Molecular Sequence Data; D009474:Neurons / Q000378:metabolism; D010641:Phenotype; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled; D017386:Sequence Homology, Amino Acid; D015398:Signal Transduction; D013997:Time Factors; D051153:Wnt Proteins; D029961:Zebrafish Proteins
D029742:Caenorhabditis elegans Proteins; D004268:DNA-Binding Proteins; D006609:High Mobility Group Proteins; C101684:LIN-17 protein, C elegans; D008164:Luminescent Proteins; D015778:Minor Histocompatibility Antigens; D011518:Proto-Oncogene Proteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C088203:SON protein, human; D051153:Wnt Proteins; D029961:Zebrafish Proteins; C096787:pop-1 protein, C elegans; D049452:Green Fluorescent Proteins