Wnt signaling and an APC-related gene specify endoderm in early C. elegans embryos

Christian E. Rocheleau, William D. Downs, Rueyling Lin, Claudia Wittmann, Yanxia Bei, Yoon Hee Cha, Mussa Ali, James R. Priess, Craig C. Mello

Research output: Contribution to journalArticlepeer-review

549 Scopus citations

Abstract

In a 4-cell stage C. elegans embryo, signaling by the P2 blastomere induces anterior-posterior polarity in the adjacent EMS blastomere, leading to endoderm formation. We have taken genetic and reverse genetic approaches toward understanding the molecular basis for this induction. These studies have identified a set of genes with sequence similarity to genes that have been shown to be, or are implicated in, Wnt/ Wingless signaling pathways in other systems. The C. elegans genes described here are related to wnt/ wingless, porcupine, frizzled, β-catenin/armadillo, and the human adenomatous polyposis coli gene, APC. We present evidence that there may be partially redundant inputs into endoderm specification and that a subset of these genes appear also to function in determining cytoskeletal polarity in certain early blastomeres.

Original languageEnglish (US)
Pages (from-to)707-716
Number of pages10
JournalCell
Volume90
Issue number4
DOIs
StatePublished - Aug 22 1997
Externally publishedYes

Bibliographical note

Funding Information:
We thank Bruce Bowerman for communicating unpublished results and Iva Greenwald, Tae Ho Shin, and Sue Euling for helpful discussions. Some strains were obtained from the C. elegans Genetic Stock Center, which is funded by a grant from the National Institutes of Health National Center for Research Support. Special thanks to Yuji Kohara and to the entire Worm Genome Consortium for providing the clones and sequences that made this work possible. Support was provided in part by a grant from the NIH, a PEW scholarship, and career development awards from the American Cancer Society and March Of Dimes birth defects foundation to C. C. M. W. D. D. was supported by the Damon Runyon-Walter Winchell Cancer Research Fund, and R. L., Y.-H. C., and J. R. P. were supported by the HHMI and a grant from the NIH.

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