Worm Breeder's Gazette 15(2): 34 (February 1, 1998)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
|1||Department of Pathology, Division of Cancer Research, University of Zurich, CH-8091 Switzerland|
|2||Department of Biological Sciences, University of Maryland, Baltimore, MD 21250|
|3||Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305|
|4||Department of Pathology, Division of Cancer Research, University of Z!rich, CH-8091 Switzerland|
The six vulval precursor cells (VPCs) P3.p through P8.p are equivalent in their potential to adopt one of three vulval cell fates that are specified by the anchor cell signal. VPCs are connected to each other and to hyp7 through adherens junctions that stain with the MH27 antibody, while Pn.p cells that do not belong to the vulval equivalence group loose their adherens junctions and fuse with hyp7 during the first larval stage. We are interested in the role of the apr-1 gene in vulval development. apr-1 encodes a protein similar to the human Adenomatous Polyposis Colon tumor suppressor APC. APR-1 co-localizes with the MH27 antigen at the adherens junctions of the VPCs, the seam cells and the lateral hypodermis of the embryo. Since RNAi experiments have indicated that loss of apr-1 function causes an embryonic lethal phenotype (C. Rocheleau et al., Cell 90:707-716 (1997)), we have specifically down regulated APR-1 expression in the VPCs by expressing antisense apr-1 cDNA under control of the Pn.p cell-specific lin-31 promoter. VPCs expressing antisense apr-1 RNA exhibit no detectable APR-1 staining, lack adherens junctions in 53% of the cases (n=114) and adopt an undivided, non-vulval cell fate in 70% of the cases (n=30), resulting in an 80% penetrant vulvaless phenotype. Mutations in the beta-catenin/armadillo related gene bar-1 and in the HOX gene lin-39 cause a similar phenotype, and APR-1 specifically interacts with BAR-1 in a yeast two-hybrid assay. These observations have suggested two possible models: (1) APR-1 might act together with BAR-1 to specify the vulval equivalence group by inducing lin-39 expression in the VPCs, or (2) APR-1 might be required to maintain the adherens junctions and thus prevent the VPCs from fusing with hyp7 before the vulva is induced.