Worm Breeder's Gazette 14(3): 61 (June 1, 1996)

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.


Jonathan Pettitt1, William B. Wood2, Ronald H. A. Plasterk1

1 The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.
2 Dept. of MCDB, University of Colorado, Boulder, CO 80309-0347, USA.

cdh-3 encodes a member of the cadherin superfamily. We have previously reported the determination of the expression pattern of cdh-3 in embryos undergoing morphogenesis, as well as the isolation of a deletion allele of cdh-3 (WBG 13 (2), 76, 1994; 1995 Meeting Abstracts, #416). We have continued our analysis of cdh-3 expression using a GFP reporter construct and have further characterized the phenotype resulting from the pk87 deletion allele.

Expression of the cdh-3::GFP reporter construct is confined to ectodermally derived cells. We observe expression, beginning just prior to the start of embryonic morphogenesis, in the seam cells, both arcade cells, F, U, the excretory cell, and hyp10 and hyp11. Expression in these cells continues throughout postembryonic development, with the exception of hyp10, hyp11 and the excretory cell; expression in these cells continues only into the L1. During the L3 stage we see cdh-3::GFP expression in the anchor cell and the invaginating vulval epidermis, continuing throughout the development of the vulva. At the same time we also see expression in the VC neurons and the two HSNs.

More careful examination of animals homozygous for the pk87 mutation revealed abnormalities in the morphogenesis of hyp10 (see table). These defects can be rescued by a wild-type copy of cdh-3 and are consistent with the expression of cdh-3::GFP in this cell during the period that it is undergoing a change in cell shape. However, we have not been able to detect any other defects in pk87 homozygotes. The absence of defects in the other cells that express cdh-3 reporter constructs hints that other genes may substitute for cdh-3 function. Future work will address this possibility, both by isolating mutations in the other cdh genes that have been identified and by carrying out screens for mutations that cause additional phenotypes in a cdh-3(pk87) background.

                                         hyp10 morphology#
Genotype                             N     wild-type      abnormal
cdh-3(+)                            115       100%          0.0%   
cdh-3(pk87)                         170        24%         76.0% 
cdh-3(pk87; pkIs243)*               112        97%          2.5% 
# Abnormalities include ectopic protrusions as well as complete failure to elongate.
* Strain carrying an integrated array of cdh-3(&#43).