Worm Breeder's Gazette 15(1): 47 (October 1, 1997)
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||Institute of Zoology, University of Fribourg, Perolles, CH-1700 Fribourg, Switzerland|
|2||MPI fuer Biochemie, D-82152 Martinsried, Germany|
Homeotic (Hox) genes participate in the specification of differentiating structures along the anteroposterior body axis of animals. The third chromosome of C. elegans contains a cluster (HOM-C) of four Hox genes: lin-39, ceh-13, mab-5 and egl-5 . Mutants defective for three of these genes, lin-39, mab-5 and egl-5, show modifications in cell fate along the anteroposterior body axis of the nematode during post-embryogenesis1. In order to study the function of ceh-13, which is the C. elegans labial orthologue, a Tc1 insertion was isolated from the frozen mutant bank in the laboratory of R. H. A. Plasterk2. This Tc1 insertion is located in the first intron of ceh-13 (pk20::Tc1). Since the ceh-13 intron insertion has no phenotype, a bidirectional deletion derivative, ceh-13 (sw1), was isolated. This deletion removes most of the first intron, all of the second and third exons, which contain the homeodomain and 22 bases of the 3'UTR. The ceh-13 mutant shows a Vab (variable abnormal morphophology) phenotype which ranges from embryonic lethality to larval arrest with a low frequency of "sick" escapers (<10%), suggesting that the phenotype is not fully penetrant. The ceh-13 larvae do not elongate properly and most of them arrest at the L1 larval stage. 54% of ceh-13 (sw1) broods arrest during embryogenesis, with the earliest stage of arrest occuring soon after elongation begins. In C. elegans, body-wall muscles and hypodermal cells play a crucial role during the elongation process. Indeed, the hypodermal cells change their relatively spherical shape into a long, thin one. This morphogenetic transformation is driven by a microfilament-dependent force3. We looked, therefore, at the pattern of the hypodermis in ceh-13 mutants using a 4D microscope and by staining with the MH27 and anti-LIN-26 antibodies (kindly provided by R. Waterson and M. Labouesse, respectively). We found that the lateral hypodermal cells, called the seam cells, show an anterior mispatterning, whereas the commitment to hypodermal fate is normal. At the stage of embryonic morphogenesis, the lateral hypodermis is composed of a row of ten cells: H0, H1, H2, V1-6 and T. In ceh-13 mutants, the row of seam cells is disorganized at the position of H2 and V1. These defects in the patterning of the hypodermis correlate with the expression pattern of ceh-13. At this stage, CEH-13 has been detected in many cell types including some of the seam cells, H2 to V6 (Wittmann et al., submitted). Furthermore, the preliminary lineaging of ceh-13 embryos has not revealed any "homeotic" transformations of the lineage, however, this does not exclude transformations at later larval stages, as has been shown to be the case for the other members of the HOM cluster of C. elegans 1. ceh-13 is also expressed at later stages, including the male tail, and we are currently characterizing its role in this morphogenetic process. 1 Salser and Kenyon, 1994, TIG 10: 159-164. 2 Zwaal et al.,PNAS, 1993, 90: 7431-7435. 3 Priess and Hirsh, 1986, Dev. Biol. 117: 156-173.