Worm Breeder's Gazette 14(4): 59 (October 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.
IGBMC, BP163, 67404 Illkirch Cedex, France.
We are interested in understanding how the fates of ectodermal cells are specified during embryogenesis. The gene lin-26 is expressed in all non-neuronal ectodermal cells and is required for normal development of these cells. One approach to identify genes that specify the fates of ectodermal cells is to identify zygotic genes that would control lin-26 expression. Using antibodies against the LIN-26 protein, we have examined 3600 genomes after EMS mutagenesis for abnormal LIN-26 expression patterns, concentrating on zygotic lethal mutations. We identified a single penetrant mutation that affected lin-26 expression. This mutation was called mc14 and defined the gene ale-1, an acronym for abnormal lin-26 expression (in a preliminary report at the 1996 European Worm Meeting, this gene was temporarily named emb-36). ale-1(mc14) mapped close to spe-6 (LGIII). ale-1(mc14) embryos arrested at the comma/1.5-fold stage with approximately 25% fewer LIN-26 positive hypodermal nuclei in their bodies (i.e. between the ADE sheath nucleus and the rectum) and 35% fewer in their tails. MH27 staining was also strongly abnormal in the body. By comparison, ale-1 embryos had essentially normal numbers of LIN-26 positive nuclei in their heads. To try and understand why ale-1 embryos do not express lin-26 normally we lineaged two embryos (1). In one embryo 23 of the 32 AB precursors that generate hypodermal cells 240 min after fertilization failed to divide; similarly the last round of cell divisions failed to occur within the D lineage (see Figure); in the other embryo defects were less severe. In addition certain cell deaths failed to occur in AB and MS lineages. The observed lineage defects are in good agreement with the reduced number of LIN-26 positive cells. We imagine that ale-1 could be a gene required to allow normal cell divisions in AB-derived hypodermoblasts and in D-derived myoblasts or to specify the fates of these cells (one aspect of their normal fate could be to divide). We find it striking that emb-29, a gene which was previously shown to be required for normal cell divisions mostly in EMS and C (2), affects lineages that are largely complementary to those affected by ale-1. We are wondering whether different lineages require different cell division machines. (1) We thank Dr. Ralf Schnabel for allowing us to use his 4D lineage microscope. (2) Denich et al., Roux's Archiv. Dev. Biol. 193: 164. Hecht et al., J. Cell Sci. 87: 305. Figure: Examples of lineage defects observed in ale-1(mc14) embryos.