Worm Breeder's Gazette 11(5): 89

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.

skn-1 ("skinhead"): A Maternal-Effect Mutant in which the Pharynx and Intestine have been Replaced by Extra Hypodermal Cells

Bruce Bowerman and James R. Priess

We have isolated a mutant in C.  elegans which we call 'skinhead' (
skn-1).  The progeny of homozygous skn-1 mutants lack two major body 
organs, the pharynx and the intestine.  Instead, these mutant embryos 
have extra hypodermal cells abnormally located inside their bodies.  I 
have shown that the EMS blastomere, which in a wild type embryo 
produces the posterior pharynx and the intestine, is transformed in 
skn-1 mutant embryos such that it instead makes hypodermal and muscle 
cells.  Although skn-1 embryos lack a pharynx and an intestine, they 
show extensive differentiation of other cell types, including anterior 
sensory neurons, suggesting that the defect is specific to the 
pharyngeal and intestinal lineages.  By genetic analysis, I have shown 
that the mutation is recessive and that the skn-1 gene product is 
maternally contributed to the oocyte.
Analysis of skn-1 mutants.  skn-1 embryos appear to have additional 
hypodermal cells by several criteria.  (i) Using Nomarski optics, one 
can see what appear by morphological criteria to be hypodermal cells 
on successive focal planes throughout the bodies of these mutant 
embryos.  This is in contrast to wild type embryos in which hypodermal 
cells are seen only on the surface of the embryo.  (ii) Joel Rothman 
found that antibodies that recognize the Drosophila protein engrailed 
recognize hypodermal cell nuclei on the surface of C.  elegans embryos 
(WBG 10:3).  We see additional nuclei staining inside the bodies of 
skn-1 embryos using these antibodies.  (iii) Another characteristic of 
skn-1 embryos is the presence of internal cavities which are 
surrounded by the putative internal hypodermal cells.  After fixing 
embryos and sectioning them for transmission electron microscopy, we 
have been able to confirm that these internal cavities are lined by 
cuticle.  Most significantly, the cuticle lining the cavities includes 
a striated layer, which is normally seen only in the cuticle that 
surrounds the hypodermal cells on the exterior of wild type animals.
When I use a laser beam to kill all the blastomeres except for EMS 
in a wild type 4-cell embryo, EMS produces a posterior pharynx and an 
intestine, as it would in an intact animal.  When I ablate all the 
blastomeres except EMS in a skn-1 embryo, EMS produces instead a clump 
of hypodermal cells (a cell type never produced by a wild type EMS) 
and muscle cells.  Therefore, by the 4-cell stage of embryogenesis, 
the lineage that normally produces the posterior pharynx and the 
intestine has been transformed into a new lineage in skn-1 mutants.
A Model.  One way to interpret the phenotype of skn-1 mutants is to 
propose that the wild type skn-1 gene product normally programs EMS to 
make a pharynx and an intestine.  Strikingly, a reduction of function 
mutation in this gene causes EMS to adopt a fate very much like that 
of its sister cell in the 4-cell embryo, which normally makes almost 
exclusively hypodermal and muscle cells.  Experimental and genetic 
analyses have suggested that cell determination in C.  elegans partly 
involves the asymmetric segregation of maternal factors (often called 
determinants) to specific embryonic blastomeres.  Perhaps the skn-1 
gene encodes such a maternally provided, segregated determinant.
skn-1 maps near unc-5 on LGIV.  I am currently working to identify 
deficiencies that include skn-1 and to isolate additional alleles of 
the gene.