The postembryonic mesoderm in C. elegans develops from two cell types, the M cell and the gonadal Z(1,4) cells, both of which contribute to the egg-laying apparatus. At hatching, the single mesoblast M is poised to produce all of the non-gonadal mesodermal cells that will be produced during larval development, namely 14 striated body wall muscles, two sex myoblasts (SM), and two non-muscle cells (coelomocytes). The two SM cells, one on each side of the animal, are born midway between gonad and rectum and migrate to their final position in the center of the animal. After migration, both SM cells divide and form a total of 16 progeny, eight non-striated vulval and uterine muscles, respectively. SM migration in C. elegans hermaphrodites is controlled by multiple guidance mechanisms. In Pristionchus pacificus, the M cell lineage is identical to C. elegans, but has a novel role in vulva formation. The mesoblast M participates in lateral inhibition, a process that influences the fate of the vulval precursor cells P(5,7).p. Interestingly, the analysis of
Ppa-mab-5 mutants revealed important differences during M cell lineage specification at the cellular and molecular levels between P. pacificus and C. elegans. In
Ppa-mab-5 mutants, the complete M lineage is misspecified. The first two cell divisions occur along a longitudinal axis instead of the dorsoventral and the left/right division axes, resembling the phenotype known of mutations in the C. elegans twist gene. In order to gain more insight into the molecular determinants of the M cell lineage, we performed a screen for postembryonic mesoderm defective mutants (pmd). We obtained mutants of three complementation groups named
pmd-1, -2, and -3. The first mutant,
pmd-1, has a novel phenotype, which has not been reported in C. elegans. After the first cell division of M, the two daughter cells exhibit an aberrant growth and division pattern causing the misspecification of the M descendants.
pmd-2 mutants fail to form SM cells but have excessive body wall muscles. Molecular analysis indicated
pmd-2 to represent the
Ppa-sem-4 gene. The third mutant,
pmd-3, has posteriorly displaced SM cells. Since we ruled out that
egl-15 is affected,
egl-17 is a probable candidate gene.