Worm Breeder's Gazette 11(2): 94
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.
The nematode gonad rapidly, and dramatically, converts into an epithelium late in larval development. In hermaphrodites, for example, six uterine precursor cells draw together during L2, forcing germ cells from the center of the gonad. These mesoblasts divide during L3, forming a small mesenchyme attached to the ventral body wall. In early L4, before the final round of uterine divisions, this mesenchyme converts into an epithelium. An indicator of this conversion is the appearance of the uterine lumen, i.e., the apical surface of the epithelium. The anchor cell fuses the emerging uterine epithelium to the vulval epithelium. We have isolated several mutants with abnormal uterine morphogenesis, recognized by the presence of germ cells near the center of the gonad, or the absence of a lumen, in early L4 hermaphrodites. Unexpectedly, these mutants also affect the outgrowth of the excretory canals. In unc-6 and unc-40 mutants, adhesion of the uterine precursors to the hypodermis may be defective and these cells are easily pried from the body wall, or apart, by proliferating germ cells (Hedgecock, Culotti, and Hall, 1990). In emb (rh54; LGIII) mutants, conversion of the uterus into an epithelium may be abnormal. In a MS.p(-) mosaic, the anterior half of the gonad failed to epithelialize while the posterior half developed normally. AB(-) mosaics are viable but have defects in AB derived muscles and the excretory cell. In exc cell (-) mosaics, the canals fail to grow along the hypodermis (Hedgecock, Culotti, Hall, and Stern, 1987). A sterile mutant let (rh151; LGIII) fails in both uterine morphogenesis and canal outgrowth (1989 CSH Abstracts, p.117). A usually sterile mutant rh152 (LGIV) has frequent defects in uterine morphogenesis and occasional defects in canal outgrowth. The gonadal basal lamina is weak and can herniate, allowing germ cells to escape into the body cavity. John Yochem and Iva Greenwald (see this WBG) have identified a new laminin gene, possibly encoding an A chain, on LGIV near mec-3. Laminin A, a structural component of basal laminae, is essential for development of epithelial cell polarity in vertebrates (Klein et al., Cell 55, 331 (1988)). We re-examined the phenotype and map position of rh152 to learn whether it might be an allele of the laminin gene on LGIV. A new allele, rh165, has stronger pleiotropic effects on basal laminae and cell adhesion. The gonadal basal lamina is absent in rh165 larvae and germ cells proliferate throughout the body cavity, often in close association with the hypodermis. Gonadal development is severely abnormal. The basal laminae of the intestine and hypodermis may fuse together in places of contact. The canals fail to grow or, in rare cases, grow along the dorsal hypodermal ridge. These mutants have variable defects in hypodermal and muscle cell positions and probably nervous system defects.