Worm Breeder's Gazette 11(3): 67
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.
Zygotic lethal, emb(rh54: III), mutants arrest during embryonic elongation. Embryos can pump and hatch but are paralyzed and soon die. Mosaics were generated using the unstable free duplication, sDp3, covering dpy-1 emb(rh54) ncl-1 chromosomes (duplication losses in individual mosaics are shown by stars below). AB(-), EMS(-), and C(-) larvae are viable and reach adulthood. (D(-) larvae have not yet been observed but are also expected to be viable.) Cell autonomous defects were observed in the excretory cell, gonad, and non-pharyngeal muscles. Mutant excretory cells fail to extend canals along the hypodermis but instead form a convoluted canal within their cell body. Mutant gonads have apparently normal cell lineages, but uterus, spermatheca, and ovarian sheath fail to assemble and flatten normally. Mutant body muscles attach to the hypodermis but fail to spread and form a myofilament lattice. Similarly, mutant anal depressor muscles attach normally but have little if any birefringence using polarized light. Mutant sex myoblasts (SMs) fail to migrate to the hermaphrodite gonad but generate apparently normal lineages in situ. Vulval and uterine muscles remain attached to the body wall but are apparently not contractile. These defects suggest that emb(rh54) is required for the differentiation of certain cells, including the expression or assembly of myofilaments in non-pharyngeal muscles, SM migrations, and excretory canal outgrowth. It is somewhat surprising that these different phenotypes should occur together. Zygotic mutants on LGIII with similar embryonic phenotypes, reported independently by J. Rothman and by B. Williams and R. Waterston (pat-2), could be allelic to emb (rh54).[See Figure 1]