Worm Breeder's Gazette 3(1): 23
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 isolation of mutants with altered body wall muscle has led to the identification of 12 complementation groups--unc-89 I, unc-87 I, unc-15 I, unc-54 I, unc-52 II, unc-45 III, unc-82 IV, unc-22 IV,unc-60 V, unc-23 V, unc-78 X, and unc-90 X. A paper describing the mutants of these genes is in preparation. Disorganization of the body wall muscle can be severe without resulting necessarily in lethality. Pharyngeal muscle, however, was generally found to be unaffected in these mutants. This observation has been interpreted to mean not that no genes are common to both pharyngeal and body wall muscles, but that alterations of pharyngeal muscles would be lethal since adequate pharyngeal function is presumably an indispensable function. However over the past few months we have detected abnormal pharyngeal muscle structure in mutants of three different genes, which indicates that not all pharyngeal abnormalities are incompatible with life. As previously reported, paramyosin is a normal component of the pharynx, and, in accordance with this fact, mutants of unc-15, the putative structural gene for paramyosin, show alterations of thick filament structure. In unc-15(e1214),a null mutant, dissection experiments reveal that paramyosin is absent from the pharynx. Serial electron micrographs indicate that the pharyngeal thick filaments of this mutant have hollow cores throughout their lengths, whereas the wild type possesses solid cores in the central portion of the filaments. In unc-15(e73), a putative missense mutant, the thick filaments are occasionally of an abnormally large diameter. Nonetheless pharyngeal function seems relatively unimpaired in both strains. Mutants of unc-82 also have pharyngeal abnormalities, but again without apparent functional impairment. Both isolates of this gene ( E1220 and E1323) move only slightly more slowly than wild type and have been complemented and mapped primarily by their polarized light phenotypes. With electron microscopy, the body wall muscle abnormalities include the presence of thick filaments of larger than normal diameter--up to more than 1000 angstrom. In longitudinal sections a periodicity is apparent (this has yet to be determined accurately). Electron micrographs of pharyngeal muscle reveals similar abnormalities, although the abnormal filaments are present less frequently than in the body wall. unc-89 also apparently specifies a product important in assembly of both body wall and pharyngeal muscle. The only isolate, E1460, has obvious pharyngeal abnormalities. Phenotypically, E1460 moves as well as wild type but grows no larger than the wild type young adult size. The body wall muscle shows a loss of A and I banding, but both thin and thick filaments are present in approximately normal numbers. In the second pharyngeal bulb, birefringence is present at the circumference of the bulb, and electron microscopy reveals numerous thick filaments oriented longitudinally just inside the perimeter of the second bulb. These are not present in the wild type. We are presently determining which cells are involved. This defect maps with both the body wall muscle phenotype and the small adult size. ( Doubles with mutants less than 2 map units away have consistently shown all three features.) It is tempting to conclude that the small size might result from poor nutrition, attributable to pharyngeal dysfunction. Thus mutants in genes that function in both body wall and pharyngeal muscles can be obtained, although obviously certain limits still exist. Other genes, e.g. unc-54, function only for body wall muscle. Thus there is an incomplete overlap of genes determining the genetic specification of distinct but related tissues.