Worm Breeder's Gazette 12(2): 84 (January 1, 1992)
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.
Mutations in the srf-4 , srf-8 ,or srf-9 genes produce a collection of phenotypic defects, including ectopic lectin binding, uncoordinated movement, egg laying defects, and abnormal copulatory bursa morphogenesis. To determine the cellular basis of the Unc phenotype, we first looked for muscle abnormalities in these mutants using the fluorescent actin probe Bodipy-phallacidin. Muscle structure appeared normal, suggesting that the Unc phenotype may have a neuronal basis. We therefore checked the morphology of the GABAnergic neurons (using anti-GABA antisera) and the touch cells [using the anti-acetylated tubulin antibody 6-11B-1 and transgenic animals containing a mec-7 /lacZfusion (courtesy of M. Hamelin)].
The GABAnergic neurons of the pleiotropic srf mutants did not show gross abnormalities (such as seen in unc-6 mutants), but did differ quantitatively from wild-type neurons in some respects. Specifically, we determined the fraction of DD and VD commissures that crossed or fasiculated with neighboring commissures, and the number of varicoities per commissure. For all of the pleiotropic srf mutants, the frequency of crossed or fasiculated commissures was roughly twice that of wild-type, while the number of varicosities was approximately five-fold higher.
We restricted our touch cell scoring to the anterior lateral touch cells (ALML and ALMR). These cells send anterior processes to the nerve ring; in wildtype animals, a short posterior process can be observed by 6-11B-1 staining in rare instances (1/50 ALM by our scoring). Posterior processes were much more common (~15-55% of ALMs scored) in the pleiotropic srf mutants. To confirm that we were scoring the right cells, ALM morphology in srf mutants containing mec-7 /lacZtransgenes was observed by ß-galactosidase staining. Posterior processes were also observed by this method, although at a reduced frequency (compared to 6-11B-1 staining). This reduced frequency may result because (presumably nonfunctional) posterior processes may contain microtubules but may not be able to accumulate ß-galactosidase.
These results may not directly account for the srf mutant Unc phenotype, but do support the idea that this phenotype has a neuronal basis.