Worm Breeder's Gazette 10(1): 87
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.
We have used the monoclonal antibody MAb44 to identify mutants with abnormal PVP neurons. These are monopolar cells in the pre-anal ganglion which extend axons anteriorly along the ventral nerve cord and then dorsally through the nerve ring where they meet and terminate at the dorsal midline. An unusual feature is that the axons cross in the pre-anal ganglion so that PVPL and PVPR travel in the major (right- hand side) and the minor (left-hand side) fascicles of the ventral nerve cord, respectively (White et al., 1986). R. Durbin and N. Thomson have shown that the PVP axons are the first neurons to grow anteriorly along the ventral nerve cord from the tail ganglia and they may help organize latter arrivals. The PVP neurons in unc-30 (e191) mutants fail to stain with MAb44. Nomarski DIC examination of newly hatched larvae confirmed that the somata are present in their normal positions in the pre-anal ganglion. The DDn and VDn motor axons are abnormal in unc-30 mutants. These cells also lack their neurotransmitter GABA and at least one other characteristic antigen (S. McIntyre, R. Horvitz, and J. White; S. Siddiqui and J. Culotti, pers. comms.). Conceivably, defects in the PVP interneurons are responsible for the motorneuron defects or vice versa but these two neuron classes are only weakly connected in the adult nervous system. Incompletely differentiated classes of neurons have also been observed in mec-3 and unc-86 mutants. Conceivably, unc- 30 is a third homeotic gene which controls the differentiation of certain cell types. The PVP neurons in pvp-1 (rh114; LGX) fail to stain with MAb44. In contrast to unc-30, move and mate normally and are indistinguishable from wild-type animals except for the lack of detectable antigen on the PVP neurons. We have not yet confirmed that the somata are present. The PVP somata stain faintly in unc-33 (e204) and unc-44 (rh86) mutants but their axons are too faint to follow. In unc-33 (rh112) mutants, the MAb44 staining is somewhat brighter and axonal abnormalities are observed, i.e., both axons often run in the same fascicle in the ventral nerve cord, the axons have small varicosities, and the cells are sometimes bipolar, having short posterior processes. The PVP neurons stain brightly in unc-14 (rh115), unc-73 (rh108), unc-76 (rh116), and unc (rh38; LGI). In each of these mutants both axons often run in the same fascicle in the ventral nerve cord. The axons have small varicosities in all four mutants. The PVP axons in unc (rh38) mutants terminate in large swellings where they meet in the nerve ring. The cells are sometimes bipolar. The PVP axons in unc-76 mutants have short, ectopic branches in the pre-anal region. The PVP neurons stain brightly in unc-51 (e369) mutants and their axons have normal trajectories. The axons occasionally have very large varicosities. Similar varicosities have been observed in other classes of neurons in these mutants (Hedgecock et al., 1985). The PVP neurons stain more brightly than normal in unc(rh110; LGX) mutants. Extra processes are observed in the nerve ring. These may be ectopic branches in the ring with swollen endings, or as we first reported, the axons of monopolar neurons in the head that do not stain in wild-type animals. The pattern is apparently not reproducible suggesting that the staining is of swollen branch terminals rather than additional cells. The PVP neurons stain brightly with MAb44 in unc (rh20; A). The somata have multiple axons which branch extensively in the preanal region. The branches often extend dorsally or posteriorly and they may end in swellings. Axons growing anteriorly usually end before the midbody. Most classes of neurons have abnormal axons in these mutants. It has been proposed that the unc-40 gene is required for guiding axons from lateral somata to the ventral midline and for keeping pioneer axons, such as the PVP neurons, at the midline. Similarly, the unc-6 gene is required for guiding axons from lateral somata to the ventral midline and for guiding axons from ventral somata to the dorsal midline (E. Hedgecock, J. Culotti, and D. Hall, unpublished data). The PVP axons in unc-40 (rh66) frequently leave the ventral nerve cord and grow anteriorly along the lateral epidermal ridge. The PVP axons in unc-6 (ev400), a null mutant, are more normal. Often both axons run in the same fascicle in the ventral nerve cord but they have not been observed to leave the nerve cord as in unc-40 mutants. In a spontaneous unc-6 (ev400) partial revertant, the PVP axons often leave the ventral nerve cord. Interestingly, this revertant restores dorsalward (unc-5-like) guidance but not ventralward (unc-40-like) guidance. This neomorphic unc-6 phenotype strenghtens the conjecture that unc-6 and unc-40 are functionally, and perhaps molecularly, related.