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.

Mutations Affecting the PVP Interneurons

H. Bhatt and E. Hedgecock

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,