Worm Breeder's Gazette 9(1): 81

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.

Alterations In The Synaptic Connections Made By VAn Ventral Cord Motoneurones In Mutants Of unc-4

J.G. White, E. Southgate and J.N. Thomson

Mutants in the gene unc-4 were first isolated by Sydney Brenner in 
1969 and since that time they have become well known and loved genetic 
markers.  The phenotype of these mutants is quite characteristic, they 
are healthy and grow well but have a striking locomotory defects They 
can move forward, albeit with a certain amount of difficulty, but, 
when provoked to move backwards by a tap on the head, the body coils 
up with the dorsal side innermost.  The tail does not coil up in these 
circumstances and usually curves in the opposite sense 
We have reconstructed regions of the ventral cord from three unc- 4(
e120) animals.  The morphology and disposition of motoneurone 
processes is much the same as is seen in wild type animals There is a 
striking difference in the synaptic connections that are made onto 
certain VAn motoneurones however.  Normally VAn motoneurones receive 
chemical synapses from AVA, AVU and AVE interneurones and also make 
gap junctions to AVA.  In unc-4(e120) animals VA2, VA3 and VA10 
motoneurones do not make these synapses, but instead make prominent 
gap junctions onto AVB interneurones, which is characteristic of the 
connections made by VBn and DBn motoneurones.  Thus, although these 
neurones have the same morphological features as VAn motoneurones (eg. 
have anteriorly directed axones), they make synaptic connections that 
are appropriate to VBn motoneurones.  Only certain VAn motoneurones 
are affected, neurones at either end of the cord (VAl, VAll and VA12) 
are normal (VA4 to VA9 have not been reconstructed).  
In wild type animals VAn and DAn motoneurones receive the same 
synaptic inputs and respectively provide excitatory input to ventral 
and dorsal body muscles during forward locomotion.  Conversely, VBn 
and DBn motoneurones inervate the ventral and dorsal body muscles 
during backward locomotion (Chalfie et al. 1985, J.  Neuroscience, 5: 
956).  The behavioral phenotype of unc-4 is consistent with its 
anatomical phenotype; forward locomotion is presumably mediated by the 
VBn and DBn neurones in the normal way however there will be a certain 
amount of interference from the transformed VA neurones which will 
presumably be also activated because they have the same synaptic 
inputs as VBn and DBn neurones.  During backward movement the 
transformed VAn motoneurones will not be activated.  This will have 
the consequence that only dorsal muscles will receive excitatory input 
in the middle regions of the body, giving rise to the dorsal coiling 
behavior that is observed.  The tight coil of the body additionally 
suggests that VA4 to VA9 are also transformed.  The reverse curve of 
the tail is presumably a reflection of the normal VA11 and VA12 
It is interesting to consider why only certain VAn neurones are 
transformed.  Leakiness is an unlikely explanation because the same 
behavioral phenotype as unc-4(e120) is seen in animals with two trans 
deficiencies that overlap in the unc-4 region (Sigurdson et al.  1984, 
Genetics 108: 331), suggesting that this represents the null phenotype.
A possible clue is that all the transformed VAn neurones are sisters 
of VBn neurones whereas none of the untransformed VAn, or for that 
matter DAn neurones, are sisters of VBn or DBn neurones.  The 
significance of this coincidence is not clear, but it does provide 
food for speculation.