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.
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 neurones. 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.