Worm Breeder's Gazette 9(3): 91

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.

More Observations on Embryonic Cell Migration Mutants

J. Manser and W.B. Wood

In the last WORM BREEDER'S GAZETTE (Vol. 9, NO. 2, p.63), we 
reported on five genetic loci affecting the embryonic migration of the 
neurons CAN, HSN, and ALM. Since then we have more closely examined (
Nomarski of newly-hatched L1's) the cellular phenotype of one mutation,
mig-3(ct73)V, that appeared to affect only CAN migration with high 
penetrance. We have found that ALM is misplaced toward the anterior 
with low penetrance in mig-3(ct73)V, and we have also discovered a 
possible effect on the embryonic migration of M, the postembryonic 
mesoblast. In 2 of 17 animals examined a nucleus with the morphology 
characteristic of M was found misplaced. In one animal it was found 
misplaced toward the anterior and in the other it was found to be in 
its proper position along the anterior-posterior axis, but on the left 
side of the intestine. In 7 of the 17 animals examined, M was not seen,
suggesting more drastic misplacement. We have also constructed the 
double mutant mig(ct78)III;vab- 8(ct33)V 
)
ln previously as mig(7a)III] and examined its 
cellular phenotype in newly-hatched L1's. Both single mutants affect 
CAN migration primarily. In the double mutant, only CAN migration is 
apparently affected with high penetrance. On all 9 sides examined CAN 
is not seen, suggesting that it is misplaced over the nerve ring as in 
vab- 8(ct33). ALM was found misplaced toward the anterior on 2 of 9 
sides examined. In the future, we would like to define the null 
phenotypes of the mig loci we are currently studying (only for vab-8 
do we know that the alleles we have studied behave like nulls when 
placed over a deficiency). Knowledge of null phenotypes will be useful 
both for defining more precisely the roles of these loci in embryonic 
cell migrations and in planning strategies for isolating Tc1-induced 
alleles for use in possible cloning.