Worm Breeder's Gazette 9(1): 57

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.

The Phenotype of the HSNs in egl-44 and egl-46 Animals May Depend on Interaction with their Targets

C. Desai and B. Horvitz

We have previously described 45 mutations that disrupt the 
functioning of the HSN motorneurons, which drive egglaying.  Of these 
mutations, seven that define the two genes egl-44 and egl-46 display 
low levels of serotonin in the HSNs as visualized by indirect 
immunoflourescent staining.  The other serotonergic cells (the NSMs 
and six or seven additional neurons in the head and pharynx) appear to 
have normal levels of serotonin.
While constructing and characterizing strains containing pairs of 
mutations affecting the HSNs, we noticed that the HSNs in egl-43: 
egl-46 animals have increased levels 
of anti-serotonin staining compared to the levels seen in egl-44 and 
egl-46 mutants alone.  The HSNs in egl-43 mutants fail to migrate from 
their birthplaces in the tail to their wild-type positions just 
posterior to the midpoint of the gonad.
This result led us to theorize that the lower antiserotonin staining 
in egl-44 and egl-46 HSNs may be dependent on synapse formation 
between the HSN processes and their targets, the vulval muscles.  To 
further test this hypothesis, we constructed four more double mutant 
strains, designed to disrupt these synapses.  These double mutant 
strains are: egl-44: egl-44; 
egl-46: egl-31.  
The egl-15 mutation results in the incomplete migrations of the sex 
myoblasts, the ancestors of the vulval muscle cells.  The egl-31 
mutation results in abnormalities in the M cell divisions that 
generate the sex myoblasts.  The level of anti-serotonin staining in 
the HSNs of each of these four strains is enhanced, compared to that 
seen in egl-44 and egl-46 alone.
All six of the double mutant strains described above either remove 
the targets from the HSNs or the HSNs from their targets.  Thus, the 
low level of anti-serotonin staining found in the HSNs of egl-44 and 
egl-46 animals seems to depend on HSN-vulval muscle synapse formation. 
This reduced anti-serotonin staining could be due to synaptic leakage 
of serotonin, faulty reuptake, or some other defect.