Worm Breeder's Gazette 9(2): 88

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.

Focus of Action of unc-3(+)

B. Herman

In earlier work (Herman, 1984), I showed that an unc-3 phenotype is 
produced when cells derived from AB.p lack the unc-3(+) gene and that 
a semi-unc-3 phenotype is produced when cells derived from either AB.
pl or AB.pr lack unc-3(+).  I suggested, on the basis of this evidence,
that the prime candidates for the cell-specific action of the unc-3 
gene were the dorsal and ventral cord motor neurons (or some subset of 
these neurons), since all but one of the 75 cord motor neurons of the 
adult hermaphrodite descend, in about equal measures, from AB.pl and 
AB.pr.  At the last C.  elegans Meeting, John White reported on the 
neuroanatomy of unc-3.  He reported that the anatomy of the nerve ring 
of unc-3 animals seemed to be normal; this result seems consistent 
with the phenotype of unc-3 animals, because although they are unable 
to propagate the dorsoventral bends along the body necessary for 
movement, they seem able to move their heads normally and the motor 
neurons driving head movement make their synapses in the ring.  In 
addition, I think it is of interest that many of these motor neurons 
descend from AB.a rather than AB.p.  John also reported that the 
neuroanatomy of the cord was so deranged that it was difficult to 
distinguish specific neurons and he suggested that perhaps the focus 
of action of unc-3(+) might be in the surrounding hypodermis rather 
than the neurons themselves.  I've been testing this suggestion by 
identifying semi-unc-3 animals derived from unc-3 
d unc-3 sup-10 
Ten of the 22 embryonically-generated cord motor neurons descend 
from AB.plp and 11 descend from AB.prp (one descends from AB.a).  The 
post-embryonically derived cord motor neurons descend from AB.pla and 
AB.pra.  Virtually all of the relevant hypodermal nuclei, however, 
descend from AB.pla and AB.pra only; the only hypodermal nuclei 
descending from AB.plp and AB.prp are situated in positions posterior 
to the anus.  The question I have been asking, therefore, is whether 
loss of unc-3(+) by AB.plp or AB.prp results in a semi-unc-3 phenotype.
I am working on the assumption that osm-1 behaves cell autonomously 
with respect to its effect of FITC staining of certain amphid and 
phasmid sensory neurons.  Thus, loss of osm-1(+) on mnDp7 from the unc-
3 gote at AB.plp is signified by lack of 
staining by PHAL (which descends from AB.plpp) and ASHL (which 
descends from AB.plpa); similarly, loss at AB.prp is signified by lack 
of staining by PHAR (which descends from AB.prpp) and ASHR (which 
descends from AB.prpa).  Although I'm not finished with these 
experiments, a significant fraction of the semi-unc-3 animals show 
precisely these patterns of non-staining (with all other neurons 
staining) as if duplication loss at AB.plp or AB.prp does indeed 
result in the semi-unc-3 phenotype; it therefore seems unlikely that 
the focus of action of unc-3 is in (or at least limited to) the 
hypodermis.  I note that mnDp7 carries Marty Chalfie's dominant 
mutation mec-4(e1611), which promotes death of the touch cells; 
duplication loss at either AB.plp or AB.prp does not rescue the 
posterior touch cells, PLML and PLMR, which descend from AB.pla and AB.
pra, respectively.  Finally, I've been using the unc-3 
sup-20 imals because 
duplication loss at AB.plp or AB.prp leads to quite different 
consequences for expected FITC staining patterns depending on whether 
the focus of action of daf-6 is sockets, sheaths or both.  The results 
should also confirm expectations for the cell-specific actions of unc-
3 and mec-4(e1611).  (The presence of sup-10 in this strain is simply 
a consequence of how the strain was constructed and is irrelevant to 
the mosaic analysis.)  The results, which are still very fragmentary, 
so far support the notion that daf-6 action is limited to sheath cells.