Worm Breeder's Gazette 5(1): 21a

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.

Title unknown.

Authors unknown.

Ultrastructural study of L2 larvae of the non-chemotactic, dauer-
defective mutant E1379 have shown that the morphology of amphid and 
phasmid cilia are both severely affected in this mutant.  The cilia 
are enlarged, irregular in shape and filled with an electron-dense 
matrix.  Microtubules are generally absent from the afferent endings 
of the neurons, while the basal bodies appear normal.  The morphology 
of E1379 phasmid neurons closely resembles that of the amphids 
although phasmid microtubules were less severely affected in a second 
specimen.  The amphid morphology of this strain is similar to that 
exhibited by the che-3 mutant, E1124, studied by Lewis and Hodgkin (J. 
Comp.  Neurol.  172: 489-510, 1977).  Both mutations are on LGI.
In addition to being dauer-defective and nonchemotactic, E1379 males 
do not mate successfully although they do contain sperm, and they 
attempt to copulate.  This behavior could be related to chemosensory 
impairment.  The phasmids in the male may respond to a substance 
released through the hermaphrodite vulva, and this response may be an 
essential step in successful mating.  The fact that a single mutation 
causes similar amphid and phasmid defects supports the idea suggested 
by Sam Ward that these structurally similar sense organs share common 
developmental steps.