Worm Breeder's Gazette 1(2): 21

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.

Fertilization Defective Mutants

S. Ward, J. Carrel, J. Miwa, G. Nelson

We are continuing to study sperm morphology and the process of 
fertilization in order to characterize temperature sensitive 
fertilization defective mutants.  We have begun studying the process 
of male fertilization.  When wild-type males are mated to young wild-
type adult hermaphrodites, the male sperm are deposited in the region 
of the vulva amidst the hermaphrodite zygotes.  Within five hours all 
the male sperm migrate to the region of the spermatheca.  Most 
surprisingly, five hours after mating some hermaphrodites will begin 
producing only outcross progeny.  Thus not only can male sperm reach 
the spermatheca rapidly, but when they do so they fertilize oocytes 
preferentially in spite of the presence of hermaphrodite sperm.  We 
are investigating the basis of both the male sperm motility and the 
mechanism of preferential fertilization.  Sam will get back to 
studying chemotaxis yet.
The temperature sensitive sterility of Che 1 mutants, E1034 and 
E1035, is not due to deficient sperm production.  At 25 C 
spermatogenesis is normal and the mutant sperm have normal morphology 
by light and scanning electron microscopy.  The sperm contact the 
oocytes in the hermaphrodite but fertilization does not take place.  
The mutant sperm are swept into the uterus and expelled when oocytes 
are laid.  We are pursuing the nature of this defect by further 
scanning and transmission electron microscopy and by immunological and 
biochemical study of sperm membrane proteins.  Several other 
temperature sensitive sterile mutants in different genes also make 
sperm that fail to function.
We have not been able to resolve the question of whether the sterile 
defect in these strains is due to the same genetic defect as the 
behavioral and anatomical defects.  Neither the behavioral nor the 
anatomical defects are temperature sensitive; we have been unable to 
revert the sterile phenotype and we have been unable to separate the 
phenotypes by recombination.  Other alleles of the behavioral locus 
isolated in our lab and obtained from Dave Dusenbery are not sterile 
at 25 C.  Perhaps we have a small deletion that alters two linked 
genes.  Does anyone have direct evidence for EMS inducing deletions in 
C.  elegans or any other organism?  Does anyone know of a deletion 
that gives a temperature sensitive phenotype?