Worm Breeder's Gazette 3(2): 23

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.

Transmission Ratio of fer Mutations

Y. Argon, S. Bodmer

Figure 1

We have identified eight genes that can mutate to give a 
fertilization-defective (FER) phenotype due to defective sperm.  Our 
mutants are all recessive, but because of their effect on sperm we 
asked if both classes of sperm produced in a heterozygote were equally 
fertile.  Heterozygous males, grown permissively or restrictively, 
were mated to their corresponding sterile hermaphrodites.  The 
genotype of the progeny of such crosses was then determined by placing 
them on plates containing 1.5 mM Tramisol.  The animals are paralyzed 
within minutes and expel the contents of their uterus revealing 
whether they are sterile or fertile.  In some cases, closely linked 
UNC or DPY markers were used to identify progeny fertilized by sperm 
bearing the fer chromosome.  The results are presented in the table as 
the fraction of progeny fertilized by a fer sperm (the transmission 
[See Figure 1]
As shown, hc1 and hc3 have the 0.5 ratio expected from Mendelian 
principles.  However, sperm bearing the hc4 and hc34 mutations have 
reduced fertility.  For hc34 the effect is temperature sensitive.  For 
hc4, it is less so, which may reflect the fact that the phenotype is 
partially defective at 16 C.  We have examined the sperm from the 
hc4/+ males with the scanning electron microscope and find there are 
two classes of sperm, one of which is indistinguishable from wild-type.
This observation, together with the observation that homozygous 
mutant males make sperm in normal number and transfer them to 
hermaphrodites, makes it unlikely that the cause of the reduced 
transmission of mutant bearing sperm is due to sperm death or 
These results show that the hc4 and hc34 mutations are expressed 
autonomously in the sperm and that gene expression must continue after 
the first reductive division in meiosis in order to cause a defect in 
the sperm bearing the mutant allele.

Figure 1