From fertilization throughout development cell fusion is an essential process in multicellular organisms. Recently, we isolated and characterized
eff-1, a gene encoding type-I membrane proteins that is essential for all epithelial cell fusion events in C. elegans [1]. To investigate whether
eff-1 has a function in the fertilization process we looked for fertility defects in
eff-1(
hy21) and
eff-1(
oj55). We also generated and tested strains carrying mnDf105 deficiency over a mutated
eff-1 gene and preformed RNAi. We have found in all these experiments a significant percent of sterility and reduced number of progeny. In the
eff-1 strongest allele
hy21ts there was 12.4% sterility at the restrictive temperature (25C) compared to 1% at the permissive temperature (15C). In the strain carrying
eff-1(
hy21) over mnDf105 deficiency we found 25%, 9.6% and 29% sterility at 15C, 20C and 25C respectively. To study the reduced function of
eff-1, we used RNAi experiments by injecting N2 and eff- 1
(hy21) worms with 800bp dsRNA complementary to
eff-1 cDNA. We found 28% sterility in eff- 1
(hy21) injected animals at 15C (the permissive temperature) and F1s of either N2 or
eff-1 injected animals showed 9% to 40% sterility. In addition to the increase in sterility and a reduction in the number of progeny (for non sterile worms) there was an increase in the number of worms exhibiting other morphological defects associated with the
eff-1(
hy21ts) mutant (e.g., Dpy, Unc and Egl). Two alternative hypotheses can explain the fertility problems in
eff-1 worms: 1) Somatic cell fusion failure in vulva, uterus and hypodermis cause low fertility. And 2) EFF-1 activity is directly required for egg-sperm fusion. In order to distinguish between these hypotheses, we crossed sterile hermaphrodites to N2 males. These crosses resulted in a restoration of the fertility, suggesting a putative role for EFF-1 in egg-sperm fusion and/or spermatogenesis. Our results show correlation between worms with reduced
eff-1 activity and fertility problems. The results of the genetic crosses may imply that indeed some fertility defects are a result of sperm defects. The above results suggest that our strongest
eff-1 allele (
hy21ts) is not a null. We are doing non-complementation screens in order to find new
eff-1 alleles. New alleles of
eff-1 will help us to better understand the role of cell fusion in the development of C. elegans and in fertility.