After fertilization, the oocyte undergoes a series of conserved cellular events termed egg activation, which drive the transition from oocyte to embryo. When these events are compromised, embryogenesis fails. Several oocyte-contributed genes are required for this process, but only one sperm gene has been implicated. The paternal effect lethal gene, spe-11, encodes a sperm-specific novel protein (Browning and Strome,1996). Mutants in spe-11 have early embryonic phenotypes: failure to complete meiosis, formation of a fragile eggshell and lack of cytokinesis (Hill et al., 1989). The terminal phenotype of the null allele, spe-11(hc90), is arrest as a one-cell multinucleate embryo. To identify the primary defect in the spe-11 mutant embryos, we have undertaken a detailed phenotypic analysis. Because spe-11 exhibits eggshell defects, we have examined two diagnostics of eggshell integrity. We show that spe-11(hc90) mutant embryos are osmotically sensitive, indicating a disruption in the inner layer of the eggshell. The chitin layer of the eggshell is also defective in these mutants. No chitin is observed at the surface of the embryo in the null spe-11(hc90) embryos, and chitin staining is greatly reduced in the conditional spe-11(hc77) mutant. The spe-11 mutants are not compromised in the cell cycle dependent process of cortical granule fusion. CAV-1::GFP, a marker of cortical granules, exhibits normal trafficking in spe-11 mutants. We also asked if the localization of other egg activation genes was normal in the absence of SPE-11 and found that EGG-3::GFP is normally localized following fertilization in spe-11(hc90) mutants. Thus, the earliest defects we have detected are in eggshell formation. It has been shown that injection of a spe-11 transgene into the hermaphrodite germline is sufficient to rescue the loss of spe-11 in sperm (Browning and Strome, 1996). We have investigated if a stable spe-11::GFP transgene is able to perform the same function. We have generated lines expressing axIs1489 [pie-1p::spe-11::GFP::pie-1]. spe-11(hc90) hermaphrodites expressing this transgene are fertile, indicating rescue of the egg activation defect. In addition, hermaphrodites that have exhausted their sperm supply produce live progeny when mated to spe-11(hc90) males. Thus, the spe-11::GFP transgene is competent to replace endogenous SPE-11, pointing to the existence of a regulatory mechanism to ensure proper activation of SPE-11 activity following fertilization.