Polarity is established in the one-cell C. elegans embryo shortly after fertilization and determines the anterior-posterior body axis. This polarization is cued by the sperm-donated centrosome, which triggers changes in the posterior cortex. It is not well understood how the centrosome is positioned in the early embryo to trigger this polarization. Our previous work uncovered a role for the PAM-1 aminopeptidase in positioning the centrosome at the cortex to allow for proper axis polarization. PAM-1 is a highly conserved aminopeptidase that targets unknown proteins for degradation. In the absence of functional PAM-1, centrosomes are mispositioned and the anterior-posterior axis fails to establish correctly. In order to identify novel regulators of centrosome positioning and targets of the PAM-1 aminopeptidase, we took advantage of the maternal-effect embryonic-lethal phenotype of pam-1 mutants to conduct a suppressor screen. We have identified six suppressors, which significantly increase the pam-1 hatch rates from 2% to between 25-96%. Two of these suppressors are dominant while the others are recessive. Using DIC microscopy we have found that each suppressor significantly rescues the polarity defects, such as the lack of pseudocleavage and the symmetric cleavage, found in pam-1 mutants. We have also discovered that some, but not all, of our suppressors can rescue more than pam-1 allele, pointing to different mechanisms of action. We are currently mapping the suppressor mutations to identify the molecular identity. Toward this end, we have used whole genome sequencing on two of our suppressors and are currently verifying the lesions to identify the suppressors in these strains. Future characterization of these suppressors is likely to uncover new insights into the role of this aminopeptidase in centrosome positioning and polarity establishment.