Caenorhabditis elegans are microscopic worms that are a great model organism for examining genes and proteins involved in the
reproductive system because of their fecundity, easy manipulation, and easy to look at gonad. Lyczak’s lab has studied two versions of a
puromycin aminopeptidase known as PAM-1. We have identified a missense mutation pam-1(or347), a partial loss-of-function of PAM-1.
Also, a nonsense mutation, pam-1(or403), a complete loss of PAM-1. This PAM-1 protein is 36 – 37% similar to the
humans Npepps protein. pam-1 mutants lay fewer viable embryos than wild-type worms because they have trouble completing meiosis due
to it being significantly extended. However, we have also found another protein that rescues pam-1 mutants’ low hatch rate, known as WEE1.3. WEE-1.3 inhibits the maturation-promoting factor (MPF) in oocytes to keep the immature oocytes from being fertilized. A suppressing
mutation in wee-1.3 raised the hatch rate of pam-1 embryos from 2% to about 50%. Due to this, we believe PAM-1 has a direct or indirect
effect on MPF. MPF is made up of cyclin B and cyclin-dependent kinase 1(CDK-1). To examine this interaction, I have
been conducting localization studies of CDK-1 in wildtype, pam-1(or347), and pam-1(or403) using the confocal. I am also
examining interaction studies of PAM-1 with MPF components in oocytes by using CDK-1 and WEE-1.3 RNAi with different variations of
the strains. With these in hand, they will help further characterize PAM-1 and MPF’s interaction.