The maternal-effect phenotype of the delorean mutation in Drosophila melanogaster. Georgette Sass, Sarah VanOeveren. Biology, Grand Valley State University, Allendale, MI.

   We have previously described the delorean mutation in Drosophila melanogaster; a recessive, gain-of-function allele of the protein kinase N (pkn) gene (Sass, VanOeveren, Burke, and Ostrow 2012 A. Dros. Res. Conference 53; 572B). The PKN protein is required for the process of dorsal closure during embryogenesis and has been identified as an effector of Rho1, a member of the Ras GTPase superfamily (Betson and Settleman 2007 Genetics). To further investigate the role of PKN in embryogenesis, we have characterized embryonic phenotypes associated with the delorean mutation. Females that are homozygous for the pkn^dln allele were found to exhibit a maternal-effect phenotype. Embryos derived from these mothers show moderate to severe head defects as well as alterations in denticle patterning. To expand upon these results, we have generated germ-line clones of the pkn^dln allele and find that the embryos produced have similar embryonic defects. Furthermore, the head and segmental defects that we see are analogous to those seen in other systems such as in germline clones of a loss-of-function allele of nemo (Mirkovic et al, 2002 Mechanisms of Development). The cause of such defects is postulated to be due to disruption of programmed cell death and we are specifically interested in how apoptosis via the JNK pathway may be perturbed in delorean mutants. For this reason, we will present our analysis of genetic interactions between the pkn^dln allele and mutants of the JNK signaling pathway.