Faculty Scholarly Dissemination Grants


The Phenotypic Effects Associated With Loss of PKN Function Are Manifest upon Perturbation of Cell Death in Drosophila Melanogaster


Biology Department


College of Liberal Arts and Sciences

Date Range



Life Sciences


The Drosophila homolog of the mammalian PKN family kinases is required during the embryonic process of dorsal closure and has been identified as an effector of Rho1, a member of the Ras GTPase superfamily. The loss-of-function, dorsal closure phenotype associated with the mutant allele pkn06736 is relatively mild (~10% of embryos with the phenotype) and may reflect functional redundancy with components of the Jun-terminal kinase (JNK) pathway that are also required for dorsal closure in Drosophila. We have investigated post-embryonic phenotypic consequences associated with loss of PKN function using this same mutant allele and via ectopic expression of pkn RNAi. Low levels of lethality are seen throughout early stages of development in pkn06736 homozygotes, however all are individuals are dead by the end of the third instar with accompanying defects in formation of imaginal discs. In contrast, ectopic expression of PKN RNAi does not result in a mutant phenotype associated with loss of PKN function in any of the adult structures examined (i.e. using ovary, wing and eye GAL4 drivers). However, overexpression of the death-inducing gene, head involution defective (Hid) in the eye while also removing PKN using the eye specific promoter (GMR-Pkn RNAi) results in a larger eye size suggesting that PKN loss leads to cell survival. Cell survival does not seem to be impacted by Erks inactivation of Hid since the same effect is also seen when a mutant of hid (hidala5) is used. These results suggest that PKN may promote cell death and that its function is independent of the Ras/MAPK survival pathway. We find that phenotypic effects of PKN loss of function in the adult are not seen in the absence of ectopic perturbations of cell death. This indicates that even though PKN is required earlier for larval development, PKN function in adult tissues is only important if the cell death/survival pathways are altered.

Conference Name

56th Annual Drosophila Research Conference

Conference Location

Chicago IL

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