This report describes a model of malignant glioma using the Drosophila Par complex gene aPKC. In Drosophila, the Par complex consists of Dmel\baz (PARD3, PARD3B in human), Dmel\Cdc42 (CDC42 in human), Dmel\par-6 (PARD6A, PARD6B, PARD6G in human) and Dmel\aPKC (PRKCI, PRKCZ in human). This complex is variously called the PAR3-aPKC-PAR6 complex, the Cdc42-Par6-aPKC complex, the aPKC-PAR complex, or other combinations of the components; the junctional apical-basal polarity complex or the junctional ABP complex. The four component fly genes have been extensively studied: classical loss-of-function mutations, RNAi-targeting constructs, and alleles caused by insertional mutagenesis have been generated for each; physical and genetic interactions have been described for each; see below and in the respective gene reports.
Multiple Drosophila genes of the Par complex have been investigated in models of epithelial cancer (see FBhh0000810).
Animals homozygous for severe loss-of-function alleles of Dmel\aPKC typically die in the embryonic or early larval stages; homozygous larvae have a reduced number of brain neuroblasts. When aPKC is overexpressed in the larval and adult brain, hyperplastic proliferation is observed, resulting in masses of undifferentiated immature neural progenitor cells. These undifferentiated masses continue to proliferate, escape proper controls during metamorphosis, and persist in the adult, where they keep growing and result in reduced adult lifespan. Many physical and genetic interactions have been described for Dmel\aPKC; see below and in the aPKC gene report.
[updated Dec. 2018 by FlyBase; FBrf0222196]