The ventral Corazonin (vCrz) neurons provide a model system to study neuronal programmed cell death (PCD) in Drosophila, as they undergo caspase-dependent PCD during early metamorphosis between 1 and 7 hours after puparium formation (APF). DIAP1 (Drosophila inhibitor of apoptosis) is a key survival factor, preventing accidental cell death at the wrong stage. In response to death signals, caspase activation resulting from DIAP1 degradation is a primary cause of the PCD in many tissues. However, transgenic over-expression of the wild type diap1 gene in vCrz neurons failed to block PCD completely. This previous result suggested its role as a survival factor in the vCrz neurons. To gain definitive evidence for diap1's roles as a survival factor, two P-elements, UAS-diap1(6-3s) and UAS-diap1ΔRF, were constructed and injected into Drosophila embryos. Transgenic lines were established and crossed to a Crz-gal4 line for targeted over-expression. The result showed that this type of transgenic manipulations blocked vCrz neuronal PCD significantly, supporting the critical role of diap1 in the prevention of premature vCrz death.
Creekmore, Faith V.
"Neurogenetic Studies on the Role of DIAP1 in Neuronal Programmed Cell Death in Drosophila,"
Pursuit - The Journal of Undergraduate Research at the University of Tennessee: Vol. 3
, Article 8.
Available at: http://trace.tennessee.edu/pursuit/vol3/iss1/8