Regulation of Programmed Cell Death by Diap 1 and Dronc During Drosophila Metamorphosis



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Programmed Cell Death (PCD) is a tightly regulated process in which organismal cells and tissues undergo self-destruction (Green & Llambi, 2015). In the fruit fly, Drosophila melanogaster, most of the larval tissues undergo PCD during metamorphosis under tight regulation by 20-hydroxyecdysone (ecdysone) signaling. During the first 12 hours of metamorphosis, ecdysone signaling works in two pulses; one at the end of the third instar larval stage and one at 12 hours after puparium formation (puparium formation is the onset of metamorphosis) (Lee et al., 2002). This signaling pathway induces the death activator genes that drive PCD. In contrast, the E3-ubiquitin ligase Diap1 inhibits PCD (Steller, 2008; Yin & Thummel, 2004). Several studies have examined the interaction between Diap1 and Dronc in regulating PCD in Drosophila. While Diap1 is necessary for the inhibition of unwanted cell death, Dronc, the initiator caspase, is necessary for promoting PCD. Dronc is activated when Diap1 undergoes auto-ubiquitination by the death activator genes, stopping the inhibitory actions of Dronc (Lee et al., 2002; Steller, 2008; Yin & Thummel, 2004). Not all the tissues in Drosophila undergo PCD during metamorphosis; the larval fat body undergoes remodeling rather than destruction during metamorphosis (Agulia et al., 2007). The fat body cells are resistant to PCD, unlike other larval tissues such as the larval salivary glands. The larval fat body has the function of storing energy for the development of the pupa (Agulia et al., 2007). Following previous studies, this study examines programmed cell death and its regulatory pathways in more depth. The hypothesis is that high Dronc expression and low Diap1 expression in the larval salivary gland cells will lead to the destruction of that organ by PCD, and that low Dronc and high Diap1 expression in the larval fat body cells inhibit PCD. My findings indicate that Dronc is underexpressed in the larval fat body relative to the larval salivary gland, supporting my hypothesis. Unfortunately, the results of my experiment with Diap1 are inconclusive due to poor RT-PCR primer efficiency. The findings from this study provide valuable insights into the regulation of PCD, which aid in our understanding of disorders caused by PCD misregulation.



Programmed Cell Death, Apoptosis, Misregulation, Pathways of cellular death, Drosophila melanogaster, Larval salivary gland, Larval fat body, Ecdysone signaling