THE ROLE OF DROSOPHILA INHIBITOR OF APOPTOSIS (DIAP1) IN FAT BODY REMODELING
Date
2012-05-29
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Abstract
During metamorphosis in Drosophila melanogaster some larval tissues are destroyed through programmed cell death (PCD) (Aguila et al., 2007). The steroid hormone 20-hydroxyecdysone (ecdysone) regulates several genes that induce PCD in Drosophila (McBrayer et al 2007). Apoptosis, which is a type of PCD, occurs when the antiapoptotic gene diap1 is downregulated in larval tissues. DIAP1 regulates apoptosis by deactivating caspases (Orme and Meier, 2009). During metamorphosis, the larval fat body, which is composed of a sheet of connected cells, is not destroyed by PCD. This organ is instead remodeled and is transformed into individual, spherical, and loose cells (Nelliot et al., 2006).
I hypothesize that diap1 is expressed in the larval fat body throughout metamorphosis and that this helps to inhibit PCD in this organ. To test this hypothesis, I examined diap1 transcript levels in wild type Drosophila using qPCR. In addition, I determined the expression of diap1 in larval fat body of flies with a diap1 RNAi construct. My results demonstrate that diap1 is expressed in the larval fat body during prepupal and early pupal development. Preliminary findings showed that Drosophila expressing the diap1 RNAi construct failed to undergo normal fat body remodeling. This finding suggests that diap1 is necessary for the normal timing of fat body remodeling and the successful development of Drosophila.
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Keywords
Apoptosis, Fat body remodeling, Programmed cell death, diap1, Autophagy, 20-hydroxyecdysone