Download or read book HOW DROSOPHILA MELANOGASTER LARVAL FAT BODY ESCAPES EARLY CELL DEATH written by Zhivka Hristova and published by . This book was released on 2013 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: During metamorphosis in Drosophila melanogaster, various larval tissues, such as the salivary glands (SG) are destroyed through PCD (programmed cell death). However, an exception is the larval fat body, which undergoes changes during metamorphosis resembling those of metastatic cancer cells. Instead of being destroyed by PCD, the fat body tissue remodels from a sheet of closely attached cells into loosely associated individual cells. The study of the fat body is of great importance because it can aid in our understanding of processes such as tumor metastasis and wound healing. The steroid hormone 20-hydroxyecdysone (20E) plays a key role in the development of Drosophila melanogaster (Woodard et al., 1994). 20E functions by binding to a heterodimer of two nuclear receptors, EcR (ecdysone receptor) and USP (ultraspiracle) (Bond et al., 2011). Two 20E pulses signal the end of the larval and prepupal developmental stages, respectively. Changes in 20E levels regulate the transcription of genes involved in the fly metamorphosis. Among the regulated genes are betaftz-f1 and E74A (Woodard et al., 1994). betaftz-f1 encodes a nuclear receptor required for 20E function. betaftz-f1 transcription is necessary for fat body remodeling and salivary gland PCD. Premature expression of betaftz-f1 in third instar larval fat body leads to premature fat body remodeling, but only in the presence of 20E (Bond et al., 2011). E74A is required for PCD in the salivary glands, but its function in fat body remodeling has not yet been determined (Chimeh, 2012). Previously it has been shown that blocking of betaftz-f1 expression increases E74A expression in the fat body (Almonacid, 2012). This suggests the hypothesis that betaFTZ-F1 represses E74A expression. Thus, my prediction is that premature expression of betaftz-f1 will result in E74A downregulation and premature fat body remodeling. To test my hypothesis, I worked with late third instar larvae in which betaftz-f1 was expressed prematurely in the fat body. I compared E74A transcript levels in the fat body of these transgenic animals to those in wild-type controls by using real-time quantitative PCR to analyze the effect of betaFTZ-F1 on E74A transcription. My findings support my hypothesis and suggest that betaFTZ-F1 represses E74A transcription in the larval fat body. This provides a potential mechanism for inhibiting PCD in the fat body during metamorphosis.