The Role of E93 in Fat Body Remodeling and Autophagy in Drosophila Melanogaster Third Instar Larvae - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook The Role of E93 in Fat Body Remodeling and Autophagy in Drosophila Melanogaster Third Instar Larvae write by Loretah Chibaya. This book was released on 2012. The Role of E93 in Fat Body Remodeling and Autophagy in Drosophila Melanogaster Third Instar Larvae available in PDF, EPUB and Kindle. In this study, I proposed that the ectopic expression of Bftz-fl in D. melanogaster third instar larvae during the first 20E pulse will trigger the premature expression of E93, resulting in premature fat body remodeling. My results to date have shown that ectopic expression of Bftz-f1 in third instar larva leads to premature expression of E93 and fat body remodeling. Transmission electron microscopy showed that autophagosomes are present in dissociating fat bodies suggesting that the fat body fuels the process of metamorphosis by releasing nutrients.
The Role of E93 in Fat Body Remodeling in Drosophila Melanogaster
The Role of E93 in Fat Body Remodeling in Drosophila Melanogaster - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook The Role of E93 in Fat Body Remodeling in Drosophila Melanogaster write by Wai Yan Lam. This book was released on 2012. The Role of E93 in Fat Body Remodeling in Drosophila Melanogaster available in PDF, EPUB and Kindle. In wild-type animals, E93 is expressed in the fat body at 12 hours after puparium formation (APF), coinciding with the last stage of fat body remodeling, detachment, during which individual fat cells are redistributed into the head capsule and body cavity. E93 is known to regulate various tissue specific developmental changes such as programmed cell death of larval salivary glands and the midgut. Given E93's role in triggering the death of larval tissue, it is interesting that it does not trigger the death of fat tissue. However, considering the numerous roles E93 takes on during development, it is possible that E93 might also be involved in influencing fat body remodeling. Microscopy work utilizing light microscopy, fluorescence microscopy, transmission electron microscopy, scanning electron microscopy, and confocal microscopy reveals phenotypic differences between the wild-type and E93 mutant fat body after 12 hours APF. While wild-type fat body dissociates into individual and spherical fat cells, E93 mutant fat body is frequently found as aggregates of undetached fat cells and some individual, dissociated fat cells. I hypothesize that E93 may play a role in facilitating the detachment phase of fat tissue remodeling and that its absence would hinder proper fat body remodeling.
Mapping a Genetic Mutation Involved in Larval Fat Body Remodeling Disruption in Drosophila Melanogaster
Mapping a Genetic Mutation Involved in Larval Fat Body Remodeling Disruption in Drosophila Melanogaster - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Mapping a Genetic Mutation Involved in Larval Fat Body Remodeling Disruption in Drosophila Melanogaster write by Honami Tanaka. This book was released on 2020. Mapping a Genetic Mutation Involved in Larval Fat Body Remodeling Disruption in Drosophila Melanogaster available in PDF, EPUB and Kindle. Tissue remodeling plays an important role in the development of many multicellular organisms. It is also a key process in wound healing and tumor metastasis, and studying the control of tissue remodeling could lead to important developments in medicine, such as treatment and prevention of cancer and other diseases. Drosophila melanogaster, more commonly known as the fruit fly, is a great model organism to study such processes, due to their short life cycle and genomic similarities to humans. When Drosophila develop from larva into adult flies, they undergo metamorphosis, in which most of the larval tissues are destroyed by programmed cell death and replaced by adult tissues. However, the larval fat body is exempt from such cell death and is maintained until a few days into adulthood. During metamorphosis, the larval fat body cells remodel structurally through detaching from one another and moving to the head cavity. The larval fat body remodeling is a critical process, as failure to do so leads to lethality. Past members of the Woodard Lab performed complementation tests on fly lines that each had a single mutation on the third chromosome that resulted in abnormal fat body morphology and pharate adult lethality. The current study focuses on line l(3)LL-15413:L 04 PA, one of the seven lines that were identified to have completely lost the ability to remodel fat bodies during metamorphosis. In order to identify the location of the mutation causing the loss of fat body remodeling, I used the mapping methodology developed by Sapiro et al. (2013), and was able to determine the approximate location of the mutation to be between the dominant marker pair, Stubble and Hairless. Following that, line l(3)LL-15413:L 04 PA was crossed with 13 deficiency stocks, each missing a small fragment of the third chromosome, to further narrow down the location of the mutation. Despite having the gene mapped between the two dominant markers, I was unable to find a deficiency line that uncovered the mutation gene. Further experiments are required to determine the exact location and role of this gene, as well as other lines with abnormal fat body morphology. I hope this study will be a groundwork for further studies in the field.
Identifying Genes Involved in Larval Fat Body Remodeling in Drosophila Melanogaster
Identifying Genes Involved in Larval Fat Body Remodeling in Drosophila Melanogaster - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Identifying Genes Involved in Larval Fat Body Remodeling in Drosophila Melanogaster write by Miriam Levy. This book was released on 2017. Identifying Genes Involved in Larval Fat Body Remodeling in Drosophila Melanogaster available in PDF, EPUB and Kindle. Tissue remodeling is an essential process that occurs in multicellular organisms and is essential for the growth, development, and health of any organism. Drosophila melanogaster is an important organism for the study of this process as tissue remodeling is crucial for proper metamorphosis, during which the larval fat body remodels from a sheet of connected, polygonal cells into single, spherical cells which can then move throughout the body and head cavity of the fly. In this study, complementation tests were performed on lines of flies that each had a single mutation on the third chromosome that resulted in both abnormal fat body morphology and pharate adult lethality. The F1 progeny were scored for fat body morphology and adult lifespan post-eclosion in order to elucidate the relationship between the two phenotypes and better understand the role of potential novel genes. Abnormal fat body morphology was found to result in a reduced lifespan post-eclosion, where the degree of remodeling shows a slightly positive correlation with lifespan. In addition, I have begun to linkage map some of the mutations using pairs of dominant markers to identify the region of the third chromosome where each mutation is present.
HOW DROSOPHILA MELANOGASTER LARVAL FAT BODY ESCAPES EARLY CELL DEATH
HOW DROSOPHILA MELANOGASTER LARVAL FAT BODY ESCAPES EARLY CELL DEATH - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook HOW DROSOPHILA MELANOGASTER LARVAL FAT BODY ESCAPES EARLY CELL DEATH write by Zhivka Hristova. This book was released on 2013. HOW DROSOPHILA MELANOGASTER LARVAL FAT BODY ESCAPES EARLY CELL DEATH available in PDF, EPUB and Kindle. 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.
