Download or read book Mapping a Genetic Mutation Involved in Larval Fat Body Remodeling Disruption in Drosophila Melanogaster written by Honami Tanaka and published by . This book was released on 2020 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.