Download or read book The Role of Aurora-A in Drosophila Melanogaster Fat Body Cell Migration written by Marlena Starrs and published by . This book was released on 2022 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: After Drosophila melanogaster undergoes metamorphosis, the fly breaks free of the pupal case in a process called eclosion. Pharate adult lethality is a phenomenon in which the developed fly fails to eclose and dies inside the pupal case. Early in metamorphosis, the larval fat body in Drosophila melanogaster undergoes tissue remodeling, going from attached sheets of cells to individual spherical cells. These remodeled cells are motile and are able to migrate and provide energy to target tissues. Incomplete fat body remodeling has been linked to pharate adult lethality, likely due to insufficient energy for eclosion. Two lines of flies, aurA14641 and aurA8839 are both pharate adult lethal and are known to have incomplete fat body remodeling, and both have different point mutations in the gene Aurora-A (aurA). Aurora-A is a protein kinase known to be a regulator of the cytoskeleton. It has been found to promote actin-driven cell motility in other types of motile cells, by promoting activation of the actin-depolymerizing protein cofilin. I hypothesize that aurA mutations inhibited cofilin activity, resulting in alterations to the actin cytoskeleton that prevented fat body cell migration. The fat body remodeling and actin organization of the aurA mutants was compared to a wild-type control. Both aurA lines showed incomplete fat body remodeling, and one of the lines had irregularities in the actin cytoskeleton. Crosses were generated that overexpressed and underexpressed cofilin in the fat body. These lines also both showed incomplete fat body remodeling and altered actin organization. The similarities between this cofilin knockdown and the aur-A8839 line suggest that the mutation in aurA may be affecting the cofilin activation in fat body cells. However, the cofilin knockdown line was not pharate adult lethal, which indicates that disruption of cofilin alone is not sufficient to cause the pharate adult lethality seen in the aurA mutants and instead is likely one of a number of pleiotropic effects.