The role of Aur-A in Drosophila melanogaster fat body remodeling

Abstract

Tissue remodeling is an important process in multicellular organisms that is necessary for processes such as wound healing and tumor metastasis. For remodeling to occur, connective proteins of the extracellular matrix (ECM) must be cleaved so that cells can migrate. The migration of cells in wound healing promotes wound closure and ECM degradation allows cancerous cells to separate from the tumor to metastasize. Drosophila melanogaster undergoes metamorphosis from larva to adult. Most larval tissues undergo apoptosis, but the larval fat body undergoes remodeling and persists until after the adult has eclosed. During remodeling, the larval fat body cells change from being polygonal cells connected in sheets to spherical cells that are free floating. Since D. melanogaster possess multiple tools for genetic analysis, this organism is a commonly used model organism in biomedical research. Drosophila were fed EMS to establish mutations on their third chromosome and were then scored for lethality. Twenty of these lines are pharate adult lethal, wherein the newly formed adult flies fail to eclose from their pupal case, and have larval fat body remodeling abnormalities. The fat body phenotype was screened and categorized according to the level of remodeling. The chromosomal location of four of the mutated genes that cause pharate adult lethality and abnormal fat body remodeling was attempted to be established. Three of the mutated lines were determined to have mutations in the aur-A gene. This gene is known to affect the cytoskeleton arrangement in neuroblasts, but its role in fat body remodeling is unknown. The results from this study suggest that that this mutated gene does affect the actin filament organization.