The role of Aur-A in Drosophila melanogaster fat body remodeling
Date
2017-06-29
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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.
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Keywords
Drosophila melanogaster, metamorphosis, Tissue remodeling, pharate adult lethality, fat body, fat body remodeling, aur-A, actin filament organization, actin filaments, cytoskeleton