Title:
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Characterisation of histoblast development in Drosophila Melanogaster
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During metamorphosis, the larval form of a holometabolous insect is restructured
to create the adult form. In Drosophila melanogaster, histoblasts are the
precursor imaginal cells that generate the adult abdominal epithelium. Ecdysone
triggers the histoblasts to proliferate, resulting in the expansion of the histoblast
nests and the complete coverage of the abdomen. Concurrently, the larval
epidermal cells (LEGs) are removed. Potentially, histoblast development can be
a good system to study morphogenesis, cell migration, programmed cell death,
ecdysone signaling and differentiation. However, to date, histoblast development
has not been extensively studied.
In this thesis, I characterised the pattern of histoblast nest expansion and fusion,
.and explored behaviour of LECs during histoblast development with time-lapse
analysis using novel genetic markers I identified in existing collections of Gal4
and GFP trap lines. During metamorphosis, histoblast nests spread and fuse in a
strict spatial and temporal manner. Spreading is highly controlled and directed,
as histoblast cells produce filopodial outgrONths and actively migrate towards the
appropriate partner during fusion. LECs removal is concurrent with histoblast
nest expansion. Not only are LECs removed at the histoblast migrating front as
previously proposed (Madhavan and Madhavan, 1980), a significant amount of
LECs located distant from histoblast nests are also destroyed.
To further investigate the relationship between histoblast nest expansion and
LEC removal, I disrupted cell death in LECs using genetic manipulation. I also
studied the effect on the pattem of LEC removal in a mutant background which
histoblast nests are severely reduced. The results from both studies suggest that
histoblasts and LECs signal to one another to coordinate the events during
histoblast development. Moreover, in order to explore the involvement of
histoblast signalling during histoblast development, I disrupted endocytosis to
inhibit histoblasts. The results point to the conclusion that signalling is important
during histoblast development.
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