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Fig. 8. Extrinsic and intrinsic signals on the process of generating an
epithelial sheet de novo: LEC replacement by histoblasts. During larval
stages, histoblasts are arrested in G2 and increase their size. LECs
endoreduplicate, become polyploid and secrete the larval cuticle. At the onset
of metamorphosis, the histoblasts undergo a series of G1-less synchronous cell
divisions and reduce their size. Histoblast nests do not expand and remain
confined to their original territories. LECs undergo apolysis, detach from the
old larval cuticle and secrete the pupal cuticle. Images show the increment in
number and the reduction in size of histoblasts from a ventral nest during
pupariation. Histoblasts express GFP under the control of the Esg-Gal4 driver.
The cell cytoplasm is marked in red with Propidium Iodide. In pupal stages,
histoblasts undertake stochastic cell divisions and nests expand to replace
LECs. These extrude from the epithelia, die and are cleared by the action of
circulating haemocytes. In the images, histoblasts and LECs can be
distinguished by their size (nuclear DAPI staining). Images show in false
colour the spreading of nests in the period between 18 and 30 hours APF.
Colour coding is as in Fig. 1
(i.e. green, anterior dorsal; red, posterior dorsal; yellow, spiracular; blue,
ventral nest). The proliferation and expansion of histoblasts and the death of
LECs are very precisely triggered by external (hormonal) inputs. An early
Ecdysone peak of expression activates the synchronous divisions of histoblasts
in prepupae. A late peak of Ecdysone correlates with histoblast loss of
synchrony and it is essential for the initiation of cell replacement.
Nonetheless, intrinsic interactive mechanisms involved in the coordination of
histoblast proliferation and LEC death are also in place. LECs do not die in
the absence of histoblast proliferation; conversely, histoblasts do not expand
when LEC death is blocked. Mutual exchange of distinct signals thus appears to
be necessary, beyond hormonal triggering events, to implement and harmonize
the behaviour of histoblasts and LECs during abdominal epithelial
morphogenesis
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