Biology Reference
In-Depth Information
CHAPTER
17
Closure of Holes
The closure of holes within an embryonic or foetal epithelium is an essential part of normal
development in many animals. It is also important in the repair of wounds: these are not part
of normal 'programmed' development, but may nevertheless occur accidentally or through
attempted predation of free-living embryos, or because of foetal surgery on mammalian
embryos.
DORSAL CLOSURE IN
DROSOPHILA MELANOGASTER
The morphogenetic movements of the D. melanogaster embryo leave a gap on the dorsal
side of the egg, in which the embryonic epidermis fails to cover the underlying amnioserosa.
This gap, the 'dorsal hole', is later covered by an upwards spreading of the epidermis from
the flanks of the embryo ( Figure 17.1 ).
In principle, inward movement of an epidermis to seal a hole might be driven either by
active advance of the edge cells into the space or by their passive advance under pressure
from cell expansion or proliferation in the epidermis behind them. Ablation of areas of
epidermis near but not at the leading edge, using an ultraviolet laser, fails to prevent dorsal
closure. 1 Indeed, it accelerates it a little. This indicates that, far from pushing the edges
together, the bulk epidermis resists the closure and the advance across the hole must be
driven by mechanisms local to the area of the hole and its immediate borders. As with
convergent extension (the mechanism of bulk epithelial movement described in the previous
chapter), the mechanics of the process make use of actin-myosin contraction, and cells
become plane-polarized in order to apply forces in the right place.
There are at least two sources of force involved in hole closure. The first to be discovered
lies in the epidermis itself, which develops a thick cable of actin and myosin that runs adja-
cent to and parallel to the hole's edge. 1 The actin bands terminate at cell-cell junctions and are
attached to them; indeed, the junctions here show modified accessibility to epitope-specific
anti-cadherin antibodies and may be especially strong. 2 The alternating fibre-junction e
fibre-junction system therefore constitutes a band that runs right around the edge of the
hole, appearing to be continuous at the resolution of light microscopy ( Figure 17.2 a). Forma-
tion of this actin band is dependent on Rho GTPase, which is also responsible for causing
formation of stress fibres in fibroblasts (see Chapters 5 and 8), and it fails to form around
the dorsal hole of embryos lacking Rho activity. 3
It is also dependent on the activity of the
 
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