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Figure 1.

Mean zooxanthellae density (± SE) over time post-injury.

H = healthy tissue, n = 27 (K-W x2 (4) = 88.35, P<0.001).

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Figure 2.

Mean melanin volume fraction (Vf; ± SE) over time post-injury (n = 27).

H Epid = healthy coral epidermis. Melanin Vf compared among H. Gast. ( = healthy gastrodermis) and gastrodermis within injured tissue (K-W x2 (4) = 35.94, P<0.001).

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Figure 3.

Healthy Porites cylindrica tissue sections stained with a) Haematoxylin and Young's Eosin-Erythrosin stain (H&E) and b) Fontana-Masson stain.

E = epidermis, G = gastrodermis, Me = melanin and/or melanin-containing granular cell, Mes = mesentery, Z = zooxanthella (Symbiodinium cell) and N = cnidae.

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Figure 4.

H&E stained free-body wall area of Porites cylindrica 0 h post-injury with surface body wall epidermis having been removed by the injury.

G = gastrodermis, Un-id. = unidentified cells, Sm = smooth (hyaline) cell, N = cnida.

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Figure 5.

Disorganised tissues of Porites cylindrica immediately post-injury (0 h) stained with a) H&E and b) Fontana-Masson stain.

Un-id. = unidentified cells, Am = granular amoebocytes, Me = melanin-containing granular cells, Sm = smooth (hyaline) cell, N = cnida.

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Figure 6.

The edge of a lesion on Porites cylindrica 6 hours post-injury demonstrating amoebocyte aggregations, disrupted tissue and expelled, dead or dying tissue with microorganisms.

Exp. = expelled, dead and dying tissue, W. ed. = wound edge, Am = granular amoebocytes, Me = melanin-containing granular amoebocytes, Cil = ciliate, N = cnida.

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Figure 7.

Porites cylindrica 6 hours post-injury with a) aggregating amoebocytes and expelled and/or disrupted tissue components, b) amoebocytes aggregating with melanin-containing-granular cells, c) granular amoebocytes forming a front, with melanin and Symbiodinium cells forming a second front immediately interior to the first one, and d) fibroblasts displaying characteristic pseudopodia potentially secreting connective collagen fibres.

Me = melanin and/or melanin-containing granular cell, N = cnidae, Mu = mucocyte, Am = granular amoebocyte, fib = fibroblast and Pseud = pseudopodia.

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Figure 8.

Agranular amoebocytes indicated with an arrow, present at 6 hours post-injury.

Stained with H&E.

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Figure 9.

Porites cylindrica tissue 24 hours post-injury demonstrating a) granular amoebocytes aligning along the newly-forming epithelial layer, at the edge of the lesion b) granular amoebocytes being reinforced by melanin-containing granular cells.

E = epidermis, G = gastrodermis, Me = melanin and/or melanin-containing granular cell, Sm = smooth (hyaline) cell, Am = granular amoebocyte.

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Figure 10.

Porites cylindrica tissue 48 hours post-injury demonstrating a) a developing epithelial front and b) merging granular amoebocytes and melanin-containing granular cells.

E = epidermis, M = mesogloea, G = gastrodermis, Me = melanin and/or melanin-containing granular cells, N = cnida, E. nuc = enlarged nucleus, Am = granular amoebocyte.

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Figure 11.

Potentially apoptotic cells as indicated by blebbing nuclei (arrow heads).

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Figure 12.

A series of schematic diagrams representing the wound healing process between 0 and 48 h in P. cylindrica.

1) Healthy coral tissue is composed of a surface body wall layer including the epidermis, a thin mesogloea and a gastrodermal layer. The epithelial layers are then mirrored on the other side of the gastrovascular cavity, to form the basal body wall, with a squamous epithelium forming the calicodermis. 2) Upon injury of the surface body wall epithelial layer, cell lysis and degranulation of melanin-containing granular cells starts to form a rudimentary clot, or plug. 3) Infiltration of granular amoebocytes, some potentially via the mesogloea, occurs at 6 h to form a cell barrier behind which melanin-containing granular cells aggregate, along with agranular amoebocytes and some fibroblasts. 4) At 24 h, infiltrated cells have begun to proliferate and the granular amoebocytes are reorientated and elongated to form an undifferentiated epidermis. 5) By 48 h, differentiation begins to occur and the epithelial layers begin to form from the lesion edge. The high abundance of amoebocytes and fibroblasts, potentially due to proliferation, is reduced by apoptosis.

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