Levi G et al. (1991), The distribution of E-cadherin during Xenopus l...

XB-ART-25171

Development 1991 Jan 01;1111:159-69.

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The distribution of E-cadherin during Xenopus laevis development.

Levi G , Gumbiner B , Thiery JP .

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A vast amount of experimental evidence suggests that cell surface molecules involved in cell-to-cell and/or cell-to-substrate interactions participate in the control of basic events in morphogenesis. E-cadherin is a cell adhesion molecule directly implicated in the control of Ca2(+)-dependent interactions between epithelial cells. We report here the patterns of expression of E-cadherin in developmental stages of Xenopus laevis ranging from early embryo to adult using immunofluorescence microscopy. Although its distribution shares some similarities with those of L-CAM in the chicken and E-cadherin/Uvomorulin in the mouse, the distribution of E-cadherin in Xenopus presents several peculiar and unique features. In early stages of Xenopus development, E-cadherin is not expressed. The molecule is first detectable in the ectoderm of late gastrulas (stage 13-13.5 NF). At this time both the external and the sensory layer of the nonneural ectoderm accumulate high levels of E-cadherin while the ectoderm overlying the neural plate and regions of the involuting marginal zone (IMZ) not yet internalized by the movements of gastrulation are E-cadherin-negative. Unlike most other species, endodermal cells express no or very low levels of E-cadherin up to stage 20 NF. Endodermal cells become strongly E-cadherin-positive only when a well-differentiated epithelium forms in the gut. No mesodermal structures are stained during early development. In the placodes, in contrast to other species, E-cadherin disappears very rapidly after placode thickening. During further embryonic development E-cadherin is present in the skin, the gut epithelium, the pancreas, many monostratified epithelia and most glands. Hepatocytes are stained weakly while most other tissues, including the pronephros, are negative. In the mesonephros, the Wolffian duct and some tubules are positive. During metamorphosis a profound restructuring of the body plan takes place under the control of thyroid hormones, which involves the degeneration and subsequent regeneration of several tissues such as the skin and the gut. All newly formed epithelia express high levels of E-cadherin. Surprisingly, degenerating epithelia of both skin and intestine maintain high levels of the protein even after starting to become disorganized and to degenerate. In the adult, staining is strong in the skin, the glands, the lungs, the gut epithelium and the pancreas, weak in the liver and absent from most other tissues. Our results show that the expression of E-cadherin in Xenopus is strongly correlated with the appearance of differentiated epithelia.

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Species referenced: Xenopus laevis
Genes referenced: cdh1
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	Fig. 1. Distribution of anti-E-cadherin immunoreactivity in Xenopus gastrula. (A-C,G,1) Section corresponding to the regions designed in the drawings (the left drawing is a sagittal section of the gastrula passing through the neural plate, the solid line corresponds to the horizontal plane of section which gives rise to the right drawing). (D) Tangential section through the gastrula ectoderm, (H) Transverse section through the neural plate. (E,F) Phase-contrast images corresponding to B,C. In stage 13.5-14 Xenopus gastrula E-cadherin is present in most of the ectoderm (A,C,D,G) in the region of cell-cell contact (D), the ectoderm overlying the neural plate (B.H) and in the region surrounding the yolk plug (I) is not labeled. The mesoderm and the endoderm are negative. The region of the embryo expressing E-cadherin is indicated by the chessboard filling in the summary drawings, ar, archenteron; bl, blastocoele; e, ectoderm; en, endoderm; m, mesoderm; n, notochord; np, neural plate; yp, yolk plug. Magnification: A-C,I, x200; D, X500; G,H, xlOO.
	Fig. 2. Distribution of anti-E-cadherin immunoreactivity in Xenopiis neurula. (A) Stage 18 neurula, the ectoderm overlying the neural plate region is not stained, B is the phase-contrast image corresponding to A; (C-E) transverse sections at different levels of a stage 23 embryo; C is the most rostral section and E is the most caudal, a, cement gland; en endoderm, h, hypophysis; n, notochord; nt, neural tube; s, somite. Magnification: xlOO.
	Fig. 3. Distribution of anti E-cadherin immunoreactivity during placode formation. Otic placode stage 22 (A), 24 (B), 27 (C) and 37 (D). E-cadherin immunostaining disappears very rapidly from the otic placode after thickening. Olfactory placode stage 37 (E); E-cadherin immunoreactivity diminishes sharply in the olfactory cells, a, cement gland; olf, olfactory organ; op, otic placode; ov, otic vesicle; nt, neural tube; ph, pharynx. Magnification: A-C,E, X150; D, x75.
	Fig. 4. Distribution of anti-E-cadherin immunoreactivity in the skin. (A) Embryonic skin, stage 19; (B) pre-larval skin, stage 32; (C) larval skin, stage 51, note the numerous large unicellular glands; (D) premetamorphic skin, stage 55, a new epidermis has formed beneath the larval skin, and glands are starting to form beneath the epidermis; (E) region of metamorphosed skin (stage 61) containing mucus glands; (F) granular and mucous glands in postmetamorphic skin (stage 64); (GjH) junction (arrow) between areas of metamorphosing and degenerating skin (G) and metamorphosing and larval skin (H); (I) adult skin. Magnification: A-E.I x200; G,H, x75.
	Fig. 5. Distribution of anti-E-cadherin immunoreactivity in the limb and tail at metamorphosis. (A,B) Forelimb stage 51, both the newly forming epidermis of the limb and the degenerating epidermis of the body are E-cadherin positive. (C) Stage 59. On the left is the metamorphosing skin of a developing forelimb while on the right is a degenerating, disorganized portion of the body skin; both are labeled by anti-E-cadherin antibodies. (D,E) Degenerating fin tip at stage 59, note the invasion of melanocytes and the cornification of part of the epidermis which continues to be E-cadherin-positive. lb, limb bud. Magnification: A, x75; C, xlOO; B,D,E, x!50.
	Fig. 6. Distribution of anti-E-cadherin immunoreactivity in the digestive tract. (A) Midgut of a stage 41 embryo, staining of the tall columnar epithelium is barely visible; (B) stomach and duodenum of a stage 41 embryo; (C) larval intestine (stage 53); (D) prometamorphic intestine (stage 59); (E) degenerating intestine during the metamorphic climax (stage 61); (F) postmetamorphic intestine (stage 64). li, liver; p, pancreas; st, stomach. Magnification: xlOO.
	Fig. 7. Distribution of anti-E-cadherin immunoreactivity in the liver, pancreas and gall bladder. (A) A section through the liver, bile duct and gall bladder in a stage 53 tadpole; (B) section through the liver, pancreas and intestine in a stage 51 tadpole. Although some low-level immunoreactivity could always be detected in the liver this was much fainter than that present in the epithelia of the gall bladder, ducts and pancreas, bd, bile duct; li, liver; gb, gall bladder; p, pancreas. Magnification x100.
	Fig. 8. Distribution of anti-E-cadherin immunoreactivity in adult organs. (A) Lungs; (B) kidney, the tubules, particularly surrounding the glomeruli, which were negative, are strongly E-cadherin positive; (C) stomach; (D) liver, the bile duct epithelium (arrows) is much more strongly stained than the hepatocytes. (g) glomerulus. Magnification: xlOO.