Ectodermal Cell Layer Research Articles

Mature mediastinal teratoma with adhesions to the pericardium: A rare case report.

Mature mediastinal teratoma (MMT) is a benign tumor that is composed of well-differentiated tissues from all three germ cell layers. Malignant tumors have a distinct feature of adhering to the surrounding organs. Therefore, adhesion of MMT to the adjacent tissues, as a benign tumor, is rare and considered a surgical challenge. It leads to incomplete tumor resection to avoid damage to the surrounding tissues. MMT is a germ cell tumor that contains well-differentiated tissues from ectodermal, mesodermal, and endodermal germ cell layers. MMT comprises approximately 3%-12% of mediastinal tumors in adults and 60%-70% of mediastinal germ cell tumors. Complete surgical resection is the standard treatment. When adhesion to the surrounding tissues is present, residual tissues could be retained to reduce the injury of the peripheral blood vessels and nerves. We are reporting a rare case of MMT with adhesions to the pericardium and discussing the diagnostic and surgical challenges.

Understanding the impact of missense mutations on the structure and function of the EDA gene in X-linked hypohidrotic ectodermal dysplasia: A bioinformatics approach.

X-linked hypohidrotic dysplasia (XLHED), caused by mutations in the EDA gene, is a rare genetic disease that affects the development and function of the teeth, hair, nails, and sweat glands. The structural and functional consequences of caused by an ectodysplasin-A (EDA) mutations on protein phenotype, stability, and posttranslational modifications (PTMs) have not been well investigated. The present investigation involves five missense mutations that cause XLHED (L56P, R155C, P220L, V251M, and V322A) in different domains of EDA (TM, furin, collagen, and tumor necrosis factor [TNF]) from previously published papers. The deleterious nature of EDA mutant variants was identified using several computational algorithm tools. The point mutations induce major drifts in the structural flexibility of EDA mutant variants and have a negative impact on their stability, according to the 3D protein modeling tool assay. Using the molecular docking technique, EDA/EDA variants were docked to 10 EDA interacting partners, retrieved from the STRING database. We found a novel biomarker CD68 by molecular docking analysis, suggesting all five EDA variants had lower affinity for EDAR, EDA2R, and CD68, implying that they would affect embryonic signaling between the ectodermal and mesodermal cell layers. In silico research such as gene ontology, subcellular localization, protein-protein interaction, and PTMs investigations indicates major functional alterations would occur in EDA variants. According to molecular simulations, EDA variants influence the structural conformation, compactness, stiffness, and function of the EDA protein. Further studies on cell line and animal models might be useful in determining their specific roles in functional annotations.

Invention sharing is the mother of developmental biology.

Invention sharing is the mother of developmental biology.

A differentiation program induced by bone morphogenetic proteins 4 and 7 in endodermal epithelial cells provides the molecular basis for efficient nutrient transport by the chicken yolk sac.

BackgroundThe mammalian yolk sac provides nutrients for the growing fetus during critical early developmental processes such as neural tube closure, which precedes the functional maturation of the placenta. In contrast, oviparous species such as the chicken rely solely on the yolk sac for transfer of nutrients from the yolk to the developing embryo. However, the molecular mechanisms that provide the yolk sac with nutrient transfer competence remain poorly understood.ResultsWe demonstrate that the chicken endodermal epithelial cells (EEC), which are in close contact with the yolk, gain their nutrient‐transport competence by a paracrine crosstalk with the blood‐vessel forming mesodermal cell layer. Bone morphogenetic proteins (BMP) 4 and 7 produced by ectodermal and mesodermal cell layers likely initiate a differentiation program of EECs during the transition from the area vitellina to the area vasculosa. BMPs, by inducing SMAD signaling, promote the up‐regulation of endocytic receptor expression and thereby provide the EECs with the molecular machinery to produce triglyceride‐rich lipoprotein particles.ConclusionThis paracrine signaling cascade may constitute the basis for the EEC‐mediated mechanism underlying the efficient uptake, degradation, resynthesis, and transfer of yolk‐derived nutrients into the embryonic circulation, which assures proper energy supply and development of the growing fetus.

Cytological and Histological Study of Adult and Neonate Epidermis in Thick and Thin Skin of Various Anatomical Sites

The integumentary system covers the surface of the embryo (skin) and its specialized skin structures including hair, nails, sweat glands, mammary glands and teeth. During fetal skin development, the epidermis changes from a single layer of ectodermal cells at 7–8 days of gestation into a more apparent stratified, keratinized epithelium at 22–24 weeks. The aim of the study is to identify the histological and cytological changes that take place during neonatal and adult epidermis development. Human neonatal and adult samples were obtained from fully informed, consenting parent or releatives from Al-hilla mortary / Iraq. Neonatal samples were obtained from neonates after sudden deaths from maternity wards. Anatomical Sites included abdomen, forehead, back, shoulder and feet sole. A totoal of 15 neonates and 10 mature adults were used for this study. Fresh tissues were sectioned using a freezing cryostat. Tissues were sectioned at 5µm in -24°C and collected on microscopic slides. Slides were allowed to air dry for 30 min prior to hematoxyline and eosin staining. Tissues were also photographed using scanning electron microscopy SEM. Cytological measurements were taken using image j software and data was analysed using graph prism. Various cytological and histological changes takes place during neonatal and adult and epidermis development. Our study shows the stages of fair follicule formation as well as number of nucleated layers present at each stage of development and at different anatomical sites. Major histological changes takes places during the transition frm a neonate to a mature adult including the number of basal cells and epidermal thickness depending on the anatomical site.

Purinergic receptor detection in human embryonic epidermis

The integumentary system covers the surface of the embryo (skin) and its specialized skin structures including hair, nails, sweat glands, mammary glands and teeth. During fetal skin development, the epidermis changes from a single layer of ectodermal cells at 7–8 days of gestation into a more apparent stratified, keratinized epithelium at 22–24 weeks. Skin development is driven by the complex inter-play between intrinsic and extrinsic pathways. There has been significant interest in determining the molecular cues that regulate the proliferation of human epidermal cells.P2Y receptors are membrane bound G protein coupled receptors. Purinergic signalling mediated by nucleotides such as Adenosine Triphosphate (ATP) and Adenosine Diphosphate (ADP) has also been shown to play a significant role in embryogenesis. Aim:The aim of the study is to identify the presence of purinergic receptors P2Y1,P2Y2,and P2Y4 during human embryonic epidermis development. The expression of purinergic receptors is examined in various anatomical sites and embryonic stages. Human embryonic samples were obtained from fully informed,consenting patients undergoing spontaneous terminations of pregnancy from emergency department at Al-Hilla maternity. Anatomical Sites included abdomen,forehead,back and feet sole. A total of 15 embryos aged between 2-3 months were used for this study. Fresh tissues were sectioned using a freezing cryostat. Tissues were sectioned at 5µm in -24°C and collected on microscopic slides. Slides were allowed to air dry for 30 min prior to immunohistochemical processing. Our study shows strong positivestaining for purinergic receptors P2Y1,P2Y2,and P2Y4 in all selected anatomical sites. Immunohistochemical staining increases with gestational development in all selected anatomical sites. A strong expression of purinergic receptors is seen in anatomical areas which possess high rate of development and strong differentiation rate.purinergic receptors as stem cell markers are actively seen in human epidermis histogeneis and development. Their role is important is epidermal layer proliferation and differentiation.

Neuromuscular structure of the larva to early ancestrula stages of the cyclostome bryozoan Crisia eburnea

AbstractFor the first time, the development of a cyclostome bryozoan has been studied with immunochemistry and confocal laser scanning microscopy, with emphasis on nerves and muscles. The larva is covered by multiciliated cells, which are latitudinally strongly elongated and show phalloidin‐stained cell junctions. We hypothesize that these cells contract at metamorphosis and squeeze the apical invagination and the adhesive sac out. Ectodermal, longitudinal muscle cells extend from the cells of the inner, conical cuticularized part of the apical invagination to the lower part of the corona, around the adhesive sac pore. These muscles are retained in the ancestrula. Scattered monociliated nerve cells are interspersed between the coronal ciliary cells. An equatorial nerve in the larva disappears at metamorphosis. The central, conical part of the cuticle becomes the terminal membrane of the ancestrula, and the underlying ectodermal and mesodermal cell layers differentiate into the polypide bud, forming a deep narrow invagination, differentiating into vestibule–atrium, mouth ring and pharynx–stomach–rectum. Tentacles develop from the ring of cells around the mouth, and a small ganglion with four nerves innervating each of the tentacles develops at the anal side of the mouth. These new findings yield further support for previous homology statements of bryozoan larvae and development.

Sulfur utilization of corals is enhanced by endosymbiotic algae.

ABSTRACTSulfur-containing compounds are important components of all organisms, but few studies have explored sulfate utilization in corals. Our previous study found that the expression of a sulfur transporter (SLC26A11) was upregulated in the presence of Symbiodinium cells in juveniles of the reef-building coral Acropora tenuis. In this study, we performed autoradiography using 35S-labeled sulfate ions (35SO4 2−) to examine the localization and amount of incorporated radioactive sulfate in the coral tissues and symbiotic algae. Incorporated 35SO4 2− was detected in symbiotic algal cells, nematocysts, ectodermal cells and calicoblast cells. The combined results of 35S autoradiography and Alcian Blue staining showed that incorporated 35S accumulated as sulfated glycosaminoglycans (GAGs) in the ectodermal cell layer. We also compared the relative incorporation of 35SO4 2− into coral tissues and endosymbiotic algae, and their chemical fractions in dark versus light (photosynthetic) conditions. The amount of sulfur compounds, such as GAGs and lipids, generated from 35SO4 2− was higher under photosynthetic conditions. Together with the upregulation of sulfate transporters by symbiosis, our results suggest that photosynthesis of algal endosymbionts contributes to the synthesis and utilization of sulfur compounds in corals.

Identification of heat shock protein 10 within the equine embryo, endometrium, and maternal peripheral blood mononuclear cells

Early pregnancy factor has been identified as a 10-kDa extracellular homolog of heat shock protein 10 (Hsp10). Hsp10 has been detected during early pregnancy in serum of mice, sheep, pigs, horses, cows, and humans by the rosette inhibition test. Hsp10 has also been associated with several neoplastic and autoimmune diseases. The goal of the present study was to determine if Hsp10 could be detected in the early equine embryo through the use of immunohistochemistry and quantitative real-time PCR. Additionally, analysis of systemically harvested peripheral blood mononuclear cells (PBMCs) from both pregnant and nonpregnant mares was evaluated to determine expression levels of HSP10. Embryos were collected from Quarter Horse mares by uterine lavage at either 8 or 25 days after ovulation. Collection and separation of PBMCs occurred on Day 8 for both pregnant and nonpregnant mares. Immunohistochemistry revealed cytoplasmic localization of HSP10 throughout the single layer of ectodermal cells forming the trophoblast in Day-8 embryos. Day-25 embryos demonstrated intense localization focally along the apical border of ectodermal cells forming the trophoblast layer of the developing chorion. There was no nuclear staining in either embryonic population. Quantitative real-time PCR detected the presence of mRNA for HSP10 in both 8- and 25-day equine embryos. Day-25 embryos exhibited an elevated degree of expression (P = 0.006) compared with the 8-day embryos for HSP10. Endometrial samples did not display any significant difference in degree of expression for HSP10 (P = 0.10). Finally, PBMCs from pregnant mares demonstrated elevated (P = 0.03) expression of HSP10 compared to the nonpregnant mares on Day 8 of the estrous cycle. This study confirmed the presence of HSP10 protein and mRNA expression of HSP10 in equine embryos at two maturation stages. Additionally, the presence of increased gene expression within PBMCs of pregnant mares suggests communication, possibly leading to necessary immunomodulatory effects between the embryo and mare.

Polarized Wnt Signaling Regulates Ectodermal Cell Fate in Xenopus

How cells convert polarity cues into cell fate specification is incompletely understood. Here, we show that Wnt/β-catenin and Wnt/PCP signaling cooperate in this process in early Xenopus embryos. We find that the Wnt coreceptor Lrp6 is asymmetrically localized to the basolateral membrane in ectodermal blastomeres. Lrp6 asymmetry is controlled by Wnt/PCP signaling, indicating that this pathway regulates not only planar- but also apicobasal cell polarity. Following asymmetric cell division, Lrp6 preferentially sorts to the deep ectodermal cell layer and becomes depleted in the epithelial cell layer. This is accompanied by elevated Wnt/β-catenin signaling in deep cells, which in turn promotes their differentiation into ciliated cells. We conclude that coordinated Wnt/PCP and Wnt/β-catenin signaling convert apicobasal polarity information to specify ectodermal cell fate.

Insect immune responses to nematode parasites

Host innate immunity plays a central role in detecting and eliminating microbial pathogenic infections in both vertebrate and invertebrate animals. Entomopathogenic or insect pathogenic nematodes are of particular importance for the control of insect pests and vectors of pathogens, while insect-borne nematodes cause serious diseases in humans. Recent work has begun to use the power of insect models to investigate host-nematode interactions and uncover host antiparasitic immune reactions. This review describes recent findings on innate immune evasion strategies of parasitic nematodes and host cellular and humoral responses to the infection. Such information can be used to model diseases caused by human parasitic nematodes and provide clues indicating directions for research into the interplay between vector insects and their invading tropical parasites.

ADP-ribosylation Factor-like GTPase ARFRP1 Is Required for Trans-Golgi to Plasma Membrane Trafficking of E-cadherin

ADP-ribosylation factor-related protein 1 (ARFRP1) plays a specific role in Golgi function controlling recruitment of GRIP domain proteins and ARL1 to the trans-Golgi. Deletion of the mouse Arfrp1 gene causes embryonic lethality during early gastrulation, because epiblast cells detach from the ectodermal cell layer and do not differentiate to mesodermal tissue. Here we show that in Arfrp1(-/-) embryos E-cadherin is mistargeted to intracellular compartments, whereas in control embryos it is present at the cell surface of trophectodermal and ectodermal cells. In enterocytes of intestine-specific Arfrp1 null mutants (Arfrp1(vil)(-/-)), E-cadherin is associated with intracellular membranes, partially colocalizing with the cis-Golgi marker GM130 or with punctae close to the cell surface. In contrast, in control enterocytes E-cadherin is exclusively located in the lateral membranes. In addition, ARL1 is dislocated from Golgi membranes to the cytosol of Arfrp1(vil)(-/-) enterocytes. Depletion of endogenous ARFRP1 by RNA interference leads to a dislocation of E-cadherin from the cell surface in HeLa cells and to a reduced cell aggregation in Ltk(-)Ecad cells. ARFRP1 was coimmunoprecipitated in a complex with E-cadherin, alpha-catenin, beta-catenin, gamma-catenin, and p120(ctn) from lysates of Madin-Darby canine kidney cells stably expressing myc-ARFRP1. These data indicate that knock-out of Arfrp1 disrupts the trafficking of E-cadherin through the Golgi and suggest an essential role of the GTPase in trans-Golgi network function.

Transcriptional Control of the Differentiation Program of Interfollicular Epidermal Keratinocytes

Mammalian epidermis is a stratified squamous epithelium that serves as a protective barrier against external harmful elements. The development of the epidermis is a highly regulated process that begins by the commitment of a single layer of multipotent ectodermal cells to a keratinocyte cell fate. This is followed by stratification and a subsequent elaborate program of differentiation leading to the generation of a multilayered epidermis and patterned cutaneous appendages such as the hair follicles and sebaceous glands. The stratified epidermis occupying the space between skin appendages is referred to as the interfollicular epidermis (IFE) and is the focus of this review. Within the IFE, keratinocytes in the innermost basal layer are mitotically active. Upon specific cues, these cells undergo cell cycle arrest and execute a terminal differentiation program as they progress through spinous, granular, and cornified layers. This program operates continually throughout the life of an organism; dead cells sloughed off from the skin surface are replenished by basal cells moving outward in a highly synchronized fashion. Not surprisingly, at the heart of the control process is a dedicated group of transcription factors that ensure the integrity of the keratinocyte differentiation program by regulating gene expression in a temporally and spatially coordinated manner. Here we review the transcription factors that play important roles in the development and maintenance of IFE as evidenced by biochemical and genetic studies.

Shield formation at the onset of zebrafish gastrulation

During vertebrate gastrulation, the three germ layers, ectoderm, mesoderm and endoderm are formed, and the resulting progenitor cells are brought into the positions from which they will later contribute more complex tissues and organs. A core element in this process is the internalization of mesodermal and endodermal progenitors at the onset of gastrulation. Although many of the molecules that induce mesendoderm have been identified, much less is known about the cellular mechanisms underlying mesendodermal cell internalization and germ layer formation. Here we show that at the onset of zebrafish gastrulation, mesendodermal progenitors in dorsal/axial regions of the germ ring internalize by single cell delamination. Once internalized, mesendodermal progenitors upregulate E-Cadherin (Cadherin 1) expression, become increasingly motile and eventually migrate along the overlying epiblast (ectodermal) cell layer towards the animal pole of the gastrula. When E-Cadherin function is compromised, mesendodermal progenitors still internalize, but, with gastrulation proceeding, fail to elongate and efficiently migrate along the epiblast, whereas epiblast cells themselves exhibit reduced radial cell intercalation movements. This indicates that cadherin-mediated cell-cell adhesion is needed within the forming shield for both epiblast cell intercalation, and mesendodermal progenitor cell elongation and migration during zebrafish gastrulation. Our data provide insight into the cellular mechanisms underlying mesendodermal progenitor cell internalization and subsequent migration during zebrafish gastrulation, and the role of cadherin-mediated cell-cell adhesion in these processes.

Cnidarian and Bilaterian Promoters Can Direct GFP Expression in Transfected Hydra

Complete sexual development is not easily amenable to experimentation in hydra. Therefore, the analysis of gene function and gene regulation requires the introduction of exogenous DNA in a large number of cells of the hydra polyps and the significant expression of reporter constructs in these cells. We present here the procedure whereby we coupled DNA injection into the gastric cavity to electroporation of the whole animal in order to efficiently transfect hydra polyps. We could detect GFP fluorescence in both endodermal and ectodermal cell layers of live animals and in epithelial as well as interstitial cell types of dissociated hydra. In addition, we could confirm GFP protein expression by showing colocalisation between GFP fluorescence and anti-GFP immunofluorescence. Finally, when a FLAG epitope was inserted in-frame with the GFP coding sequence, GFP fluorescence also colocalised with anti-FLAG immunofluorescence. This GFP expression in hydra cells was directed by various promoters, either homologous, like the hydra homeobox cnox-2 gene promoter, or heterologous, like the two nematode ribosomal protein S5 and L28 gene promoters, and the chicken β-actin gene promoter. This strategy provides new tools for dissecting developmental molecular mechanisms in hydra; more specifically, the genetic regulations that take place in endodermal cells at the time budding or regeneration is initiated.

Embryonic Lethality Caused by Apoptosis during Gastrulation in Mice Lacking the Gene of the ADP-Ribosylation Factor-Related Protein 1

ADP-ribosylation factor (ARF)-related protein 1 (ARFRP1) is a membrane-associated GTPase with significant similarity to the family of ARFs. We have recently shown that ARFRP1 interacts with the Sec7 domain of the ARF-specific guanine nucleotide exchange factor Sec7-1/cytohesin and inhibits the ARF/Sec7-dependent activation of phospholipase D in a GTP-dependent manner. In order to further analyze the function of ARFRP1, we cloned the mouse Arfrp1 gene and generated Arfrp1 null-mutant mice by gene targeting in embryonic stem cells. Heterozygous Arfrp1 mutants developed normally, whereas homozygosity for the mutant allele led to embryonic lethality. Cultured homozygous Arfrp1 null-mutant blastocysts were indistinguishable from wild-type blastocysts. In vivo, they implanted and formed egg cylinder stage embryos that appeared normal until day 5. Between embryonic days 6 and 7, however, apoptotic cell death of epiblast cells occurred in the embryonic ectoderm during gastrulation, as was shown by histological analysis combined with terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling. Epiblast cells that would normally differentiate to mesodermal cells detached from the ectodermal cell layer and were dispersed into the proamniotic cavity. In contrast, the development of extraembryonic structures appeared unaffected. Our results demonstrate that ARFRP1 is necessary for early embryonic development during gastrulation.

Xoom is required for epibolic movement of animal ectodermal cells in Xenopus laevis gastrulation.

Gastrulation is the most dynamic cell movement and initiates the body plan in amphibian development. In contrast to numerous molecular studies on mesodermal induction, the driving force of gastrulation is as yet poorly understood. A novel transmembrane protein, Xoom, was previously reported, which is required for Xenopus gastrulation. In the present study, the role of Xoom during Xenopus gastrulation was further examined in detail. Overexpression and misexpression of Xoom induced overproduction of Xoom protein, but not a changed phenotype. However, Xoom antisense ribonucleic acid (RNA) injection reduced the Xoom protein and caused gastrulation defects without any influence on the involution and translation levels of mesodermal marker genes. Normal migrating activity of dorsal mesodermal cells was recognized in the antisense RNA-injected explant. Morphological examination using artificial exogastrulation showed that convergent extension of mesodermal cells occurred normally, but the ectodermal cell layer significantly shrank in the antisense RNA-injected embryo. Comparison of cell shape among various experimental conditions showed that inhibition of cell spreading occurs specifically in the outer ectodermal layer of the antisense RNA-injected embryo. Cytochemical examination indicated disorganization of F-actin in the ectodermal cells of the antisense RNA-injected embryo. These results suggest that Xoom plays an important role in the epibolic movement of ectodermal cells through some regulation of actin filament organization.

Dual role of the basic helix-loop-helix transcription factor scleraxis in mesoderm formation and chondrogenesis during mouse embryogenesis.

Scleraxis is a basic helix-loop-helix (bHLH) transcription factor shown previously to be expressed in developing chondrogenic cell lineages during embryogenesis. To investigate its function in embryonic development, we produced scleraxis-null mice by gene targeting. Homozygous mutant embryos developed normally until the early egg cylinder stage (embryonic day 6.0), when they became growth-arrested and failed to gastrulate. Consistent with this early embryonic phenotype, scleraxis was found to be expressed throughout the embryo at the time of gastrulation before becoming restricted to chondrogenic precursor cells at embryonic day 9.5. At the time of developmental arrest, scleraxis-null embryos consisted of ectodermal and primitive endodermal cell layers, but lacked a primitive streak or recognizable mesoderm. Analysis of molecular markers of the three embryonic germ layers confirmed that scleraxis mutant embryos were unable to form mesoderm. By generating chimeric embryos, using lacZ-marked scleraxis-null and wild-type embryonic stem cells, we examined the ability of mutant cells to contribute to regions of the embryo beyond the time of lethality of homozygous mutants. Scleraxis-null cells were specifically excluded from the sclerotomal compartment of somites, which gives rise to the axial skeleton, and from developing ribs, but were able to contribute to most other regions of the embryo, including mesoderm-derived tissues. These results reveal an essential early role for scleraxis in mesoderm formation, as well as a later role in formation of somite-derived chondrogenic lineages, and suggest that scleraxis target genes mediate these processes.

Serum response factor is essential for mesoderm formation during mouse embryogenesis

The transcription factor serum response factor (SRF), a phylogenetically conserved nuclear protein, mediates the rapid transcriptional response to extracellular stimuli, e.g. growth and differentiation signals. DNA- protein complexes containing SRF or its homologues function as nuclear targets of the Ras/MAPK signalling network, thereby directing gene activities associated with processes as diverse as pheromone signalling, cell-cycle progression (transitions G0-G1 and G2-M), neuronal synaptic transmission and muscle cell differentiation. So far, the activity of mammalian SRF has been studied exclusively in cultured cells. To study SRF function in a multicellular organism we generated an Srf null allele in mice. SRF-deficient embryos (Srf -/-) have a severe gastrulation defect and do not develop to term. They consist of misfolded ectodermal and endodermal cell layers, do not form a primitive streak or any detectable mesodermal cells and fail to express the developmental marker genes Bra (T), Bmp-2/4 and Shh. Activation of the SRF-regulated immediate early genes Egr-1 and c-fos, as well as the alpha-Actin gene, is severely impaired. Our study identifies SRF as a new and essential regulator of mammalian mesoderm formation. We therefore suggest that in mammals Ras/MAPK signalling contributes to mesoderm induction, as is the case in amphibia.

Mechanisms of carbon acquisition for endosymbiont photosynthesis in Anthozoa

In contrast to free-living photoautotrophs, endosymbiontic dinoflagellates of the genus Symbiodinium must absorb their inorganic carbon from the cytoplasm of their host anthozoan cell rather then from seawater. The purpose of this paper is to review the present knowledge on the source of dissolved inorganic carbon supply for endosymbiont photosynthesis and the transport mechanisms involved. Symbiodinium spp., generally known as zooxanthellae, live within the endodermal cells of their hosts, corals and sea anemones. They are separated from the surrounding seawater by the host tissues (oral ectodermal cell layer, collagenous basal membrane, endodermal cell, and perisymbiotic vesicles). The symbiotic association is therefore faced with the problem of delivering dissolved inorganic carbon to an endodermal site of consumption from an, essentially, ectodermal site of availability. Studies using original methods demonstrated that neither the internal medium (coelenteric fluid) nor paracellular diffusion could supply enough dissolved inorganic carbon for endosymbiont photosynthesis. A transepithelial active mechanism must be present in the host tissues to maintain the photosynthetic rate under saturating irradiance. A pharmacological approach led to propose a working model of dissolved inorganic carbon transport from seawater to zooxanthellae. This vectorial transport generates a pH gradient across the epithelium. The role of this gradient as well as the physiological adaptation of Symbiodinium spp. to symbiotic life are discussed.Key words: carbon concentrating mechanism, anthozoan, dinoflagellates, anion transport, symbiosis, transepithelial transport.