Xclaudin 1 is required for the proper gastrulation in Xenopus laevis

Chang, Da-Jung; Hwang, Yoo-Seok; Cha, Sang‐Wook; Chae, Jeong-Pil; Hwang, Sung-Hun; Hahn, Jang-Hee; Bae, Yong Chul; Lee, Hyun‐Shik; Park, Mae Ja

doi:10.1016/j.bbrc.2010.05.068

Cited by 4 publications

(3 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The chick intestinal epithelium also expresses claudin-3, -5, and -16, with localization observed along the entire villus, in the crypt and lower villus, and in upper villus goblet cells, respectively (Ozden et al, 2010). In Xenopus , Xclaudin controls left-right patterning (Brizuela et al 2001), and gain or loss of the Xenopus claudin-1 homolog, XClaudin-1 , disrupts normal convergent-extension during gastrulation (Chang et al 2010). The Xclaudin-5 genes ( 5a and 5b ) are observed in the mesoderm and are required for heart tube formation (Yamagishi et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

The tight junction protein claudin-1 influences cranial neural crest cell emigration

Fishwick

Neiderer

Jhingory

et al. 2012

Mechanisms of Development

View full text Add to dashboard Cite

The neural crest is a population of migratory cells that follows specific pathways during development, eventually differentiating to form parts of the face, heart, and peripheral nervous system, the latter of which includes contributions from placodal cells derived from the ectoderm. Stationary, premigratory neural crest cells acquire the capacity to migrate by undergoing an epithelial-to-mesenchymal transition that facilitates their emigration from the dorsal neural tube. This emigration involves, in part, the dismantling of cell-cell junctions, including apically localized tight junctions in the neuroepithelium. In this study, we have characterized the role of the transmembrane tight junction protein claudin-1 during neural crest and placode ontogeny. Our data indicate that claudin-1 is highly expressed in the developing neuroepithelium but is down-regulated in migratory neural crest cells, although expression persists in the ectoderm from which the placode cells arise. Depletion or overexpression of claudin-1 augments or reduces neural crest cell emigration, respectively, but does not impact the development of several cranial placodes. Taken together, our results reveal a novel function for a tight junction protein in the formation of migratory cranial neural crest cells in the developing vertebrate embryo.

show abstract

Section: Discussionmentioning

confidence: 99%

The tight junction protein claudin-1 influences cranial neural crest cell emigration

Fishwick

Neiderer

Jhingory

et al. 2012

Mechanisms of Development

View full text Add to dashboard Cite

show abstract

“…Tight junction proteins are detected as early as the gastrulation stage and persist until full development (4). The presence of tight junction claudin-1 proteins is crucial during gastrulation in X. laevis embryos (65), but general observations of tight junction proteins in adult frogs are lacking. In early larvae, tripartite junctional complexes of tight junction, adherens junction, and desmosomes are observed, wherein these complexes appear to lose significant contribution from adherens junctions in larvae approaching metamorphosis and in adult frogs (4).…”

Section: Skin As a Physical Barriermentioning

confidence: 99%

Frog Skin Innate Immune Defences: Sensing and Surviving Pathogens

2019

View full text Add to dashboard Cite

Amphibian skin is a mucosal surface in direct and continuous contact with a microbially diverse and laden aquatic and/or terrestrial environment. As such, frog skin is an important innate immune organ and first line of defence against pathogens in the environment. Critical to the innate immune functions of frog skin are the maintenance of physical, chemical, cellular, and microbiological barriers and the complex network of interactions that occur across all the barriers. Despite the global decline in amphibian populations, largely as a result of emerging infectious diseases, we understand little regarding the cellular and molecular mechanisms that underlie the innate immune function of amphibian skin and defence against pathogens. In this review, we discuss the structure, cell composition and cellular junctions that contribute to the skin physical barrier, the antimicrobial peptide arsenal that, in part, comprises the chemical barrier, the pattern recognition receptors involved in recognizing pathogens and initiating innate immune responses in the skin, and the contribution of commensal microbes on the skin to pathogen defence. We briefly discuss the influence of environmental abiotic factors (natural and anthropogenic) and pathogens on the immunocompetency of frog skin defences. Although some aspects of frog innate immunity, such as antimicrobial peptides are well-studied; other components and how they contribute to the skin innate immune barrier, are lacking. Elucidating the complex network of interactions occurring at the interface of the frog's external and internal environments will yield insight into the crucial role amphibian skin plays in host defence and the environmental factors leading to compromised barrier integrity, disease, and host mortality.

show abstract

“…Cldn-1, Ocln, ZO-1), have been shown to respond to changes in environmental conditions (Castillo et al, 1991;Chasiotis and Kelly, 2009;Tokuda et al, 2010). Over 30 genes encoding amphibian TJ proteins have now been reported, yet little is known about their contribution to TJ permeability (Cardellini et al, 1996;Cordenonsi et al, 1997;Fesenko et al, 2000;Klein et al, 2002;Chasiotis and Kelly, 2009;Chang et al, 2010;Saharinen et al, 2010;Yamagishi et al, 2010;Baltzegar et al, 2013;Sun et al, 2015). In addition, the majority of these genes have been identified in the strictly aquatic anurans Xenopus laevis and Xenopus tropicalis; thus, almost nothing is known about the characteristics of TJ proteins in terrestrial and semi-aquatic amphibians (Günzel and Yu, 2013).…”

Section: Introductionmentioning

confidence: 99%

A lethal fungal pathogen directly alters tight junction proteins in the skin of a susceptible amphibian

Gauberg

Cramp

et al. 2018

Journal of Experimental Biology

View full text Add to dashboard Cite

Bacterial and viral pathogens can weaken epithelial barriers by targeting and disrupting tight junction (TJ) proteins. However, comparatively little is known about the direct effects of fungal pathogens on TJ proteins and their expression. The disease chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd), is threatening amphibian populations worldwide. Bd is known to infect amphibian skin and disrupt cutaneous osmoregulation. However, exactly how this occurs is poorly understood. This study considered the impact of Bd infection on the barrier properties of the Australian green tree frog (Litoria caerulea) epidermis by examining how inoculation of animals with Bd influenced the paracellular movement of FITC-dextran (4 kDa, FD-4) across the skin in association with alterations in the mRNA and protein abundance of select TJ proteins of the epidermal TJ complex. It was observed that Bd infection increased paracellular movement of FD-4 across the skin linearly with fungal infection load. In addition, Bd infection increased transcript abundance of the tricellular TJ (tTJ) protein tricellulin (Tric) as well as the bicellular TJ (bTJ) proteins occludin (Ocln), claudin (Cldn)-1, Cldn-4 and the scaffolding TJ protein zonula occludens 1 (ZO-1). However, while Tric protein abundance increased in accord with changes in transcript abundance, protein abundance of Cldn-1 was significantly reduced and Ocln protein abundance was unchanged. Data indicate that disruption of cutaneous osmoregulation in L. caerulea following Bd infection occurs, at least in part, by an increase in epidermal paracellular permeability in association with compromised integrity of the epidermal TJ complex.

show abstract

Xclaudin 1 is required for the proper gastrulation in Xenopus laevis

Cited by 4 publications

References 17 publications

The tight junction protein claudin-1 influences cranial neural crest cell emigration

The tight junction protein claudin-1 influences cranial neural crest cell emigration

Frog Skin Innate Immune Defences: Sensing and Surviving Pathogens

A lethal fungal pathogen directly alters tight junction proteins in the skin of a susceptible amphibian

Contact Info

Product

Resources

About