Abstract
During early vertebrate development, epithelial cells establish and maintain apicobasal polarity, failure of which can cause developmental defects or cancer metastasis. This process has been mostly studied in simple epithelia that have only one layer of cells, but is poorly understood in stratified epithelia. In this paper we address the role of the polarity protein Partitioning defective-6 homolog beta (Par6b) in the developing stratified epidermis of Xenopus laevis. At the blastula stage, animal blastomeres divide perpendicularly to the apicobasal axis to generate partially polarized superficial cells and non-polarized deep cells. Both cell populations modify their apicobasal polarity during the gastrula stage, before differentiating into the superficial and deep layers of epidermis. Early differentiation of the epidermis is normal in Par6b-depleted embryos; however, epidermal cells dissociate and detach from embryos at the tailbud stage. Par6b-depleted epidermal cells exhibit a significant reduction in basolaterally localized E-cadherin. Examination of the apical marker Crumbs homolog 3 (Crb3) and the basolateral marker Lethal giant larvae 2 (Lgl2) after Par6b depletion reveals that Par6b cell-autonomously regulates the dynamics of apicobasal polarity in both superficial and deep epidermal layers. Par6b is required to maintain the “basolateral” state in both epidermal layers, which explains the reduction of basolateral adhesion complexes and epidermal cells shedding.
Highlights
Epithelial apicobasal polarity plays important roles in morphogenesis during embryogenesis [1], and is lost or dis-regulated in many disease processes, including metastatic carcinomas [2,3,4]
In this study we show that apicobasal polarity in developing stratified epidermis of Xenopus is dynamically established during gastrulation and that Partitioning defective-6 homolog beta (Par6b) regulates this process
The blastula presumptive epidermal cells have an intermediate polarity with Crumbs homolog 3 (Crb3) around the entire membranes of both the superficial and deep cells, whereas Lethal giant larvae 2 (Lgl2) is basolaterally restricted in the superficial cells but all around the entire deep cells surface (Fig. 7A)
Summary
Epithelial apicobasal polarity plays important roles in morphogenesis during embryogenesis [1], and is lost or dis-regulated in many disease processes, including metastatic carcinomas [2,3,4]. Apicobasal polarity has mostly been characterized in simple epithelia, in which cells are arranged in a single layer with clear apical and basolateral membrane domains separated by sub-apical junctions. Many epithelial tissues, such as the epidermis, are composed of multiple layers, known as stratified epithelia. Little is known about what regulates apicobasal polarity in stratified epithelia [5], especially in deep layer cells. In monolayered C. elegans, Drosophila and cultured mammalian epithelial cells, key polarity proteins Par, aPKC and Crb are apically localized [6,7,8]. In the newborn stratified mouse skin, aPKC is localized in basal keratinocytes at the dermal/epidermal junction, Par is enriched in the cytoplasm of the granular layer, and Crb exhibits a diffuse pattern at the basal side of basal cells [9]. The different distributions of conserved polarity proteins and different architecture between simple and stratified epithelia raise the question of how the core polarity machinery acts in stratified epithelia
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