Desmosomes are cell-cell junctions present in the epithelia and heart and provide mechanical resistance to these tissues in adults. Thus, it is of no surprise that people born with defects in desmosomal proteins can have numerous defects affecting the skin, hair, and heart. However, unlike other junctional complexes, the role of the desmosomes in epidermal development has largely been unexplored. Therefore, this work fills a major knowledge gap by probing the function and regulation of a critical desmosomal protein, desmoplakin (Dsp) during the development of the Xenopus epidermis. Using morpholinos and CRISPR/ Cas9, we demonstrate that Dsp is required for proper epidermal morphogenesis and mechanical resistance in the embryo. These embryos also display defects in keratin organization and development of ectodermally-derived structures such as the mouth, eye and fin. Importantly, Dsp is required for radial intercalation, a morphogenetic process where basally-located cells move into the outer epidermal layer. Decrease in Dsp results in "halted" radial intercalation, affecting the development of small secretory cells and multiciliated cells. Finally, this study highlights a role for c-Jun N-terminal Kinase (JNK) in regulating desmosome dynamics in the epidermis of the developing embryo. In this study, we use a tractable in vivo system to demonstrate that desmosomes perturb epidermal morphogenesis and uncover a novel role for desmosomes in radial intercalation.
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