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Dev Biol 2016 Jan 15;4092:489-501. doi: 10.1016/j.ydbio.2015.11.002.
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Ptbp1 and Exosc9 knockdowns trigger skin stability defects through different pathways.

Noiret M , Mottier S , Angrand G , Gautier-Courteille C , Lerivray H , Viet J , Paillard L , Mereau A , Hardy S , Audic Y .

In humans, genetic diseases affecting skin integrity (genodermatoses) are generally caused by mutations in a small number of genes that encode structural components of the dermal-epidermal junctions. In this article, we first show that inactivation of both exosc9, which encodes a component of the RNA exosome, and ptbp1, which encodes an RNA-binding protein abundant in Xenopus embryonic skin, impairs embryonic Xenopus skin development, with the appearance of dorsal blisters along the anterior part of the fin. However, histological and electron microscopy analyses revealed that the two phenotypes are distinct. Exosc9 morphants are characterized by an increase in the apical surface of the goblet cells, loss of adhesion between the sensorial and peridermal layers, and a decrease in the number of ciliated cells within the blisters. Ptbp1 morphants are characterized by an altered goblet cell morphology. Gene expression profiling by deep RNA sequencing showed that the expression of epidermal and genodermatosis-related genes is also differentially affected in the two morphants, indicating that alterations in post-transcriptional regulations can lead to skin developmental defects through different routes. Therefore, the developing larval epidermis of Xenopus will prove to be a useful model for dissecting the post-transcriptional regulatory network involved in skin development and stability with significant implications for human diseases.

PubMed ID: 26546114
Article link: Dev Biol

Species referenced: Xenopus laevis
Genes referenced: col17a1 col1a1 col1a2 des.1 des.2 exosc9 fermt1 foxa1 foxi1 hmcn1 itga6 itgb4 itln2 krt12.1 krt15.2 lama3 lamb3 lamc2 pcna ptbp1 tgm5 tuba1a tuba1cl.3
Morpholinos: exosc9 MO1 ptbp1 MO1

Disease Ontology terms: skin disease
Phenotypes: Xla Wt + exosc9 MO (fig.1.c) [+]

Article Images: [+] show captions