Ptbp1 and Exosc9 knockdowns trigger skin stability defects through different pathways
文摘

Exosc9 and ptbp1 knockdown triggers blister development in the dorsalepidermis.

Multiciliated cell development is compromised in Exosc9 morphants.

Embryos depleted in Ptbp1 and Exosc9 display phenotypically different skin defects.

Ptbp1 and Exosc9 differentially control expression of genodermatosis-related genes.

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