Introducing a null mutation in the mouse K6α and K6β genes reveals their essential structural role in the oral mucosa

Pauline Wong, Emma Colucci-Guyon, Kenzo Takahashi, Changhong Gu, Charles Babinet, Pierre A. Coulombe

Research output: Contribution to journalArticlepeer-review

Abstract

Mammalian genomes feature multiple genes encoding highly related keratin 6 (K6) isoforms. These type II keratins show a complex regulation with constitutive and inducible components in several stratified epithelia, including the oral mucosa and skin. Two functional genes, K6α and K6β, exist in a head-to-tail tandem array in mouse genomes. We inactivated these two genes simultaneously via targeting and homologous recombination. K6 null mice are viable and initially indistinguishable from their littermates. Starting at two to three days after birth, they show a growth delay associated with reduced milk intake and the presence of white plaques in the posterior region of dorsal tongue and upper palate. These regions are subjected to greater mechanical stress during suckling. Morphological analyses implicate the filiform papillae as being particularly sensitive to trauma in K6α/K6β null mice, and establish the complete absence of keratin filaments in their anterior compartment. All null mice die about a week after birth. These studies demonstrate an essential structural role for K6 isoforms in the oral mucosa, and implicate filiform papillae as being the major stress bearing structures in dorsal tongue epithelium.

Original languageEnglish (US)
Pages (from-to)921-928
Number of pages8
JournalJournal of Cell Biology
Volume150
Issue number4
DOIs
StatePublished - Aug 21 2000

Keywords

  • Bullous diseases
  • Keratin
  • Pachyonychia congenita
  • Skin
  • Transgenic mouse

ASJC Scopus subject areas

  • Cell Biology

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