Figure 3.

Altered cell adhesion properties in Tbx1 mutants. (A) Paintfilling of inner ears from Pax2-Cre;Tbx1-GFPflox/+ mutants at progressively earlier stages of development reveals a delay in SCC formation. At E12.25, fusion plates (arrows, FP) are visible in the controls, but do not appear to have formed in the mutants. Histological analysis confirms defects in the fusion plates (FP, red arrows). In controls, the vestibular epithelia can be seen to have separated from the mesenchyme (asterisks). In Tbx1-GFP mutants, there is no separation of the epithelium from surrounding tissue. (B) Immunofluorescence with anti-laminin (red). Arrows indicate the span of the fusion plate epithelia. There is more intact laminin in the Tbx1-GFP mutants. RNA in situ hybridization to netrin-1 on sections. Netrin-1 expression is reduced in the fusion plates of Tbx1-GFP mutants. Anterior canal (AC, lateral canal (LC). (C) Expression of netrin-1 mRNA on wildtype and Tbx1−/− null mice. Netrin-1 expression is increased in the mesenchyme surrounding the inner ear in the absence of endogenous Tbx1.

Freyer et al. BMC Developmental Biology 2013 13:33   doi:10.1186/1471-213X-13-33
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