Disruption of focal adhesions and extracellular matrix in E9.5 <i>RockDN;Wnt1-cre</i> embryos.

Abstract

<p>A,B,E,F are sections of the first pharyngeal arch (line i in O) and C,D,G,H,I–N are from the frontonasal processes (line ii in O). <b>A–H</b>) E–H are magnified regions shown in the boxes on A–D, respectively. Paxillin has a cortical distribution in the first pharyngeal arch in the control embryos (A,E) and also marks the boundary between the neural ectoderm and NCC-derived ectomesenchyme (arrow in C,G) in the frontonasal processes. This boundary staining is lost in the mutant (arrow in D,H) and there are intense paxillin positive foci in the pharyngeal arch and frontonasal processes (arrowheads in B,F,D,H), confirming loss of cell-substrate adhesion. <b>I–L</b>) Laminin was lost from the ectomesenchyme-neural ectoderm boundary (compare arrowhead in J with L) and was abnormally distributed in the surface ectoderm in the frontonasal processes in the <i>RockDN;Wnt1-cre</i> embryos (compare arrow in I with K). The H&E staining of the same sections are shown in M and N, allowing visualisation of the different cellular layers. fnp = frontonasal process; pa1 = first pharyngeal arch; ne = neural ectoderm; se = surface ectoderm; mes = mesenchyme. Scale bar in A–D,I,K = 50 µm; M,N = 40 µm.</p

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