Xenbase Image ID: 159774

Fig. 9. Models for the mechanisms by which Aqp3b may affect fibrillar FN matrix assembly. (A) We have shown that knockdown of Aqp3b expression (indicated by red X) caused cells to be less well organized, particularly at the tissue boundary between mesendoderm and ectoderm in Brachet's cleft in the dorsal marginal zone. This resulted in cell autonomous loss of the fibrillar FN matrix in Brachet's cleft. Cells with unaffected Aqp3b formed normal fibrillar FN matrix. (B) Aqp3b may influence fibrillar FN matrix formation by several mechanisms. Membrane protrusions are important for cell-mediated FN fibril assembly (Davidson et al., 2008) and Aqps have been localized to the leading edge of cell protrusions (Saadoun et al., 2005). Further, integrin clustering is essential for FN fibril assembly (Wu., et al., 1993), and Aqps have been shown to bind to the β1 integrin subunit, which is required for integrin endocytosis (Chen et al., 2012). Endocytosis of the α5β1 integrin receptors is necessary for FN fibril assembly (Spicer et al., 2010). Tension imparted by cadherins is required for fibrillar FN matrix formation (Dzamba et al., 2009), which has not yet been shown to be affected by aquaporins. Finally, Aqp3b may engage in cellular signaling to influence fibrillar FN matrix formation, and Aqp3 overexpression was found to upregulate FN expression in cancer cells (Chen et al., 2014). Finally, Aqp3b appears to be required for normal convergence movements during gastrulation, which may be fibrillar FN matrix-dependent or –independent. Solid arrows: relationships that have been documented; dashed arrows: possible relationships or alternate pathways. Image published in: Forecki J et al. (2018) Copyright © 2018. Image reproduced with permission of the Publisher, Elsevier B. V. Larger Image Printer Friendly View

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