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Figure 9 | BMC Developmental Biology

Figure 9

From: Serum response factor is required for cell contact maintenance but dispensable for proliferation in visceral yolk sac endothelium

Figure 9

Loss of SRF results in contact deficiency. Graphic highlighting the adhesive contacts involved in VYS function and signaling between endoderm and mesoderm tissues. Molecules affected by the loss of SRF have been marked by a red "X" (B). Extracellular matrix (ECM) containing fibronectin-1 (FN1) provides structural support and signal induction via interactions with integrins (α β) at focal adhesions (FA). FN1 is deposited into the ECM in by the mesoderm in response to autocrine transforming growth factor β (TGFβ) signals induced by retinoic acid (RA) released by the endoderm. FAs link intracellularly with the actin cytoskeleton via vinculin (VCL) and to signal cascades such as focal adhesion kinase (FAK). Adherens junctions (AJ) containing vascular endothelial cadherins (VE-Cad, CDH5) and tight junctions (TJ) consisting of claudin 5 (CLDN5) molecules provide cell-cell contacts. PECAM1 molecules provide additional intercellular contacts. Nuclear localized SRF responds to actin dynamics via interactions with MAL when released from monomeric actin. Vascular endothelial growth factor (VEGF) signals via Flk-1 to induce ERK1/2-mediated SRF-dependent proliferation. TJP1 = tight junction protein 1, a.k.a. ZO1; α-Cat = α-catenin, CTNNA1; β-Cat = β-catenin, CTNNB1; PXN = paxillin; RAR1/2 = RA receptors 1, 2; TGFβRI/II = TGFβ receptors I, II.

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