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. 2014 Jun 15;25(12):1867–1876. doi: 10.1091/mbc.E14-03-0839

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© 2014 Vaughan et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 3: — DAG is generated via the PC-PLC/SMS pathway, whereas PA is generated via PLD and DAG kinase. (A) DAG is present at wounds in control cells but blocked by the PC-PLC/SMS inhibitor D609. (A′) Quantification of wound DAG (***p < 0.005). (B) DAG is present at similar levels at wounds in control cells and those treated with FIPI, a PLD inhibitor. (B′) Quantification of wound DAG (p > 0.05). (C) DAG at wounds is elevated in cells treated with the PIP2-PLC inhibitor U-73122. (C′) Quantification of wound DAG (***p < 0.005). (D) PA is decreased in cells treated with D609 relative to controls. (D′) Quantification of wound PA (*p < 0.05). (E) PA wound signal is blocked in cells treated with FIPI. (E′) Quantification of wound PA (***p < 0.005). (F) PA levels at wounds are decreased in cells treated with R59949, a DAG kinase inhibitor. (F′) Quantification of wound PA (**p < 0.01). (G) Schematic of pathways leading to DAG and PA generation and corresponding inhibitors. Top and bottom whiskers represent maximum and minimum values, respectively. Scale bar, 20 μm.