Figure 4.
The Pak1 kinase, a potent inhibitor of Scd1, is more stable at cell ends when branched actin is lost. (A) Pak1-mEGFP localization in control cells, scd1∆, gef1∆, and rga4∆ rga6∆ mutant cells. (B) Model describing Cdc42 activation network where Pak1 kinase upon activation by Cdc42 triggers Scd1 detachment. (C) Pak1-mEGFP localization in DMSO and CK-666 treated cells. (D) Pak1-mEGFP dynamics in cells treated with DMSO or CK-666. Dynamics observed in vivo resembled the dynamics seen in model predictions (insets). (E) Quantification of Pak1-mEGFP localization at the brightest cell end in DMSO or CK-666 treated cells (N = 3, n ≥ 10 cells). (F) Quantification of the extent of Pak1-mEGFP fluctuations at the cell ends (N = 4, n ≥ 5 cells). (G) FRAP analysis showing the half-life of Pak1-mEGFP recovery in DMSO and CK-666 treated cells (n ≥ 10 cells). Scale bar, 10 µm. P value, *<0.05, Student’s t test.

The Pak1 kinase, a potent inhibitor of Scd1, is more stable at cell ends when branched actin is lost. (A) Pak1-mEGFP localization in control cells, scd1∆, gef1∆, and rga4∆ rga6∆ mutant cells. (B) Model describing Cdc42 activation network where Pak1 kinase upon activation by Cdc42 triggers Scd1 detachment. (C) Pak1-mEGFP localization in DMSO and CK-666 treated cells. (D) Pak1-mEGFP dynamics in cells treated with DMSO or CK-666. Dynamics observed in vivo resembled the dynamics seen in model predictions (insets). (E) Quantification of Pak1-mEGFP localization at the brightest cell end in DMSO or CK-666 treated cells (N = 3, n ≥ 10 cells). (F) Quantification of the extent of Pak1-mEGFP fluctuations at the cell ends (N = 4, n ≥ 5 cells). (G) FRAP analysis showing the half-life of Pak1-mEGFP recovery in DMSO and CK-666 treated cells (n ≥ 10 cells). Scale bar, 10 µm. P value, *<0.05, Student’s t test.

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