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Vidali et al. (2006) Mol. Bio. Cell. 17:2377-2390

Rac1-null mouse embryonic fibroblasts are motile and respond to platelet-derived growth factor.

Effect of blebbistatin on control immortalized Rac1 c/c cells. Nine representative control cells are shown immediately after 100 μM blebbistatin was added to serum containing media. Note the formation of large lamellipodia.

Effect of blebbistatin on cells lacking Rac1 (immortalized, c/c-k/k). Nine representative Rac1 null cells are shown immediately after 100 μM blebbistatin was added to serum containing media. Note the absence of lamellipodia and the protrusion of fine filopodia-like structures.

Comparison of wound closure between immortalized Rac1 containing c/c and depleted c/c-k/k cells. Left panel shows a wound closure time lapse sequence of cells with normal levels of Rac1, c/c. The right panel shows a similar wound being closed by cells lacking Rac1, c/c-k/k.

Initial response (20 min) to PDGF of primary MEFs containing (k/c) and depleted for (k/c-k/k) Rac1. The left panel shows control (k/c) MEFs not exposed to HTNC peptide. The right panel shows Rac1 (k/c-k/k) depleted cells after treatment with HTNC peptide. Note that the formation of lamellipodial protrusion and dorsal ruffles in response to PDGF is absent in the Rac1 depleted cells from the right panel. Also note numerous tiny blebs and filopodial protrusive activity of the Rac1 null cells in response to PDGF.
Initial response (20 min) to PDGF of primary control MEFs not treated (w/c) and treated (w/c-w/k) with HTNC. The left panel shows control (w/c) MEFs that were not exposed to HTNC peptide. The right panel shows cells containing one wild type Rac1 allele (w/c-w/k) after being exposed to HTNC peptide. Note that the formation of lamellipodial protrusion and dorsal ruffles in response to PDGF is present in cells from both panels.
Initial response (20 min) to PDGF of immortalized MEFs containing (c/c) and depleted for (c/c-k/k) Rac1. The left panel shows control (c/c) MEFs that were not exposed to HTNC peptide. The right panel shows Rac1 (c/c-k/k) depleted cells that were exposed to HTNC peptide. Note that the formation of dorsal ruffles in response to PDGF is absent in the Rac1 depleted cells from the right panel. Also note the slight cell expansion and filopodial protrusive activity of the Rac1 null cells in response to PDGF.
Motile response to PDGF of primary MEFs containing (k/c) and depleted (k/c-k/k) for Rac1. The top left panel shows control cells (k/c) not exposed to HTNC and under starved conditions. The top right panel shows control cells (k/c) not exposed to HTNC and in the presence of PDGF. The bottom left panel show cells depleted for Rac1 (k/c-k/k) under starved conditions. The bottom right panel shows cells depleted for Rac1 (k/c-k/k) in the presence of PDGF. Note the extensive tiny blebs in the k/c-k/k cells, and enhancement of motility in both sets of cells in response to PDGF.
Motile response to PDGF of primary control MEFs not treated (w/c) and treated (w/c-w/k) with HTNC. The top left panel shows cells (w/c) not exposed to HTNC and under starved conditions. The top right panel shows cells (w/c) not exposed to HTNC and in the presence of PDGF. The bottom left panel show cells treated with HTNC peptide (w/c-w/k) under starved conditions. The bottom right panel shows cells treated with HTNC peptide (w/c-w/k) in the presence of PDGF. Note the enhancement of motility on the right panels.
Motile response to PDGF of immortalized MEFs containing (c/c) and depleted (c/c-k/k) for Rac1. The top left panel shows control cells (c/c) not exposed to HTNC and under starved conditions. The top right panel shows control cells (c/c) not exposed to HTNC and in the presence of PDGF. The bottom left panel show cells depleted for Rac1 (c/c-k/k) under starved conditions. The bottom right panel shows cells depleted for Rac1 (c/c-k/k) in the presence of PDGF. Note the enhancement of motility on the right panels.

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