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The precisely coordinated spatiotemporal control of the assembly and disassembly of actin filaments is a major determinant in a wide range of fundamental cellular processes such as endocytosis, cytokinesis and cell migration. In line with this notion, loss of MyoX completely abolishes microspikes in B16-F1 cells, whereas the knockdown of MyoX in endothelial cells decreases filopodia number only by 50%. Given the typical ratio of F-actin to G-actin of approximately 1:1 in non-muscle cells, the data revealing a ratio of 7:1 in CP-KO cells further suggested a significant depletion of the polymerization-competent pool of monomeric actin in the mutants. The depletion of CP in different cell types such as B16-F1, B16-F10 and Dictyostelium cells is commonly linked to excessive formation of filopodia, as shown here for CP-deficient B16-F1 cells. Since these differences are certainly even more pronounced in diverse cell types such as the B16-F1 melanoma cells and NIH 3T3 fibroblasts used here, the specific phenotype that emerges after the loss of CP in one cell type cannot simply be transferred to the other. Whereas expression of constitutively active mDia1 for instance was found to induce filopodia-like protrusions in NIH 3T3 cells, another study using Jurkat T lymphocytes, 300.19 pre-B lymphomas and NIH 3T3 cells reached the opposite conclusion. The authors did not detect endogenous mDia1 and mDia3 at the distal tips of filopodia in EVM/CP-KO cells with the specific antibodies (data not shown), suggesting that these formins do not contribute to filopodia formation, at least in this cell type. @@
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