Centrosome Reorientation in Wound-Edge Cells Is Cell Type Specific

Abstract

The reorientation of the microtubule organizing center during cell migration into a wound in the monolayer was directly observed in living wound-edge cells expressing ␥-tubulin tagged with green fluorescent protein. Our results demonstrate that in CHO cells, the centrosome reorients to a position in front of the nucleus, toward the wound edge, whereas in PtK cells, the centrosome lags behind the nucleus during migration into the wound. In CHO cells, the average rate of centrosome motion was faster than that of the nucleus; the converse was true in PtK cells. In both cell lines, centrosome motion was stochastic, with periods of rapid motion interspersed with periods of slower motion. Centrosome reorientation in CHO cells required dynamic microtubules and cytoplasmic dynein/dynactin activity and could be prevented by altering cell-to-cell or cell-to-substrate adhesion. Microtubule marking experiments using photoactivation of caged tubulin demonstrate that microtubules are transported in the direction of cell motility in both cell lines but that in PtK cells, microtubules move individually, whereas their movement is more coherent in CHO cells. Our data demonstrate that centrosome reorientation is not required for directed migration and that diverse cells use distinct mechanisms for remodeling the microtubule array during directed migration.

Coordinate Control of Host Centrosome Position, Organelle Distribution, and Migratory Response by Toxoplasma gondii via Host mTORC2

“…For example, the orientation of the Golgi apparatus may be important because this organelle, which also associates with the PV, can provide microtubule nucleation function (11). The importance of centrosome orientation to the leading edge for directed migration has been controversial because it is not observed in some experimental systems (43)(44)(45)(46). Future studies will be directed to the use of the novel system we have described to elucidate further the mechanistic linkage between centrosome orientation and migratory response.…”

HEF1-Aurora A Interactions: Points of Dialog between the Cell Cycle and Cell Attachment Signaling Networks

“…30 In one model, of fibroblast migration, it has been demonstrated that a signal dependent on the Cdc42 GTPase is required to orient the centrosome to face the direction of migration, while microtubules emanating from the centrosome interact at their plus ends with EB1 and APC, making contact with the cell cortex at sites involving Discs-large (Dlg), and once again specified by the polarity complex (aPKC and other proteins). [31][32][33] At present, it seems likely that the phenomenon of centrosomal contribution to migration is cell type specific, 34 which may reflect the abundance of differing polarization-associated proteins in diverse cell types. It is only now becoming widely appreciated that cells migrate by a variety of different strategies, and that as cancer cells become metastatic, they can serially adapt different strategies: 35,36 hence, the importance of these observations in human disease remains to be established.…”

The Cdc14B phosphatase displays oncogenic activity mediated by the Ras-Mek signaling pathway

“…It is well established that positioning of the centrosome may determine the direction of cell movement, most probably through the microtubule system. 29,33 Overexpression of Cdc14B has been previously described to result in microtubules bundling and stabilization as well as decreased microtubule nucleation from the centrosome. 22 Thus, it is possible that some of the effects in cell movements may be due to a direct role of Cdc14B on microtubule dynamics.…”