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Fig. 8. pten–, like 3XASP, is defective in myosin II and F-actin localization to the cortex in response to an increasing temporal gradient of cAMP in the front of a temporal wave. (A,B and C,D) Indirect immunofluorescent staining of myosin II heavy chain in parental AX2 and pten– cells, respectively, migrating in buffer in the absence of attractant. Note that in both cases, there is very little cortical localization of myosin II. (E,F and G,H) Indirect immunofluorescent staining of myosin II heavy chain and laser scanning confocal microscopic (LSCM) line scans of pixel intensity of AX2 cells and pten– cells, respectively, migrating in the front of the third temporal cAMP wave in a series. Note that whereas there is a substantial increase in cortical staining in AX2 cells, there is no detectable increase in cortical staining in pten– cells. (I,J and K,L) Phalloidin staining of F-actin in Ax2 and pten– cells, respectively, migrating in buffer. Note that whereas the pseudopodia stain brightly for F-actin, there is only a hint of cortical staining in both cell types in buffer. (M,N and O,P) Phalloidin staining of F-actin and LSMC line scans of pixel intensity of AX2 cells and pten– cells, respectively, in the third of a series of temporal waves of cAMP. Note that whereas there is a substantial increase in cortical staining in AX2 cells, there is no similar increase in pten– cells. a, anterior end; u, uropod; e, cell edge. Line across cells in A-H, and M-P, indicates position of scan.
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