Deficiency of p85α in BMMs results in reduced adhesion and migration. (A) Expression of Mac-1 on WT and p85α^–/– BMMs. BMMs were stained with an anti–Mac-1 antibody or an isotype control antibody and subjected to flow cytometric analysis. Filled histograms indicate the level of Mac-1 staining on the surface of both WT and p85α^–/– BMMs; open histograms, the level of staining using an isotype control antibody. (B) WT or p85α^–/– BMMs (5 × 10⁵) were subjected to an in vitro adhesion assay on fibronectin fragments CH271 (which contains a binding site for α5β1), H296 (which contains binding sites for α4β1), and CH-296 (which contains binding sites for both α4β1 and α5β1) and VCAM-1. Adhesion was assessed by measuring absorbance at indicated times. Shown is the optical density of the adherent cells at 600 nm. *P<.05 for WT versus p85α^–/–.WTor p85α^–/– BMMs (2.5 × 10⁵) were subjected to an in vitro migration assay on fibronectin fragment CH271 (which contains a binding site for α5β1), H296 (which contains binding sites for α4β1), and CH-296 (which contains binding sites for both α4β1 and α5β1) as well as VCAM-1–coated transwell membranes. Cell migration was performed either in the absence (C) or presence (D) of M-CSF. Cell migration is expressed as the average number of cells migrated. Figure shows the average number of cells migrated ± SD. Ten fields were scored from one representative experiment. Similar results were observed in 3 other experiments. *P<.05 for WT versus p85α^–/–.