Binding of P. aeruginosa (red) increases apical PIP3 (green) and displaces apical proteins (purple).
For unknown reasons, this opportunistic bacterium prefers to enter from the basolateral surface of polarized epithelial cells. A wound provides P. aeruginosa with some access to this surface, but in intact epithelia, tight junctions generally block their paths.
Now, Kierbel and colleagues show that P. aeruginosa makes the best of the available surface. Given access only to the apical side of a cell, the bug converts the membrane around it into a more basolateral environment.
Conversion starts with phospholipid decorations. The basolateral surface is high in PIP3, which P. aeruginosa induces in the apical membrane by recruiting PI3K to its binding sites (usually just above the tight junctions).
The PIP3 then creates actin-filled protrusions that surround and eventually take in the bacterium. The protrusion membranes contain basolateral proteins instead of their previous apical occupants. This exchange also seems to be PIP3 driven: the authors previously found that exogenous apical PIP3 redirects the recycling of basolateral material to the apical surface. How this interference is achieved is not known, but the new arrivals apparently displace the former apical residents. 
