We used micropipettes to aspirate leading and trailing edges of wild-type a
nd mutant cells of Dictyostelium discoideum. Mutants were lacking either my
osin II or talin, or both proteins simultaneously. Talin is a plasma membra
ne-associated protein important for the coupling between membrane and actin
cortex, whereas myosin II is a cytoplasmic motor protein essential for the
locomotion of Dictyostelium cells. Aspiration into the pipette occurred ab
ove a threshold pressure only. For all cells containing talin this threshol
d was significantly lower at the leading edge of an advancing cell as compa
red to its rear end, whereas we found no such difference in cells lacking t
alin. Wild-type and talin-deficient cells were able to retract from the pip
ette against an applied suction pressure. In these cells, retraction was pr
eceded by an accumulation of myosin II in the tip of the aspirated cell lob
e. Mutants lacking myosin II could not retract, even if the suction pressur
es were removed after aspiration. We interpreted the initial instability an
d the subsequent plastic deformation of the cell surface during aspiration
in terms of a fracture between the cell plasma membrane and the cell body,
which may involve destruction of part of the cortex. Models are presented t
hat characterize the coupling strength between membrane and cell body by a
surface energy sigma. We find sigma approximate to 0.6(1.6) mJ/m(2) at the
leading (trailing) edge of wild-type cells.