The amoeboid myosin I's are required for cellular cortical functions such a
s pseudopod formation and macropinocytosis, as demonstrated by the finding
that Dictyostelium cells overexpressing or lacking one or more of these act
in-based motors are defective in these processes. Defects in these processe
s are concomitant with changes in the actin-filled cortex of various Dictyo
stelium myosin I mutants. Given that the amoeboid myosin I's possess both a
ctin- and membrane-binding domains, the mutant phenotypes could be due to a
lterations in the generation and/or regulation of cell cortical tension. Th
is has been directly tested by analyzing mutant Dictyostelium that either l
acks or overexpresses various myosin I's, using micropipette aspiration tec
hniques. Dictyostelium cells lacking only one myosin I have normal levels o
f cortical tension. However, myosin I double mutants have significantly red
uced (50%) cortical tension, and those that mildly overexpress an amoeboid
myosin I exhibit increased cortical tension. Treatment of either type of mu
tant with the lectin concanavalin A (ConA) that cross-links surface recepto
rs results in significant increases in cortical tension, suggesting that th
e contractile activity of these myosin I's is not controlled by this stimul
us. These results demonstrate that myosin I's work cooperatively to contrib
ute substantially to the generation of resting cortical tension that is req
uired for efficient cell migration and macropinocytosis.