Filopodia are dynamic cellular protrusions that interact with the extracellular environment. These membrane extensions are supported by parallel bundles of actin that emerge from the branched dendritic actin network in the cortex. Filopodia initiation requires the action of MyTH-FERM myosins, DdMyo7 in amoebae and Myo10 in metazoan cells that are thought to be critical for cortical actin reorganization at the plasma membrane. Filopodia initiate from the cortical cytoskeleton yet it is not known if cortical tension (CT) supports or impedes this critical process. The impact of changes in CT on filopodia formation was investigated using a set of Dictyostelium mutants that exhibit either decreased or increased CT. Reduced CT is seen in the myosin II null mutant, Myo1 double null mutants (Myo1A/B and Myo1B/C) and actin cross-linker null mutants (α-actinin and filamin) while overexpression of Myo1s (Myo1B and Myo1C) results in increased CT. Interestingly, a strong reduction in filopodia formation (68%) with no change in filopodial length is seen in the myosin II nulls. On the other hand, an increase in filopodia number is seen in α-actinin (87%) and Myo1B/C (16%) null mutants, respectively, accompanied by differences in filopodia length: the α-actinin mutant filopodia are 44% longer while the Myo1B/C nulls have 15% shorter filopodia. No change in filopodia formation was seen for Myo1A/B and filamin nulls, however, like the α-actinin null, filamin mutant filopodia were 35% longer relative to control. Mutants with increased CT (Myo1B and Myo1C overexpression mutants) produced wild type filopodia numbers yet the filopodia were ∼20% shorter compared to control. These findings reveal that changing the CT of amoeboid cells in various ways, either by altering cortical actin crosslinking or contractility, can have differing effects on filopodia initiation and extension. Work supported by NIAMS T32AR007612-24 (PW) and NIGMS R01GM122917 (MAT).
Woods et al. (Sun,) studied this question.