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Vol. 10, Issue 7, 2309-2327, July 1999
and
Department of Anatomy and Neurobiology, Washington University
School of Medicine, St. Louis, Missouri 63110
We identify an actin-based protrusive structure in growth cones
termed "intrapodium." Unlike filopodia, intrapodia are initiated exclusively within lamellipodia and elongate in a continuous
(nonsaltatory) manner parallel to the plane of the dorsal plasma
membrane causing a ridge-like protrusion. Intrapodia resemble the
actin-rich structures induced by intracellular pathogens (e.g.,
Listeria) or by extracellular beads. Cytochalasin B
inhibits intrapodial elongation and removal of cytochalasin B produced
a burst of intrapodial activity. Electron microscopic studies revealed
that lamellipodial intrapodia contain both short and long actin
filaments oriented with their barbed ends toward the membrane surface
or advancing end. Our data suggest an interaction between microtubule
endings and intrapodia formation. Disruption of microtubules by acute
nocodazole treatment decreased intrapodia frequency, and washout of
nocodazole or addition of the microtubule-stabilizing drug Taxol caused
a burst of intrapodia formation. Furthermore, individual microtubule
ends were found near intrapodia initiation sites. Thus, microtubule
ends or associated structures may regulate these actin-dependent
structures. We propose that intrapodia are the consequence of an early
step in a cascade of events that leads to the development of
F-actin-associated plasma membrane specializations.
University of Iowa, Department of Biological
Sciences, Iowa City, IA 52242.
Corresponding author.
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