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Polymerizing Microtubules Activate Site-directed F-Actin Assembly in Nerve Growth Cones
Journal article   Open access

Polymerizing Microtubules Activate Site-directed F-Actin Assembly in Nerve Growth Cones

M. William Rochlin, Michael E Dailey and Paul C Bridgman
Molecular Biology of the Cell, Vol.10(7), pp.2309-2327
07/01/1999
DOI: 10.1091/mbc.10.7.2309
PMCID: PMC25445
PMID: 10397767
url
https://doi.org/10.1091/mbc.10.7.2309View
Published (Version of record) Open Access

Abstract

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.
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