Evidence for microtubule capture by filopodial actin filaments in growth cones

Gordon-Weeks, Philip R.

doi:10.1097/00001756-199110000-00005

Cited by 52 publications

(25 citation statements)

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“…Third, direct time-lapse observations show that dynamic projections of GFP-PTP1B to the peripheral region are reversibly abrogated by a brief treatment with nocodazole. Fourth, previous work shows that microtubules dynamically explore the periphery of the growth cone, with occasional penetration into filopodia (Arregui et al, 1991;Gordon-Weeks, 1991;Sabry et al, 1991;Schaefer et al, 2002;Dent et al, 2007). We found that PTP1B coaligns with tyrosinated microtubules, which represent a highly dynamic pool of microtubules extending in a radial manner to the peripheral region of growth cones.…”

Section: Role Of Microtubules In the Dynamic Positioning Of Ptp1b At supporting

confidence: 49%

“…Growth cone responses vary, but depend on the dynamic properties of microfilaments and microtubules. Microtubules explore dynamically the periphery of growth cones and occasionally penetrate into filopodia (Gordon-Weeks, 1991;Tanaka and Kirschner, 1991;Schaefer et al, 2002;Brown and Bridgman, 2003;Schober et al, 2007). It was early proposed that a subset of exploratory microtubules become selectively stabilized in response to extracellular cues (Kirschner and Mitchison, 1986;Mitchison and Kirschner, 1988).…”

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confidence: 99%

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Microtubule and Cell Contact Dependency of ER-bound PTP1B Localization in Growth Cones

Fuentes

Arregui

2009

MBoC

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PTP1B is an ER-bound protein tyrosine phosphatase implied in the regulation of cell adhesion. Here we investigated mechanisms involved in the positioning and dynamics of PTP1B in axonal growth cones and evaluated the role of this enzyme in axons. In growth cones, PTP1B consistently localizes in the central domain, and occasionally at the peripheral region and filopodia. Live imaging of GFP-PTP1B reveals dynamic excursions of fingerlike processes within the peripheral region and filopodia. PTP1B and GFP-PTP1B colocalize with ER markers and coalign with microtubules at the peripheral region and redistribute to the base of the growth cone after treatment with nocodazole, a condition that is reversible. Growth cone contact with cellular targets is accompanied by invasion of PTP1B and stable microtubules in the peripheral region aligned with the contact axis. Functional impairment of PTP1B causes retardation of axon elongation, as well as reduction of growth cone filopodia lifetime and Src activity. Our results highlight the role of microtubules and cell contacts in the positioning of ER-bound PTP1B to the peripheral region of growth cones, which may be required for the positive role of PTP1B in axon elongation, filopodia stabilization, and Src activity. INTRODUCTIONProper discrimination and response to extracellular signals by axonal growth cones are crucial for the wiring of the nervous system. The sensing activity is performed by receptors in the plasma membrane of growth cones, from which cell adhesion receptors represent a major category. In part, information relied by these receptors regulates the behavior of the cytoskeleton and other macromolecular complexes (Suter and Forscher, 2000;Huber et al., 2003). Growth cone responses vary, but depend on the dynamic properties of microfilaments and microtubules. Microtubules explore dynamically the periphery of growth cones and occasionally penetrate into filopodia (Gordon-Weeks, 1991;Tanaka and Kirschner, 1991;Schaefer et al., 2002;Brown and Bridgman, 2003;Schober et al., 2007). It was early proposed that a subset of exploratory microtubules become selectively stabilized in response to extracellular cues (Kirschner and Mitchison, 1986;Mitchison and Kirschner, 1988). Indeed, imaging of Ti1 pioneer neurons in live grasshopper embryonic limb buds shows the selective invasion of microtubules toward growth cone branches that contact guidepost cells (Sabry et al., 1991). Furthermore, studies in bag cell neurons of Aplysia show that microtubules quickly invade regions of contact between growth cone filopodia and neighboring cells or beads coated with ApCAM (Lin and Forscher, 1993;Suter et al., 2004). This process would facilitate the translocation of vesicular and other membranous compartments to contact sites (Waterman-Storer et al., 2000;Ligon and Holzbaur, 2007; Shaw et al., 2007;Spiliotis et al., 2008). Some degree of microtubule dynamics, however, seems to be required for events induced by target interactions of growth cones, including morphological changes, the assem...

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Section: Role Of Microtubules In the Dynamic Positioning Of Ptp1b At supporting

confidence: 49%

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confidence: 99%

Microtubule and Cell Contact Dependency of ER-bound PTP1B Localization in Growth Cones

Fuentes

Arregui

2009

MBoC

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“…Low levels of phosphorylated GAP-43 were also found in both lamellae that were re-DRG cultures (Dent and Meiri, 1992), and similarly, inhibition of PKC is known to induce growth tracting and whole growth cones that were collapsing. Whole growth cone collapse differs from lamelcone collapse (Campenot et al, 1994;Theodore et al, 1995), further confirming the ability of PKC lar retraction in that it involves retraction of the central region, and often the proximal neurite as phosphorylation to confer stability to growth cones. In neither case do we know the temporal sequence well.…”

Section: Gap-43 In Motile Growth Conesmentioning

confidence: 77%

Distribution of phosphorylated GAP-43 (neuromodulin) in growth cones directly reflects growth cone behavior

Dent

Meiri

1998

J. Neurobiol.

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“…The striking effect of cAMP on actin organization has led us to propose that the retraction of actin stress fibers could be a required early event that, together with a role of microtubules, would be essential to construct new dendritic structures. Indeed, an alternation of actin-and tubulin polymerization-dependent processes in neurite development (Joshi et al, 1985;Dennerl et al, 1988;Gordon-Weeks, 1991) and in the polarity of retinal photoreceptors (Madreperla and Adler, 1989) have already been described.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Rho Is Required for cAMP-induced Melanoma Cell Differentiation

Buscà

Bertolotto

Abbe

et al. 1998

MBoC

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Up-regulation of the cAMP pathway by forskolin or ␣-melanocyte stimulating hormone induces melanocyte and melanoma cell differentiation characterized by stimulation of melanin synthesis and dendrite development. Here we show that forskolin-induced dendricity is associated to a disassembly of actin stress fibers. Since Rho controls actin organization, we studied the role of this guanosine triphosphate (GTP)-binding protein in cAMP-induced dendrite formation. Clostridium botulinum C3 exotransferase, which inhibits Rho, mimicked the effect of forskolin in promoting dendricity and stress fiber disruption, while the Escherichia coli toxin cytotoxic necrotizing factor-1 (CNF-1), which activates Rho and the expression of a constitutively active Rho mutant, blocked forskolininduced dendrite outgrowth. In addition, overexpression of a constitutively active form of the Rho target p160 Rho-kinase (P160 ROCK ) prevented the dendritogenic effects of cAMP. Our results suggest that inhibition of Rho and of its target p160 ROCK are required events for cAMP-induced dendrite outgrowth in B16 cells. Furthermore, we present evidence that Rho is involved in the regulation of melanogenesis. Indeed, Rho inactivation enhanced the cAMP stimulation of tyrosinase gene transcription and protein expression, while Rho constitutive activation impaired these cAMP-induced effects. This reveals that, in addition to controlling dendricity, Rho also participates in the regulation of melanin synthesis by cAMP.

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Evidence for microtubule capture by filopodial actin filaments in growth cones

Cited by 52 publications

References 0 publications

Microtubule and Cell Contact Dependency of ER-bound PTP1B Localization in Growth Cones

Microtubule and Cell Contact Dependency of ER-bound PTP1B Localization in Growth Cones

Distribution of phosphorylated GAP-43 (neuromodulin) in growth cones directly reflects growth cone behavior

Inhibition of Rho Is Required for cAMP-induced Melanoma Cell Differentiation

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