Attenuation of actinomyosinII contractile activity in growth cones accelerates filopodia-guided and microtubule-based neurite elongation

Rösner, Harald; Möller, Wolfgang; Wassermann, Torsten; Mihatsch, Julia; Blum, Martin

doi:10.1016/j.brainres.2007.07.081

Cited by 39 publications

(31 citation statements)

References 43 publications

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“…In order to directly investigate the implication of NM II, we pre-incubated neurons, for 20 min before WIN stimulation, with the highly selective NM II ATPase inhibitor blebbistatin (25 µM) that blocks NM II in an actin-detached state without perturbing F-actin polymerization (Kovacs et al, 2004). Blebbistatin pre-treatment induced substantial morphological changes of the growth cone, which continued to move forward in a rather disorganized fashion (Figure 2G and Video 4), typically transforming the growth cone lamellipodia into several dynamically advancing filopodia, as reported previously (Rosner et al, 2007). Remarkably, blebbistatin completely abolished WIN-mediated retraction of these dynamically advancing F-actin-rich structures (Figure 2G,H, Figure 3E and Video 4), suggesting that the main force-generating factor downstream of CB1R activation is actomyosin contractility.…”

Section: Resultssupporting

confidence: 82%

Cannabinoid-induced actomyosin contractility shapes neuronal morphology and growth

Roland

Ricobaraza

Carrel

et al. 2014

eLife

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Endocannabinoids are recently recognized regulators of brain development, but molecular effectors downstream of type-1 cannabinoid receptor (CB1R)-activation remain incompletely understood. We report atypical coupling of neuronal CB1Rs, after activation by endo- or exocannabinoids such as the marijuana component ∆9-tetrahydrocannabinol, to heterotrimeric G12/G13 proteins that triggers rapid and reversible non-muscle myosin II (NM II) dependent contraction of the actomyosin cytoskeleton, through a Rho-GTPase and Rho-associated kinase (ROCK). This induces rapid neuronal remodeling, such as retraction of neurites and axonal growth cones, elevated neuronal rigidity, and reshaping of somatodendritic morphology. Chronic pharmacological inhibition of NM II prevents cannabinoid-induced reduction of dendritic development in vitro and leads, similarly to blockade of endocannabinoid action, to excessive growth of corticofugal axons into the sub-ventricular zone in vivo. Our results suggest that CB1R can rapidly transform the neuronal cytoskeleton through actomyosin contractility, resulting in cellular remodeling events ultimately able to affect the brain architecture and wiring.DOI: http://dx.doi.org/10.7554/eLife.03159.001

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Section: Resultssupporting

confidence: 82%

Cannabinoid-induced actomyosin contractility shapes neuronal morphology and growth

Roland

Ricobaraza

Carrel

et al. 2014

eLife

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“…Several studies in chick found that Y-27632 increases lamellipodia and filopodia protrusions from multiple neuronal subtypes (Loudon et al, 2006; Rosner et al, 2007), while Y-27632 significantly decreased filopodial protrusions from Xenopus spinal cord neuronal growth cones (Woo and Gomez, 2006). Conflicting results on the role of ephrins and Rho signaling are also present in cell migration assays.…”

Section: Discussionmentioning

confidence: 99%

Ephrin‐B2 elicits differential growth cone collapse and axon retraction in retinal ganglion cells from distinct retinal regions

Petros

Bryson

Mason

2010

Developmental Neurobiology

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The circuit for binocular vision and stereopsis is established at the optic chiasm, where retinal ganglion cell (RGC) axons diverge into the ipsilateral and contralateral optic tracts. In the mouse retina, ventrotemporal (VT) RGCs express the guidance receptor EphB1, which interacts with the repulsive guidance cue ephrin-B2 on radial glia at the optic chiasm to direct VT RGC axons ipsilaterally. RGCs in the ventral retina also express EphB2, which interacts with ephrin-B2, whereas dorsal RGCs express low levels of EphB receptors. To investigate how growth cones of RGCs from different retinal regions respond upon initial contact with ephrin-B2, we utilized time-lapse imaging to characterize the effects of ephrin-B2 on growth cone collapse and axon retraction in real time. We demonstrate that bath application of ephrin-B2 induces rapid and sustained growth cone collapse and axon retraction in VT RGC axons, whereas contralaterally-projecting dorsotemporal RGCs display moderate growth cone collapse and little axon retraction. Dose response curves reveal that contralaterally-projecting ventronasal axons are less sensitive to ephrin-B2 treatment compared to VT axons. Additionally, we uncovered a specific role for Rho kinase signaling in the retraction of VT RGC axons but not in growth cone collapse. The detailed characterization of growth cone behavior in this study comprises an assay for the study of Eph signaling in RGCs, and provides insight into the phenomena of growth cone collapse and axon retraction in general.

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“…The actin filaments in the lamellipodia are also predominantly oriented with their barbed ends distal, and move retrogradely. The retrograde flow of F-actin is augmented by the action of non-muscle myosin II, as demonstrated by the finding that specific inhibition of myosin II ATPase by the small molecule inhibitor blebbistatin attenuates F-actin retrograde flow (Medeiros et al, 2006;Burnette et al, 2008;Geraldo et al, 2008) and enhances filopodia extension (Rösner et al, 2007). All known isoforms of myosin II (IIA, IIB and IIC) are present in growth cones (Turney and Bridgman, 2005) and, as blebbistatin inhibits the activity of all three, it is not clear from these experiments which isoforms are important in retrograde flow.…”

Section: The Growth-cone Cytoskeletonmentioning

confidence: 99%

Cytoskeletal dynamics in growth-cone steering

Geraldo

Gordon‐Weeks

2009

Journal of Cell Science

227

200

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Interactions between dynamic microtubules and actin filaments are essential to a wide range of cell biological processes including cell division, motility and morphogenesis. In neuronal growth cones, interactions between microtubules and actin filaments in filopodia are necessary for growth cones to make a turn. Growth-cone turning is a fundamental behaviour during axon guidance, as correct navigation of the growth cone through the embryo is required for it to locate an appropriate synaptic partner. Microtubule-actin filament interactions also occur in the transition zone and central domain of the growth cone, where actin arcs exert compressive forces to corral microtubules into the core of the growth cone and thereby facilitate microtubule bundling, a requirement for axon formation. We now have a fairly comprehensive understanding of the dynamic behaviour of the cytoskeleton in growth cones, and the stage is set for discovering the molecular machinery that enables microtubule-actin filament coupling in growth cones, as well as the intracellular signalling pathways that regulate these interactions. Furthermore, recent experiments suggest that microtubule-actin filament interactions might also be important for the formation of dendritic spines from filopodia in mature neurons. Therefore, the mechanisms coupling microtubules to actin filaments in growth-cone turning and dendritic-spine maturation might be conserved.

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Attenuation of actinomyosinII contractile activity in growth cones accelerates filopodia-guided and microtubule-based neurite elongation

Cited by 39 publications

References 43 publications

Cannabinoid-induced actomyosin contractility shapes neuronal morphology and growth

Cannabinoid-induced actomyosin contractility shapes neuronal morphology and growth

Ephrin‐B2 elicits differential growth cone collapse and axon retraction in retinal ganglion cells from distinct retinal regions

Cytoskeletal dynamics in growth-cone steering

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