New insights into the molecular mechanisms specifying neuronal polarity in vivo

Barnes, Anthony P.; Solecki, David J.; Polleux, Franck

doi:10.1016/j.conb.2008.05.003

Cited by 73 publications

(74 citation statements)

References 76 publications

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“…This process may be triggered by selective accumulation or activation of polarity determinants in the undifferentiated neurite [1,2,8]. Interestingly, we found that the active Itgb1, as indicated by immunostaining with active form-specific antibodies (HUTS4) [27], colocalized with axon marker protein GAP-43 (growth-associated protein 43) in dissociated hippocampal neurons cultured on uniform laminin substrates (Supplementary information, Figure S1A and S1B).…”

Section: Itgb1 Activation Mediates Axon Formation On Laminin Substratesmentioning

confidence: 81%

“…Many cytoplasmic signaling molecules are involved in neuronal polarization and axon development [1,2,8], most of which have been identified in cultured hippocampal or cortical neurons, widely used model systems for the study of neuronal polarity [9][10][11]. Among them, several kinases, including SAD A/B and LKB1, are essential for neuronal polarization in vivo [8,[12][13][14]. In contrast, the identity of the extracellular factors that initiate neuronal polarity in vivo is just beginning to be elucidated [15,16].…”

Section: Introductionmentioning

confidence: 99%

“…It has been shown recently that microtubule stabilization induced by pharmacological treatments is sufficient to induce the axon formation [3,6], and markedly increases axon regeneration after injury [7]. Many cytoplasmic signaling molecules are involved in neuronal polarization and axon development [1,2,8], most of which have been identified in cultured hippocampal or cortical neurons, widely used model systems for the study of neuronal polarity [9][10][11]. Among them, several kinases, including SAD A/B and LKB1, are essential for neuronal polarization in vivo [8,[12][13][14].…”

Section: Introductionmentioning

confidence: 99%

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Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

et al. 2012

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Axon specification during neuronal polarization is closely associated with increased microtubule stabilization in one of the neurites of unpolarized neuron, but how this increased microtubule stability is achieved is unclear. Here, we show that extracellular matrix (ECM) component laminin promotes neuronal polarization via regulating directional microtubule assembly through β1 integrin (Itgb1). Contact with laminin coated on culture substrate or polystyrene beads was sufficient for axon specification of undifferentiated neurites in cultured hippocampal neurons and cortical slices. Active Itgb1 was found to be concentrated in laminin-contacting neurites. Axon formation was promoted and abolished by enhancing and attenuating Itgb1 signaling, respectively. Interestingly, laminin contact promoted plus-end microtubule assembly in a manner that required Itgb1. Moreover, stabilizing microtubules partially prevented polarization defects caused by Itgb1 downregulation. Finally, genetic ablation of Itgb1 in dorsal telencephalic progenitors caused deficits in axon development of cortical pyramidal neurons. Thus, laminin/Itgb1 signaling plays an instructive role in axon initiation and growth, both in vitro and in vivo, through the regulation of microtubule assembly. This study has established a linkage between an extrinsic factor and intrinsic cytoskeletal dynamics during neuronal polarization.

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Section: Itgb1 Activation Mediates Axon Formation On Laminin Substratesmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

et al. 2012

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“…neuronal morphogenesis occurs concurrently with migration [3][4][5]. Over the past several decades, studies have mostly focused on the molecular mechanisms underlying the later stages of neuronal morphogenesis, including those mediating polarization [6][7][8][9], dendrite morphogenesis [10][11][12][13][14][15][16], synaptogenesis [17][18][19][20], and spinogenesis [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Actin Aggregations Mark the Sites of Neurite Initiation

et al. 2016

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A salient feature of neurons is their intrinsic ability to grow and extend neurites, even in the absence of external cues. Compared to the later stages of neuronal development, such as neuronal polarization and dendrite morphogenesis, the early steps of neuritogenesis remain relatively unexplored. Here we showed that redistribution of cortical actin into large aggregates preceded neuritogenesis and determined the site of neurite initiation. Enhancing actin polymerization by jasplakinolide treatment effectively blocked actin redistribution and neurite initiation, while treatment with the actin depolymerizing agents latrunculin A or cytochalasin D accelerated neurite formation. Together, these results demonstrate a critical role of actin dynamics and reorganization in neurite initiation. Further experiments showed that microtubule dynamics and protein synthesis are not required for neurite initiation, but are required for later neurite stabilization. The redistribution of actin during early neuronal development was also observed in the cerebral cortex and hippocampus in vivo.

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“…However, it is well possible that the signal transduced by LAT-1 to mediate an effect on polarity is polarized further downstream through effectors of cAMP such as protein kinases A or A kinase anchoring proteins. 30,31 It is also conceivable that polarity information in achieved by temporally restricting cues activating LAT-1.…”

Section: Camp-mediated Lat-1 Signaling Is Essential For Anterior-postmentioning

confidence: 99%

The adhesion GPCR latrophilin – a novel signaling cascade in oriented cell division and anterior-posterior polarity

Winkler

Prömel

2016

Worm

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Although several signaling pathways in oriented cell division have been well characterized such as delta/notch inductions or wnt/frizzled-based anterior-posterior polarity, there is strong evidence for additional signal pathways controlling early anterior-posterior polarity decisions. The homolog of the adhesion G protein-coupled receptor latrophilin, LAT-1 has been identified as a receptor essential for oriented cell division in an anterior-posterior direction of specific blastomeres in the early C. elegans embryo. We recently conducted a study aiming at clarifying the signals involved in LAT-1 function. We identified a G s protein/adenylyl cyclase/cAMP pathway in vitro and demonstrated its physiological relevance in oriented cell division. By interaction with a G s protein LAT-1 elevates cAMP levels. These data indicate that G-protein signaling in oriented cell division is not solely GPCR-independent. This commentary will discuss our findings in the context of the current knowledge of mechanisms controlling oriented cell division and anterior-posterior polarity. Further, we identify open questions which need to be addressed in the future.

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New insights into the molecular mechanisms specifying neuronal polarity in vivo

Cited by 73 publications

References 76 publications

Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

Laminin/β1 integrin signal triggers axon formation by promoting microtubule assembly and stabilization

Actin Aggregations Mark the Sites of Neurite Initiation

The adhesion GPCR latrophilin – a novel signaling cascade in oriented cell division and anterior-posterior polarity

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