Conditional NF-L Transgene Expression in Mice for<i>In Vivo</i>Analysis of Turnover and Transport Rate of Neurofilaments

Millecamps, Stéphanie; Gowing, Genevíève; Corti, Olga; Mallet, Jacques; Julien, Jean‐Pierre

doi:10.1523/jneurosci.5299-06.2007

Cited by 82 publications

(75 citation statements)

References 63 publications

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“…One possible explanation for a large spread in the estimates is that the half-life of tubulin may depend on a particular form of tubulin as well as on the stage of the axonal development. Nixon and Logvinenko [30] estimated the half-life of NF proteins to be approximately 20 days; however, data presented in Millecamps et al [21] suggest that the half-life of NFs in long peripheral axons with a dense NF network can exceed several months. In order to show the effect of the CE half-life, we present the results for four different values of T …”

Section: Resultsmentioning

confidence: 99%

“…This model was numerically investigated in [20]. In the present paper we extend the model developed in [19] to account for the halflife of CEs (the model suggested in Jung and Brown [19] assumes that the half-life of CEs is infinitely long while a recent work by Millecamps et al [21] suggests that there is degradation of proteins along the length of the axon). The effect of the half-life of CEs on slow axonal transport was first modeled in [22], based on the original model of slow axonal transport developed in Craciun et al [7].…”

Section: Introductionmentioning

confidence: 93%

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Effect of cytoskeletal element degradation on merging of concentration waves in slow axonal transport

2011

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Abstract:The aim of this paper is to investigate, by means of a numerical simulation, the effect of the half-life of cytoskeletal elements (CEs) on superposition of several waves representing concentrations of running, pausing, and off-track anterograde and retrograde CE populations. The waves can be induced by simultaneous microinjections of radiolabeled CEs in different locations in the vicinity of a neuron body; alternatively, the waves can be induced by microinjecting CEs at the same location several times, with a time interval between the injections. Since the waves spread out as they propagate downstream, unless their amplitude decreases too fast, they eventually superimpose. As a result of superposition and merging of several waves, for the case with a large half-life of CEs, a single wave is formed. For the case with a small half-life the waves vanish before they have enough time to merge.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Effect of cytoskeletal element degradation on merging of concentration waves in slow axonal transport

2011

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“…expressed their own neurofi lament light subunit (mNFL+) or did not (mNFL-) (Millecamps et al, 2007). In mice hNFL+/ mNFL-expressing only the human subunit, upon doxycycline treatment, the subunit disappeared at the same time along the entire sciatic nerve with a half-life of 3 weeks.…”

Section: Scrutiny Of Protein Stability In Axonsmentioning

confidence: 99%

“…The mouse that expresses only hNFL (vide supra) was used to this end. Experimentally, when the transgene was switched off with doxycycline, hNFL disappeared synchronously along the entire sciatic nerve, and when the gene was turned on, hNFL reappeared and accumulated within one week with no wavefront (Millecamps et al, 2007). Since predicted waves of proteins were not observed, STM does not pass the test and supplementary assumptions are necessary to rescue the model; alternatively, STM may choose to revise its tenets.…”

Section: Scrutiny Of the Slow Wavesmentioning

confidence: 99%

Slow axoplasmic transport under scrutiny

Court

Álvarez

2011

Biol. Res.

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We dedicate this paper to Antonio Giuditta and Edward Koenig who laid the basis to understand the origin of axoplasmic protein. ABSTRACTThe origin of axoplasmic proteins is central for the biology of axons. For over fi fty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stable, i.e., not degraded in axons. These are now textbook notions that confi gure the slow transport model (STM). The aim of this article is to cast doubts on the validity of STM, as a step toward gaining more understanding about the supply of axoplasmic proteins. First, the stability of axonal proteins claimed by STM has been disproved by experimental evidence. Moreover, the evidence for protein synthesis in axons indicates that the repertoire is extensive and the amount sizeable, which disproves the notion that axons are unable to synthesize proteins and that cell bodies supply most axonal proteins. In turn, axoplasmic protein synthesis gives rise to the metabolic model (MM). We point out a few inconsistencies in STM that MM redresses. Although both models address the supply of proteins to axons, so far they have had no crosstalk. Since proteins underlie every conceivable cellular function, it is necessary to re-evaluate indepth the origin of axonal proteins. We hope this will shape a novel understanding of the biology of axons, with impact on development and maintenance of axons, nerve repair, axonopathies and plasticity, to mention a few fi elds.

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“…Le transport des cargos pourrait s'effectuer en fonction d'une succession d'associations et de dissociations des protéines motrices. Nous avons ainsi récemment démontré que le taux de renouvellement et la cinétique du transport des NF sont inversement proportionnels à la densité du réseau de NF stationnaires dans l'axone [2]. Dans un autre modèle (« tir à la corde ») les cargos sont associés simultanément à plusieurs protéines motrices et la direction du transport dépend du moteur dominant à un moment donné.…”

Section: Mécanismes De Régulation Du Transport Axonalunclassified

Les dys-fonctionnements du transport axonal dans les neuropathies et motoneuronopathies

Millecamps

Julien

2008

Med Sci (Paris)

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Conditional NF-L Transgene Expression in Mice forIn VivoAnalysis of Turnover and Transport Rate of Neurofilaments

Cited by 82 publications

References 63 publications

Effect of cytoskeletal element degradation on merging of concentration waves in slow axonal transport

Effect of cytoskeletal element degradation on merging of concentration waves in slow axonal transport

Slow axoplasmic transport under scrutiny

Les dys-fonctionnements du transport axonal dans les neuropathies et motoneuronopathies

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