SCLIP Is Crucial for the Formation and Development of the Purkinje Cell Dendritic Arbor

Poulain, Fabienne E.; Chauvin, Stéphanie; Wehrlé, Rosine; Desclaux, Mathieu; Mallet, Jacques; Vodjdani, Guilan; Dusart, Isabelle; Sobel, André

doi:10.1523/jneurosci.1942-08.2008

Cited by 37 publications

(36 citation statements)

References 42 publications

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“…Although the roles of neuronal TLR3 and stathmins are not fully understood and are probably complex, striking similarities are starting to emerge. Both can inhibit the growth of neuronal precursors, axons, and dendrites, and both can promote dendrite branching (14,15,32). Therefore, direct stathmin-TLR3 interactions on or inside neurons, as revealed by our present data (Fig.…”

Section: Figuresupporting

confidence: 64%

“…SCG10, SCLIP, and RB3 do not differ from stathmin in their a helical properties, but they do differ in having an extended N-terminal sequence. Acylation of this sequence targets these stathmins to Golgi vesicles and to additional vesicular neuronal structures that are found along neurite shafts and in growth cones (31,32). These vesicular structures in neurons are very similar to those reported to contain TLR3 (14).…”

Section: Figuresupporting

confidence: 52%

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The Microtubule Regulator Stathmin Is an Endogenous Protein Agonist for TLR3

Bsibsi

Bajramović

Vogt

et al. 2010

The Journal of Immunology

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TLR3 recognizes dsRNAs and is considered of key importance to antiviral host-defense responses. TLR3 also triggers neuroprotective responses in astrocytes and controls the growth of axons and neuronal progenitor cells, suggesting additional roles for TLR3-mediated signaling in the CNS. This prompted us to search for alternative, CNS-borne protein agonists for TLR3. A genome-scale functional screening of a transcript library from brain tumors revealed that the microtubule regulator stathmin is an activator of TLR3-dependent signaling in astrocytes, inducing the same set of neuroprotective factors as the known TLR3 agonist polyinosinic:polycytidylic acid. This activity of stathmin crucially depends on a long, negatively charged α helix in the protein. Colocalization of stathmin with TLR3 on astrocytes, microglia, and neurons in multiple sclerosis-affected human brain indicates that as an endogenous TLR3 agonist, stathmin may fulfill previously unsuspected regulatory roles during inflammation and repair in the adult CNS.

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Section: Figuresupporting

confidence: 64%

Section: Figuresupporting

confidence: 52%

The Microtubule Regulator Stathmin Is an Endogenous Protein Agonist for TLR3

Bsibsi

Bajramović

Vogt

et al. 2010

The Journal of Immunology

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“…In other neuronal types, inhibition of SCG10 increases growth cone size and reduces axonal length (66,68). In contrast, Sclip specifically regulates axonal branching (66) and is also required for dendritic initiation and development in cerebellar Purkinje cells (37). We could not precisely determine the phosphorylation state of SCG10 or Sclip in our neuronal model.…”

Section: Kidins220/arms Associates With and Modulates The Activity Ofmentioning

confidence: 90%

Kidins220/ARMS Modulates the Activity of Microtubule-regulating Proteins and Controls Neuronal Polarity and Development

Higuero

Sánchez‐Ruiloba

Doglio

et al. 2010

Journal of Biological Chemistry

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In order for neurons to perform their function, they must establish a highly polarized morphology characterized, in most of the cases, by a single axon and multiple dendrites. Herein we find that the evolutionarily conserved protein Kidins220 (kinase D-interacting substrate of 220-kDa), also known as ARMS (ankyrin repeat-rich membrane spanning), a downstream effector of protein kinase D and neurotrophin and ephrin receptors, regulates the establishment of neuronal polarity and development of dendrites. Kidins220/ARMS gain and loss of function experiments render severe phenotypic changes in the processes extended by hippocampal neurons in culture. Although Kidins220/ARMS early overexpression hinders neuronal development, its down-regulation by RNA interference results in the appearance of multiple longer axon-like extensions as well as aberrant dendritic arbors. We also find that Kidins220/ARMS interacts with tubulin and microtubule-regulating molecules whose role in neuronal morphogenesis is well established (microtubule-associated proteins 1b, 1a, and 2 and two members of the stathmin family). Importantly, neurons where Kidins220/ARMS has been knocked down register changes in the phosphorylation activity of MAP1b and stathmins. Altogether, our results indicate that Kidins220/ARMS is a key modulator of the activity of microtubuleregulating proteins known to actively regulate neuronal morphogenesis and suggest a mechanism by which it contributes to control neuronal development.Neuronal differentiation comprises several steps, among which the acquirement of a polarized axon-dendrite phenotype, with the corresponding asymmetrical distribution of proteins, is crucial. The morphological changes, followed by a neuron in order to polarize and form a single axon and multiple dendrites, are triggered by signaling cascades evoked by both intracellular and extracellular cues (1-4).Embryonic hippocampal neurons in culture constitute a model to study the mechanisms governing the establishment of polarity (2, 5, 6). These neurons undergo clear morphological changes during in vitro polarization. First, neurons attach to the plate and form lamellipodia and filopodia (stage 1). After several hours, they extend several minor immature neurites of apparent equivalent nature (stage 2) until one of these minor processes extends rapidly and becomes the axon (stage 3). The remaining neurites develop into dendrites (stage 4), after which neurons become morphologically and functionally mature (stage 5) (5, 6).During the early events of the establishment of polarity in this model, differences in local actin polymerization among the immature neurites play a crucial role in axonal determination (5, 7). In a similar manner, microtubule dynamics influence neuronal polarization, because local microtubule stabilization in one neurite specifies an axonal fate (8). Other known regulators of neuronal polarity and axon specification include proteins involved in polarized trafficking (4, 9, 10). However, how these different molecules are linked to t...

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“…Embryonic Lethal, Abnormal Vision, Drosophila-Like 4 (Elavl4), also known as Hu-Antigen D (HuD) is a RNA-binding protein involved in neuronal maturation [18], neurite outgrowth and dendritic maintenance [19]. Stathmin 3 (Stmn3) or SCG10-Like Protein (SCLIP) is also related to dendritic formation [20] and neurite outgrowth [21]. Zinc finger, CCHC domain containing 12 (Zcchc12) or SmadInteracting Zinc Finger Protein 1 (Szn1) is a protein used in BMP [22], AP-1 and CREB signalling [23] as a co-activator.…”

Section: Resultsmentioning

confidence: 99%