The E3 ligase Cdh1-anaphase promoting complex operates upstream of the E3 ligase Smurf1 in the control of axon growth

Kannan, Madhuvanthi; Lee, Shih-Ju; Schwedhelm-Domeyer, Nicola; Stegmüller, Judith

doi:10.1242/jcs.122416

Cited by 7 publications

(12 citation statements)

References 1 publication

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“…In vivo electroporation was performed as described previously (Konishi et al, 2004;Stegmüller et al, 2006;Kannan et al, 2012a). In brief, plasmid DNA diluted in PBS (3-4 l/animal) was injected into the P4 Wistar rat cerebellar cortex together with 0.03% Fast Green using a Hamilton syringe with a 30 gauge needle.…”

Section: Methodsmentioning

confidence: 99%

“…Not surprisingly, various small GTPases that control cytoskeletal dynamics have also been implicated in neuronal migration (Govek et al, 2011;Kawauchi, 2011). Even though recent studies have characterized E3 ligases that regulate neuronal migration by acting upstream of the centrosomal proteins Par6␣ or Pard3a, the Reelin-regulated signaling component Dab1, or the small GTPase RhoA (Feng et al, 2007;Famulski et al, 2010;Kannan et al, 2012a;Kannan et al, 2012b;Vadhvani et al, 2013), E3 ligases remain poorly explored regulators of neuronal migration.…”

Section: Introductionmentioning

confidence: 99%

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Loss of the Neuron-Specific F-Box Protein FBXO41 Models an Ataxia-Like Phenotype in Mice with Neuronal Migration Defects and Degeneration in the Cerebellum

Mukherjee

Holubowska

Schwedhelm-Domeyer³

et al. 2015

Journal of Neuroscience

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The cerebellum is crucial for sensorimotor coordination. The cerebellar architecture not only requires proper development but also long-term integrity to ensure accurate functioning. Developmental defects such as impaired neuronal migration or neurodegeneration are thus detrimental to the cerebellum and can result in movement disorders including ataxias. In this study, we identify FBXO41 as a novel CNS-specific F-box protein that localizes to the centrosome and the cytoplasm of neurons and demonstrate that cytoplasmic FBXO41 promotes neuronal migration. Interestingly, deletion of the FBXO41 gene results in a severely ataxic gait in mice, which show delayed neuronal migration of granule neurons in the developing cerebellum in addition to deformities and degeneration of the mature cerebellum. We show that FBXO41 is a critical factor, not only for neuronal migration in the cerebellum, but also for its long-term integrity.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loss of the Neuron-Specific F-Box Protein FBXO41 Models an Ataxia-Like Phenotype in Mice with Neuronal Migration Defects and Degeneration in the Cerebellum

Mukherjee

Holubowska

Schwedhelm-Domeyer³

et al. 2015

Journal of Neuroscience

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“…Recent exciting evidence has uncovered unexpected neurobiological, myogenesis, or other functions for Cdh1 (26 -28). Another member of the Nedd4 family, Smad ubiquitination regulatory factor 1 (Smurf1), can be degraded by Cdh1 in its regulation of osteoblast function and axon growth in an APC/ C-independent or -dependent manner, respectively (29,30). NEDL2, whose mRNA was preferentially expressed in neuronal tissue, as previously reported (14), may function along with Cdh1 in regulation of neurobiological function or other physiological processes besides in cell cycle control.…”

Section: Discussionmentioning

confidence: 99%

The HECT Type Ubiquitin Ligase NEDL2 Is Degraded by Anaphase-promoting Complex/Cyclosome (APC/C)-Cdh1, and Its Tight Regulation Maintains the Metaphase to Anaphase Transition

Hu²,

Wei

et al. 2013

Journal of Biological Chemistry

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Background: NEDL2 is a member of the HECT type ubiquitin ligase NEDD4 family, but its function remains largely unknown. Results: NEDL2 is degraded by APC/C-Cdh1 during mitotic exit and regulates metaphase to anaphase transition. Conclusion: NEDL2 appears to dynamically modulate regulation of mitosis. Significance: Our data provide a novel substrate of APC/C-Cdh1 and reveal an additional protein by which HECT type ubiquitin ligase can regulate mitosis.

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“…in axonal growth and axon formation has been previously shown [107], but Cdk5 appears to have little or no benefit in axon regeneration [108]. Phosphorylation of pathway [109]. In vivo knockdown of Smurf1 in the developing cerebellum bolstered its role in axon growth regulation and revealed additional defects in neuronal migration [109].…”

Section: Smads and Low Levels Of Snon In Neurons Arementioning

confidence: 97%

“…Phosphorylation of pathway [109]. In vivo knockdown of Smurf1 in the developing cerebellum bolstered its role in axon growth regulation and revealed additional defects in neuronal migration [109].…”

Section: Smads and Low Levels Of Snon In Neurons Arementioning

confidence: 99%

The brake within: Mechanisms of intrinsic regulation of axon growth featuring the Cdh1-APC pathway

Stegmüller¹

2013

Translational Neuroscience

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Neurons of the central nervous system (CNS) form a magnificent network destined to control bodily functions and human behavior for a lifetime. During development of the CNS, neurons extend axons that establish connections to other neurons. Axon growth is guided by extrinsic cues and guidance molecules. In addition to environmental signals, intrinsic programs including transcription and the ubiquitin proteasome system (UPS) have been implicated in axon growth regulation. Over the past few years it has become evident that the E3 ubiquitin ligase Cdh1-APC together with its associated pathway plays a central role in axon growth suppression. By elucidating the intricate interplay of extrinsic and intrinsic mechanisms, we can enhance our understanding of why axonal regeneration in the CNS fails and obtain further insight into how to stimulate successful regeneration after injury.

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The E3 ligase Cdh1-anaphase promoting complex operates upstream of the E3 ligase Smurf1 in the control of axon growth

Cited by 7 publications

References 1 publication

Loss of the Neuron-Specific F-Box Protein FBXO41 Models an Ataxia-Like Phenotype in Mice with Neuronal Migration Defects and Degeneration in the Cerebellum

Loss of the Neuron-Specific F-Box Protein FBXO41 Models an Ataxia-Like Phenotype in Mice with Neuronal Migration Defects and Degeneration in the Cerebellum

The HECT Type Ubiquitin Ligase NEDL2 Is Degraded by Anaphase-promoting Complex/Cyclosome (APC/C)-Cdh1, and Its Tight Regulation Maintains the Metaphase to Anaphase Transition

The brake within: Mechanisms of intrinsic regulation of axon growth featuring the Cdh1-APC pathway

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