Centrosome Motility Is Essential for Initial Axon Formation in the Neocortex

Anda, Froylán Calderón de; Meletis, Konstantinos; Ge, Xuecai; Rei, Damien; Tsai, Li‐Huei

doi:10.1523/jneurosci.0381-10.2010

Cited by 123 publications

(143 citation statements)

References 46 publications

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“…17,18 Recently, it has been demonstrated that centrosomal proteins are essential for microtubule organization and centrosome motility that have important roles in axonal formation. 19 ZNF238 is a POZ/zinc finger transcriptional repressor gene. 20 Mice with targeted knock out of ZNF238 display severe hypoplasia of the cerebral cortex and the hippocampus, along with increased apoptosis of progenitors in the ventricular zone.…”

Section: Deletion Of 1q43-q44 Scs Nagamani Et Almentioning

confidence: 99%

Delineation of a deletion region critical for corpus callosal abnormalities in chromosome 1q43–q44

et al. 2011

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Submicroscopic deletions involving chromosome 1q43-q44 result in cognitive impairment, microcephaly, growth restriction, dysmorphic features, and variable involvement of other organ systems. A consistently observed feature in patients with this deletion are the corpus callosal abnormalities (CCAs), ranging from thinning and hypoplasia to complete agenesis. Previous studies attempting to delineate the critical region for CCAs have yielded inconsistent results. We conducted a detailed clinical and molecular characterization of seven patients with deletions of chromosome 1q43-q44. Using array comparative genomic hybridization, we mapped the size, extent, and genomic content of these deletions. Four patients had CCAs, and shared the smallest region of overlap that contains only three protein coding genes, CEP170, SDCCAG8, and ZNF238. One patient with a small deletion involving SDCCAG8 and AKT3, and another patient with an intragenic deletion of AKT3 did not have any CCA, implying that the loss of these two genes is unlikely to be the cause of CCA. CEP170 is expressed extensively in the brain, and encodes for a protein that is a component of the centrosomal complex. ZNF238 is involved in control of neuronal progenitor cells and survival of cortical neurons. Our results rule out the involvement of AKT3, and implicate CEP170 and/or ZNF238 as novel genes causative for CCA in patients with a terminal 1q deletion.

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Section: Deletion Of 1q43-q44 Scs Nagamani Et Almentioning

confidence: 99%

Delineation of a deletion region critical for corpus callosal abnormalities in chromosome 1q43–q44

et al. 2011

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“…However, conflicting evidence has come from studies of centrosome function in axon development. The centrosome and associated Golgi apparatus predict the site of axon formation in cultured mammalian cerebellar granule and hippocampal neurons (de Anda et al, 2005;Zmuda and Rivas, 1998) and in cortical slices (de Anda et al, 2010). Furthermore, disruption of centrosome function inhibits axon formation in cortical slices (de Anda et al, 2010) and in cultured Drosophila neurons (de Anda et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Centrosome movements in vivo correlate with specific neurite formation downstream of LIM homeodomain transcription factor activity

Andersen

Halloran

2012

Development

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SUMMARYNeurons must develop complex structure to form proper connections in the nervous system. The initiation of axons in defined locations on the cell body and their extension to synaptic targets are critical steps in neuronal morphogenesis, yet the mechanisms controlling axon formation in vivo are poorly understood. The centrosome has been implicated in multiple aspects of neuronal morphogenesis; however, its function in axon development is under debate. Conflicting results from studies of centrosome function in axonogenesis suggest that its role is context dependent and underscore the importance of studying centrosome function as neurons develop in their natural environment. Using live imaging of zebrafish Rohon-Beard (RB) sensory neurons in vivo, we discovered a spatiotemporal relationship between centrosome position and the formation of RB peripheral, but not central, axons. We tested centrosome function by laser ablation and found that centrosome disruption inhibited peripheral axon outgrowth. In addition, we show that centrosome position and motility are regulated by LIM homeodomain transcription factor activity, which is specifically required for the development of RB peripheral axons. Furthermore, we show a correlation between centrosome mislocalization and ectopic axon formation in bashful (laminin alpha 1) mutants. Thus, both intrinsic transcription factor activity and extracellular cues can influence centrosome position and axon formation in vivo. This study presents the first positive association between the centrosome and axon formation in vivo and suggests that the centrosome is important for differential neurite formation in neurons with complex axonal morphologies.

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“…Centrioles play important roles in controlling the polarity and migration of neuronal cells (de Anda et al 2005;de Anda et al 2010;Ge et al 2010;Lizarraga et al 2010;Kuijpers and Hoogenraad 2011). During evolution of the human brain, the neocortex, which is involved in higher cognitive function, has expanded greatly compared to other mammals (Borrell and Reillo 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Nuclear speckles and the nucleolus play basic roles in the metabolism of all cells (Boisvert et al 2007;Spector and Lamond 2011). Cell polarity and cell migration in human neuronal cells, in which centrioles play a key role (de Anda et al 2005;de Anda et al 2010;Ge et al 2010;Lizarraga et al 2010;Kuijpers and Hoogenraad 2011), have facilitated the unique expansion of the neocortex during evolution of the human brain (Taverna et al 2014;Florio et al 2015).…”

Section: Discussionmentioning

confidence: 99%

Dynamics of the association of heat shock protein HSPA6 (Hsp70B’) and HSPA1A (Hsp70–1) with stress-sensitive cytoplasmic and nuclear structures in differentiated human neuronal cells

Shorbagi

Brown

2016

Cell Stress and Chaperones

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Heat shock proteins (Hsps) are cellular repair agents that counter the effects of protein misfolding that is a characteristic feature of neurodegenerative diseases. HSPA1A (Hsp70-1) is a widely studied member of the HSPA (Hsp70) family. The little-studied HSPA6 (Hsp70B') is present in the human genome and absent in mouse and rat; hence, it is missing in current animal models of neurodegenerative diseases. Differentiated human neuronal SH-SY5Y cells were employed to compare the dynamics of the association of YFP-tagged HSPA6 and HSPA1A with stress-sensitive cytoplasmic and nuclear structures. Following thermal stress, liveimaging confocal microscopy and Fluorescence Recovery After Photobleaching (FRAP) demonstrated that HSPA6 displayed a prolonged and more dynamic association, compared to HSPA1A, with centrioles that play critical roles in neuronal polarity and migration. HSPA6 and HSPA1A also targeted nuclear speckles, rich in RNA splicing factors, and the granular component of the nucleolus that is involved in rRNA processing and ribosomal subunit assembly. HSPA6 and HSPA1A displayed similar FRAP kinetics in their interaction with nuclear speckles and the nucleolus. Subsequently, during the recovery from neuronal stress, HSPA6, but not HSPA1A, localized with the periphery of nuclear speckles (perispeckles) that have been characterized as transcription sites. The stress-induced association of HSPA6 with perispeckles displayed the greatest dynamism compared to the interaction of HSPA6 or HSPA1A with other stresssensitive cytoplasmic and nuclear structures. This suggests involvement of HSPA6 in transcriptional recovery of human neurons from cellular stress that is not apparent for HSPA1A.

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Centrosome Motility Is Essential for Initial Axon Formation in the Neocortex

Cited by 123 publications

References 46 publications

Delineation of a deletion region critical for corpus callosal abnormalities in chromosome 1q43–q44

Delineation of a deletion region critical for corpus callosal abnormalities in chromosome 1q43–q44

Centrosome movements in vivo correlate with specific neurite formation downstream of LIM homeodomain transcription factor activity

Dynamics of the association of heat shock protein HSPA6 (Hsp70B’) and HSPA1A (Hsp70–1) with stress-sensitive cytoplasmic and nuclear structures in differentiated human neuronal cells

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