Memo1-Mediated Tiling of Radial Glial Cells Facilitates Cerebral Cortical Development

Nakagawa, Naoki; Plestant, Charlotte; Yabuno-Nakagawa, Keiko; Li, Jingjun; Lee, Janice; Huang, Chu-Wei; Lee, Amelia; Krupa, Oleh; Adhikari, Aditi; Thompson, Suriya; Rhynes, Tamille; Arevalo, Victoria; Stein, Jason L.; Molnár, Zoltán; Badache, Ali; Anton, E. S.

doi:10.1016/j.neuron.2019.05.049

Cited by 55 publications

(59 citation statements)

References 83 publications

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“…However, importantly, our observations are in line with studies of RhoA signaling which also modulates RGC morphology and non-cellautonomously impairs neuronal migration (Cappello et al, 2012). Likewise, knockdown of Memo1, another factor linked to RhoA signaling (Zaoui et al, 2008), causes uneven distribution (tiling) of RGC basal processes, hyperbranching, and migration defects (Nakagawa et al, 2019). Altogether this indicates that both simplified and excessive RGC branching may impair neuronal migration and disrupt lamination.…”

Section: Link Between Localized Arhgap11a Expression Basal Process Msupporting

confidence: 86%

“…Further, excitatory neurons rely on the integrity of RGC basal processes to migrate from the germinal zones to the cortical plate (Belvindrah et al, 2007;Elias et al, 2007;Nakagawa et al, 2019;Noctor et al, 2004). Given that ARHGAP11A has established functions in modulating RhoA signaling and cytoskeletal morphology (Müller et al, 2018;Xu et al, 2013;Zanin et al, 2013), we hypothesized that Arhgap11a may regulate basal process morphology and thus influence excitatory neuron migration.…”

Section: Arhgap11a Controls Rgc Basal Process Morphology and Non-cellmentioning

confidence: 95%

“…The integrity of the RGC basal process is paramount for proper radial migration of excitatory neurons from the ventricular zone to the cortical plate (Belvindrah et al, 2007;Elias et al, 2007). Indeed, ectopic basal process branching can alter patterns of migrating neurons, including speed, directionality, and pausing (Nakagawa et al, 2019). Therefore, we assessed whether aberrant RGC morphology induced by Arhgap11a loss could also impact neuron migration in a non-cell-autonomous manner.…”

Section: Arhgap11a Controls Rgc Basal Process Morphology and Non-cellmentioning

confidence: 99%

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Subcellular mRNA localization and local translation ofArhgap11ain radial glial cells regulates cortical development

Pilaz

Joshi

Liu

et al. 2020

Preprint

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mRNA localization and local translation enable exquisite spatial and temporal control of gene expression, particularly in highly polarized and elongated cells. These features are especially prominent in radial glial cells (RGCs), which serve as neural and glial precursors of the developing cerebral cortex, and scaffolds for migrating neurons. Yet the mechanisms by which distinct sub-cellular compartments of RGCs accomplish their diverse functions are poorly understood. Here, we demonstrate that subcellular RNA localization and translation of the RhoGAP Arhgap11a controls RGC morphology and mediates cortical cytoarchitecture. Arhgap11a mRNA and protein exhibit conserved localization to RGC basal structures in mice and humans, conferred by a 5′UTR cis-element. Proper RGC morphology relies upon active Arhgap11a mRNA transport and localization to basal structures, where ARHGAP11A is locally synthesized. Thus, RhoA activity is spatially and acutely activated via local translation in RGCs to promote neuron positioning and cortical cytoarchitecture. Altogether, our study demonstrates that mRNA localization and local translation mediate compartmentalization of neural progenitor functions to control brain development.

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Section: Link Between Localized Arhgap11a Expression Basal Process Msupporting

confidence: 86%

Section: Arhgap11a Controls Rgc Basal Process Morphology and Non-cellmentioning

confidence: 95%

Section: Arhgap11a Controls Rgc Basal Process Morphology and Non-cellmentioning

confidence: 99%

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Subcellular mRNA localization and local translation ofArhgap11ain radial glial cells regulates cortical development

Pilaz

Joshi

Liu

et al. 2020

Preprint

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“…Genetic risk factors lead to autism by modifying early brain development and functioning,58 including synaptic signaling 5859. It is thought that advanced paternal age increases the risk of autism (pooled adjusted odds ratio 1.55, 95% confidence interval 1.39 to 1.73) by increasing rates of de novo mutations and epigenetic alterations 60.…”

Section: Risk Factorsmentioning

confidence: 99%

Linking risk factors and outcomes in autism spectrum disorder: is there evidence for resilience?

Elsabbagh

2020

BMJ

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Autism spectrum disorder (referred to here as autism) is one of several overlapping neurodevelopmental conditions that have variable impacts on different individuals. This variability results from dynamic interactions between biological and non-biological risk factors, which result in increasing differentiation between individuals over time. Although this differentiation continues well into adulthood, the infancy period is when the brain and behavior develop rapidly, and when the first signs and symptoms of autism emerge. This review discusses advances in our understanding of the causal pathways leading to autism and overlapping neurodevelopmental conditions. Research is also mapping trajectories of brain and behavioral development for some risk groups, namely later born siblings of children with autism and/or infants referred because of developmental concerns. This knowledge has been useful in improving early identification and establishing the feasibility of targeted interventions for infant risk groups before symptoms arise. However, key knowledge gaps remain, such as the discovery of protective factors (biological or environmental) that may mitigate the impact of risk. Also, the dynamic mechanisms that underlie the associations between risk factors and outcomes need further research. These include the processes of resilience, which may explain why some individuals at risk for autism achieve better than expected outcomes. Bridging these knowledge gaps would help to provide tools for early identification and intervention that reflect dynamic developmental pathways from risk to outcomes.

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“…Hence, the migrating neurons are dependent on a proper RGC fiber grid to be able to migrate properly. Indeed, disruption of the proper organization of the RGC fiber grid leads to non-cell-autonomous migration phenotypes because the main substrate of migrating neurons is perturbed (Belvindrah et al, 2007;Cappello et al, 2012;Nakagawa et al, 2019). Such findings initially emerged in a study investigating beta1 integrins in neuronal development.…”

Section: Heterogeneous Cell-cell Interactions Of Migrating Cortical Pmentioning

confidence: 99%

Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex

Hansen

Hippenmeyer

2020

Front. Cell Dev. Biol.

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Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final target lamina, is a key step in the assembly of the cerebral cortex. The cellular and molecular mechanisms regulating the specific sequential steps of radial neuronal migration in vivo are however still unclear, let alone the effects and interactions with the extracellular environment. In any in vivo context, cells will always be exposed to a complex extracellular environment consisting of (1) secreted factors acting as potential signaling cues, (2) the extracellular matrix, and (3) other cells providing cell-cell interaction through receptors and/or direct physical stimuli. Most studies so far have described and focused mainly on intrinsic cell-autonomous gene functions in neuronal migration but there is accumulating evidence that noncell-autonomous-, local-, systemic-, and/or whole tissue-wide effects substantially contribute to the regulation of radial neuronal migration. These non-cell-autonomous effects may differentially affect cortical neuron migration in distinct cellular environments. However, the cellular and molecular natures of such non-cell-autonomous mechanisms are mostly unknown. Furthermore, physical forces due to collective migration and/or community effects (i.e., interactions with surrounding cells) may play important roles in neocortical projection neuron migration. In this concise review, we first outline distinct models of non-cell-autonomous interactions of cortical projection neurons along their radial migration trajectory during development. We then summarize experimental assays and platforms that can be utilized to visualize and potentially probe non-cell-autonomous mechanisms. Lastly, we define key questions to address in the future.

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Memo1-Mediated Tiling of Radial Glial Cells Facilitates Cerebral Cortical Development

Cited by 55 publications

References 83 publications

Subcellular mRNA localization and local translation ofArhgap11ain radial glial cells regulates cortical development

Subcellular mRNA localization and local translation ofArhgap11ain radial glial cells regulates cortical development

Linking risk factors and outcomes in autism spectrum disorder: is there evidence for resilience?

Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex

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