Activated retinoid receptors are required for the migration and fate maintenance of subsets of cortical neurons

Choi, June-Seok; Park, Sung Jin; Sockanathan, Shanthini

doi:10.1242/dev.104505

Cited by 20 publications

(19 citation statements)

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“…Interestingly, we identified the mid-fetal frontal and temporal lobe, which are adjacent to each moiety, as having the most differentially expressed genes during mid-fetal neocortical development. Noteworthy, RA signaling is involved in the development of both entitites 36, 37 . In mice, the meninges covering the hippocampus, which resides next to the temporal neocortex, express the other two RA synthesizing genes ( Aldh1a1 / Raldh1 and Aldh1a2 / Raldh2 ) and RA signaling plays a critical role in hippocampal neurogenesis and function 33 .…”

Section: Resultsmentioning

confidence: 99%

“…In mice, the meninges covering the hippocampus, which resides next to the temporal neocortex, express the other two RA synthesizing genes ( Aldh1a1 / Raldh1 and Aldh1a2 / Raldh2 ) and RA signaling plays a critical role in hippocampal neurogenesis and function 33 . RA signaling is also required for the development of the olfactory system and its long-range connections with the ventrolateral forebrain 37 . Interestingly, we also identified an enrichment of RA in the ITC of humans, but not macaques.…”

Section: Resultsmentioning

confidence: 99%

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Regulation of Prefrontal Patterning, Connectivity and Synaptogenesis by Retinoic Acid

Shibata

Pattabiraman

Lorente-Galdós

et al. 2019

Preprint

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33The prefrontal cortex (PFC) and its reciprocal connections with the mediodorsal 34 thalamus (MD) are crucial for cognitive flexibility and working memory 1-4 and are 35 thought to be altered in several disorders such as autism spectrum disorder 5, 6 36 and schizophrenia 6-9 . While developmental mechanisms governing regional 37 patterning of the rodent cerebral cortex have been characterized 10-15 , the 38 mechanisms underlying the development of PFC-MD connectivity and the lateral 39 expansion of PFC with distinct granular layer 4 in anthropoid primates 16-23 have 40 not been elucidated. Here we report increased concentration of retinoic acid (RA), 41 a signaling molecule involved in brain development and function 24,25 in the 42 prospective PFC areas of human and macaque, compared to mouse, during mid-43 fetal development, a crucial period for cortical circuit assembly. In addition, we 44 observed the lateral expansion of RA synthesizing enzyme, ALDH1A3, 45 expression in mid-fetal macaque and human frontal cortex, compared to mouse. 46 Furthermore, we found that enrichment of RA signaling is restricted to the 47 prospective PFC by CYP26B1, a gene encoding an RA-catabolizing enzyme 48 upregulated in the mid-fetal motor cortex. Gene deletion in mice revealed that RA 49 signaling through anteriorly upregulated RA receptors, Rxrg and Rarb, and 50 Cyp26b1-dependent catabolism is required for the proper molecular patterning 51 of PFC and motor areas, the expression of the layer 4 marker RORB, intra-PFC 52 synaptogenesis, and the development of reciprocal PFC-MD connectivity. 53

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Regulation of Prefrontal Patterning, Connectivity and Synaptogenesis by Retinoic Acid

Shibata

Pattabiraman

Lorente-Galdós

et al. 2019

Preprint

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“…In the absence of retinoic acid (RA), migration of prospective layer V-III neurons that express the RAR403 receptor is retarded. These neurons fail to maintain their fate and instead acquire characteristics of layer II neurons (Choi et al, 2014). This RA effect on the maintenance of neuronal identity and localization relies on the stabilisation of the beta-catenin function and the stimulation of the Wnt signalling, which is necessary for migration process (Ivaniutsin et al., 2009; Morgan-Smith et al, 2014).…”

Section: Neuronal Migrationmentioning

confidence: 99%

Cellular and molecular introduction to brain development

Jiang

Nardelli

2016

Neurobiology of Disease

135

118

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Advances in the study of brain development over the last decades, especially recent findings regarding the evolutionary expansion of the human neocortex, and large-scale analyses of the proteome/transcriptome in the human brain, have offered novel insights into the molecular mechanisms guiding neural maturation, and the pathophysiology of multiple forms of neurological disorders. As a preamble to reviews of this issue, we provide an overview of the cellular, molecular and genetic bases of brain development with an emphasis on the major mechanisms associated with landmarks of normal neural development in the embryonic stage and early postnatal life, including neural stem/progenitor cell proliferation, cortical neuronal migration, evolution and folding of the cerebral cortex, synaptogenesis and neural circuit development, gliogenesis and myelination. We will only briefly depict developmental disorders that result from perturbations of these cellular or molecular mechanisms, and the most common perinatal brain injuries that could disturb normal brain development.

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“…Ephrin‐B1, for example, inhibits neurite extension and promotes their radial migration (Dimidschstein et al, ) and is a target of canonical Wnt signaling (Boitard et al, ). The migration of neurons from specific layers could also be dependent on signaling from other factors, such as retinoic acid (Choi et al, ).…”

mentioning

confidence: 99%

“…The migration of neurons from specific layers could also be dependent on signaling from other factors, such as retinoic acid (Choi et al, 2014).…”

mentioning

confidence: 99%

Rab, Arf, and Arl-Regulated Membrane Traffic in Cortical Neuron Migration

Tang

2015

J. Cell. Physiol

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The migration of projection neurons from its birthplace in the subventricular zone to their final destination in the cortical plate is a complex process that requires a series of highly coordinated cellular events. Amongst the key factors involved in the processes are modulators of cytoskeletal dynamics, as well as cellular membrane traffic. Members of the small GTPases family responsible for the latter process, the Rabs and Arfs, have been recently implicated in cortical neuron migration. Rab5 and Rab11, which are key modulators of endocytosis and endocytic recycling respectively, ensure proper surface expression and distribution of N-cadherin, a key adhesion protein that tethers migrating neurons to the radial glia fiber tracts during pia-directed migration. Rab7, which is associated with lysosomal biogenesis and function, is important for the final step of terminal translocation when N-cadherin is downregulated by lysosomal degradation. Arf6 activity, which is known to be important in neuronal processes outgrowth, may negatively impact the multipolar-bipolar transition of cortical neurons undergoing radial migration, but the downstream effector of Arf6 in this regard is not yet known. In addition to the above, members of the Arl family which have been recently shown to be important in radial glia scaffold formation, would also be important for cortical neuron migration. In this short review, we discuss recent advances in our understanding of the importance of membrane traffic regulated by the Rab, Arf, and Arl family members in cortical neuron migration.

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Activated retinoid receptors are required for the migration and fate maintenance of subsets of cortical neurons

Cited by 20 publications

References 59 publications

Regulation of Prefrontal Patterning, Connectivity and Synaptogenesis by Retinoic Acid

Regulation of Prefrontal Patterning, Connectivity and Synaptogenesis by Retinoic Acid

Cellular and molecular introduction to brain development

Rab, Arf, and Arl-Regulated Membrane Traffic in Cortical Neuron Migration

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