Foxp-Mediated Suppression of N-Cadherin Regulates Neuroepithelial Character and Progenitor Maintenance in the CNS

Rousso, D.; Pearson, Caroline Alayne; Gaber, Zachary B.; Miquelajáuregui, Amaya; Li, Shanru; Portera‐Cailliau, Carlos; Morrisey, Edward E.; Novitch, Bennett G.

doi:10.1016/j.neuron.2012.02.024

Cited by 160 publications

(209 citation statements)

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“…Several papers have described early developmental roles for Foxp2 in the embryonic forebrain [48,49] and spinal cord [50 ]. Given that expression persists into adulthood [19 ], it seems likely that the protein also has regulatory functions in postnatal animals, perhaps throughout adult life.…”

Section: Contributions Of Foxp2 To Motor-skill Learning and Performancementioning

confidence: 99%

What can mice tell us about Foxp2 function?

French

Fisher

2014

Current Opinion in Neurobiology

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Disruptions of the FOXP2 gene cause a rare speech and language disorder, a discovery that has opened up novel avenues for investigating the relevant neural pathways. FOXP2 shows remarkably high conservation of sequence and neural expression in diverse vertebrates, suggesting that studies in other species are useful in elucidating its functions. Here we describe how investigations of mice that carry disruptions of Foxp2 provide insights at multiple levels: molecules, cells, circuits and behaviour. Work thus far has implicated the gene in key processes including neurite outgrowth, synaptic plasticity, sensorimotor integration and motor-skill learning.

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Section: Contributions Of Foxp2 To Motor-skill Learning and Performancementioning

confidence: 99%

What can mice tell us about Foxp2 function?

French

Fisher

2014

Current Opinion in Neurobiology

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“…FOXP2 directly represses CDH2, leading to detachment of differentiating neurons from epithelial sheet [77]; we presume miR-3666 may suppress CDH2 indirectly via suppression of Protein Tyrosine Phosphatase, Receptor Type, J (PTPRJ). According to IntAct database, PTPRJ dephosphorylates CDH2.…”

Section: Mir-3666 Directly or Indirectly Regulates Foxp2 Functions Inmentioning

confidence: 92%

Intronic miRNA miR-3666 Modulates its Host Gene FOXP2 Functions in Neurodevelopment and May Contribute to Pathogenesis of Neurological Disorders Schizophrenia and Autism

Islam¹

2017

JABB

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MicroRNAs (miRNAs) are approximately 22-nucleotide-long, non-coding RNAs that bind to complementary mRNAs with inhibitory effect. An intronic miRNA is embedded in a particular gene called its host gene. Our study focuses on the Homo sapiens intronic miRNA-host gene pair, hsa-miR-3666 and FOXP2. Previous report of coexpression of miR-3666 and FOXP2 indicates possible regulation of FOXP2 functions by miR-3666. However, direct correlation has not been shown yet. Therefore, we took a computational approach to determine if and how such modulation occurs. ChIP-seq identified FOXP2 targets and putative miR-3666 targets showed a significant overlap of 574 common target genes. Functional enrichment analysis of common targets revealed over-representation of KEGG pathways and Gene Ontology modules associated with neurodevelopment. These modules, along with further literature mining and proteinprotein interaction analysis of FOXP2 and miR-3666 identified several specific genes associated with neurodevelopment and finally integration of transcriptomic expressions data lead to the selection of four models depicting the mechanisms by which miR-3666 can modulate FOXP2 functions. Model 1 illustrates that during neurodevelopment, miR-3666 can directly modulate the functions of FOXP2 through regulation of common targets, such as IGF1 and EFNB2, whereas model 2 shows miR-3666 can also indirectly modulate FOXP2 functions by considering targets that are not common for the intronic miRNA-host gene pair, for example CDH2 and LMO4. This direct and indirect regulation is necessary for precise spatial and temporal expression of genes during neurodevelopment. Models 3 and 4 exhibit mechanisms in which the interactions of miR-3666 and FOXP2 with target genes contribute to the pathogenesis of schizophrenia and autism respectively. a role in transcriptional activation [7]. FOXP2 hosts the intronic miRNA, miR-3666. Though not much work has been done on miR-3666, its targets have been predicted and deposited in various databases. A few recent experiments have shown the repression activity of miR-3666 on targets such as MET and ZEB1 in thyroid carcinoma and cervical carcinoma cells, respectively [9,10].

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“…FoxP subfamily member genes play essential roles in the construction and maintenance of many functional modules involved with the developmental processes and physiological activities, such as pulmonary and cardiac organogenesis, plasticity of the central nervous system and the regulation of immune systems (Fontenot et al, 2003;Hori et al, 2003;Khattri et al, 2003;Wang et al, 2004;Hu et al, 2006;Haesler et al, 2007;Shu et al, 2007;Dasen et al, 2008;Groszer et al, 2008;Rousso et al, 2008;Kurt et al, 2012;Rousso et al, 2012). In addition to involvement in key functions, these genes exhibit unique molecular structures that have been the subject of much research.…”

Section: Introductionmentioning

confidence: 99%