ArticlePloS one2014
Laf4/Aff3, a gene involved in intellectual disability, is required for cellular migration in the mouse cerebral cortex.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
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- Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.Communications biology · 2025Article
- Mdga2 deficiency leads to an aberrant activation of BDNF/TrkB signaling that underlies autism-relevant synaptic and behavioral changes in mice.PLoS biology · 2025Article
- Variant-specific pathophysiological mechanisms of AFF3 differently influence transcriptome profiles.Genome medicine · 2024Article
- Variant-specific pathophysiological mechanisms of AFF3 differently influence transcriptome profiles.medRxiv : the preprint server for health sciences · 2024Article
- Structural variation and eQTL analysis in two experimental populations of chickens divergently selected for feather-pecking behavior.Neurogenetics · 2023Article
- Transcription Pause and Escape in Neurodevelopmental Disorders.Frontiers in neuroscience · 2022Review
- Sca1Stem cell reviews and reports · 2021Article
- Variants in the degron of AFF3 are associated with intellectual disability, mesomelic dysplasia, horseshoe kidney, and epileptic encephalopathy.American journal of human genetics · 2021Article
- Language Impairment with a Partial Duplication ofMolecular syndromology · 2020Article
- Meta-analyses of genome wide association studies in lines of laying hens divergently selected for feather pecking using imputed sequence level genotypes.BMC genetics · 2020Article
- Genes with human-specific features are primarily involved with brain, immune and metabolic evolution.BMC bioinformatics · 2019Article
- De novo AFF3 variant in a patient with mesomelic dysplasia with foot malformation.Journal of human genetics · 2019Article
- Large-scale neuroanatomical study uncovers 198 gene associations in mouse brain morphogenesis.Nature communications · 2019Article
- Systematic characterization of germline variants from the DiscovEHR study endometrial carcinoma population.BMC medical genomics · 2019Article
- Genes regulated by SATB2 during neurodevelopment contribute to schizophrenia and educational attainment.PLoS genetics · 2018Article
- Article
- FoxO6 affects Plxna4-mediated neuronal migration during mouse cortical development.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- A sequence variant associating with educational attainment also affects childhood cognition.Scientific reports · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Members of the AFF (AF4/FMR2) family of putative transcription factors are involved in infant acute leukaemia and intellectual disability (ID), although very little is known about their transcriptional targets. For example, deletion of human lymphoid nuclear protein related to AF4/AFF member 3 (LAF4/AFF3) is known to cause severe neurodevelopmental defects, and silencing of the gene is also associated with ID at the folate-sensitive fragile site (FSFS) FRA2A; yet the normal function of this gene in the nervous system is unclear. The aim of this study was to further investigate the function of Laf4 in the brain by focusing on its role in the cortex. By manipulating expression levels in organotypic slices, we demonstrate here that Laf4 is required for normal cellular migration in the developing cortex and have subsequently identified Mdga2, an important structural protein in neurodevelopment, as a target of Laf4 transcriptional activity. Furthermore, we show that the migration deficit caused by loss of Laf4 can be partially rescued by Mdga2 over-expression, revealing an important functional relationship between these genes. Our study demonstrates the key transcriptional role of Laf4 during early brain development and reveals a novel function for the gene in the process of cortical cell migration relevant to the haploinsufficiency and silencing observed in human neurodevelopmental disorders.
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