| 2002 |
OLIG1 and OLIG2 are required for both motoneuron and oligodendrocyte specification in the spinal cord pMN domain; Olig1/2 double-mutant mice lose motoneurons and fail to generate oligodendrocytes, with pMN progenitors instead generating V2 interneurons and astrocytes, establishing that Olig genes couple neuronal and glial subtype specification. |
Genetic loss-of-function (Olig1/2 double-knockout mice), lineage tracing |
Cell |
High |
11955447
|
| 2005 |
Olig1 is required for oligodendrocyte myelinogenesis specifically in the brain (not spinal cord); Olig1-null mice show abolished expression of myelin-specific genes (Mbp, Plp1, Mag), failure of multilamellar myelin wrapping around axons despite axonal contact, and Olig1 suppresses astrocyte-specific Gfap expression. Oligodendrocyte progenitor formation is unaffected. |
Olig1-null mouse genetic knockout, gene expression analysis, electron microscopy |
The Journal of neuroscience |
High |
15703389
|
| 2007 |
OLIG1 physically associates with the transcription factor SOX10, and the OLIG1/SOX10 complex activates myelin basic protein (mbp) transcription through conserved DNA sequence motifs in the mbp promoter. In contrast, OLIG2 does not bind SOX10 in zebrafish, though both OLIG1 and OLIG2 bind SOX10 in mouse. |
Co-immunoprecipitation (physical interaction), promoter-reporter assays (transcriptional activation), zebrafish and mouse models |
The Journal of neuroscience |
High |
18160645
|
| 2007 |
BMP2 and BMP4 inhibit oligodendrocyte differentiation of adult OPCs by downregulating olig1 and olig2 expression; overexpression of olig1 alone blocked BMP-induced astrocyte differentiation, but overexpression of both olig1 and olig2 together was required to rescue oligodendrocyte differentiation from BMP inhibition. |
Adult OPC culture, BMP treatment, overexpression of olig1/olig2 via transfection, immunostaining |
Stem cells |
Medium |
17872503
|
| 2010 |
Olig1 and Olig2 triplication in the Ts65Dn Down syndrome mouse model causes overproduction of GABAergic interneurons and imbalance of excitatory/inhibitory tone; normalization of Olig1/Olig2 gene dosage (from 3 copies to 2) rescues the inhibitory neuron phenotype. |
Genetic dosage normalization in Ts65Dn mice, cell counting, electrophysiology |
Nature neuroscience |
High |
20639873
|
| 2012 |
Olig1 is phosphorylated at serine 138 in the helix-loop-helix domain; this phosphorylated form resides in the cytosol. A serine-to-alanine mutation (S138A) restricts Olig1 to the nucleus and permits MBP expression but limits membrane expansion, while a serine-to-aspartate (phosphomimetic S138D) mutation causes cytoplasmic localization and enhances membrane expansion and oligodendrocyte maturation. |
Site-directed mutagenesis, nuclear-specific Olig1 expression in Olig1-null OPCs, phosphorylation site identification, cell morphology quantification |
Glia |
High |
22639060
|
| 2013 |
OLIG1 functions as a Smad cofactor in TGF-β signaling: OLIG1 physically interacts with Smad2/3 (via the L3 loop of Smad3), and this interaction is regulated by the prolyl isomerase Pin1. Knockdown of OLIG1 attenuates TGF-β-induced cell motility (migration and wound healing) but has no effect on BMP-induced motility, TGF-β-induced cytostasis, or epithelial-mesenchymal transition. |
Co-immunoprecipitation (Smad2/3–Olig1 interaction), siRNA knockdown, chamber migration and wound healing assays, Pin1 knockdown, synthetic peptide inhibition |
The Journal of biological chemistry |
High |
23720758
|
| 2014 |
Olig1 directly represses the Dlx1/2 I12b intergenic enhancer, and Dlx1/2 function genetically downstream of Olig1. Olig1 deletion in mice causes ectopic Dlx1/2 upregulation in the ventral medial ganglionic eminences and a ~30% increase in adult cortical GABAergic interneuron numbers. |
Olig1 conditional knockout mice, chromatin immunoprecipitation (Olig1 binding to Dlx1/2 I12b enhancer), genetic epistasis (Dlx1/2 downstream of Olig1), cell counting |
Neuron |
High |
24507192
|
| 2014 |
TIP30 sequesters Olig1 in the cytoplasm by direct protein–protein interaction, preventing its nuclear translocation and thereby inhibiting OPC differentiation; TIP30 overexpression inhibits OPC stage progression while TIP30 knockdown enhances oligodendroglial differentiation and increases nuclear Olig1. |
Co-immunoprecipitation (TIP30–Olig1 interaction), TIP30 overexpression/knockdown in primary OPC cultures, subcellular localization by immunostaining, cuprizone demyelination model |
Glia |
Medium |
25530119
|
| 2015 |
Olig1 acetylation at Lys150 (human Olig1) drives nuclear-to-cytoplasmic translocation. The acetyltransferase CBP (CREB-binding protein) and deacetylases HDAC1, HDAC3, and HDAC10 regulate this modification. Acetylation decreases Olig1 chromatin association, increases interaction with ID2, and facilitates cytoplasmic retention in mature oligodendrocytes. Three functional nuclear export sequences (NES) were identified in the bHLH domain. |
Identification of acetylation site (Lys150) by mutagenesis, CBP/HDAC overexpression/knockdown, chromatin association assays, Co-IP (Olig1–ID2 interaction), subcellular fractionation/immunostaining in mouse and rat oligodendrocytes |
The Journal of neuroscience |
High |
26631469
|
| 2015 |
Olig1 is required for oligodendrocyte progenitor cell commitment and differentiation in the brain corpus callosum, with hypomyelination persisting into adulthood. In the spinal cord, compensatory upregulation of Olig2 protein (not seen in brain) partially rescues the deficit, explaining the regional difference in Olig1 requirement. |
Olig1-null mouse analysis, Olig2 protein quantification by Western blot and immunostaining, myelination assessment by electron microscopy and immunostaining |
The Journal of neuroscience |
High |
25762682
|
| 2010 |
Olig1 protein translocates from the cytoplasm to the nucleus in EAE (demyelination) rat brains, and progesterone treatment increases the proportion of cells showing nuclear Olig1 localization, correlating with enhanced remyelination. |
Immunostaining for Olig1 subcellular localization in EAE rat brain, electron microscopy for myelin assessment, progesterone injection paradigm |
Neuroscience letters |
Low |
20381586
|
| 2010 |
Olig1 and ID4 directly interact and form a dimer in living cells; the Olig1–ID4 complex localizes to the cytoplasm (whereas Olig1 alone is nuclear and ID4 alone is cytoplasmic), indicating that ID4 blocks nuclear transport of Olig1. |
Bimolecular fluorescence complementation (BiFC) in SW1116 cells, EGFP/DsRed2 fusion protein co-expression and colocalization |
Molecular biology reports |
Medium |
21132377
|
| 2017 |
Olig1 function is required downstream of Noggin (BMP antagonism) for OPC production after neonatal stroke; in postnatal neural progenitors, Noggin governs OL versus interneuron fate through Olig1-mediated repression of Dlx1/2 transcription factors. Olig1-null neonatal mice show hypomyelination and replacement of OPCs with proliferating neuronal precursors and GABAergic interneurons in damaged white matter. |
Olig1-null mice subjected to neonatal stroke, postnatal neural progenitor cultures with Noggin treatment, immunostaining for lineage markers |
Annals of neurology |
Medium |
28253550
|
| 2017 |
HMGN proteins regulate OLIG1 and OLIG2 expression through chromatin dynamics: loss of HMGNs increases histone H1 chromatin binding at Olig1/2 loci, recruiting the methyltransferase EZH2 and elevating H3K27me3 (repressive mark), thereby reducing Olig1/2 expression and impeding oligodendrocyte lineage specification. |
HMGN knockout ESC differentiation assays, ChIP for H1/EZH2/H3K27me3 at Olig1/2 loci, gene expression analysis, mouse behavioral and histological phenotyping |
Nucleic acids research |
Medium |
27923998
|
| 2021 |
Quetiapine upregulates Olig1 expression and promotes nuclear-to-cytoplasmic translocation of Olig1, where cytoplasmic Olig1 (not as transcription factor) drives oligodendroglial membrane expansion and maturation. Quetiapine also reverses GPR17-mediated inhibition of oligodendroglial morphological maturation, with Olig1 identified as upstream regulator of GPR17. |
Primary oligodendrocyte cultures, quetiapine treatment, Olig1 subcellular localization by immunostaining, morphological quantification, GPR17 expression analysis |
Glia |
Low |
33660902
|
| 2024 |
Olig1 promotes axonal regeneration in spinal motor neurons; Olig1 overexpression facilitates axonal regeneration in multiple injury models while deletion has the opposite effect. Olig1 acts at least partially through transcriptional regulation of the neurite extension factor Nrsn1. |
Transcriptomic profiling of motor neurons with differential regenerative capacity, Olig1 overexpression/deletion in regeneration models, identification of Nrsn1 as downstream target by differential gene expression and functional validation |
Cell reports |
Medium |
39002126
|
| 2025 |
Olig1 and Olig2 coordinately regulate cortical astrocyte maturation by directly binding the Bmp7 enhancer and repressing Bmp7 expression; genetic ablation of both Olig1 and Olig2 results in defective astrocyte morphology and immature gene expression, while Bmp7 overexpression in vivo replicates this phenotype. |
Olig1/2 double knockout mice, single-cell RNA sequencing, ChIP/CUT&Tag for Olig1/2 binding at Bmp7 enhancer, Bmp7 overexpression in vivo |
Journal of genetics and genomics |
High |
40139307
|
| 2025 |
Olig1 and Olig2 coordinately regulate Tri-IPC fate specification in cortical gliogenesis by activating OPC specification while repressing OBIN-IPC generation through direct binding to multiple conserved enhancer elements of Gsx2, suppressing its expression; Olig1/2 genetic ablation redirects progenitors from OPC to OBIN-IPC fate with Gsx2 upregulation. |
Olig1/2 double knockout mouse genetics, CUT&Tag-seq for Olig1/2 binding at Gsx2 enhancers, single-cell transcriptomics, in vivo mutagenesis |
Nature communications |
High |
41193423
|
| 2025 |
OLIG1 and OLIG2 drive GBM tumor cell proliferation by directly binding to promoter regions of cyclins (Cdk4, Ccne2, Ccnd3, Ccnd1), marked by H3K4me3 (active histone mark), leading to transcriptional activation; Olig1/2 knockout reduces proliferation but does not suppress tumor initiation or migration. |
CRISPR/Cas9 Olig1/2 knockout in GBM mouse model, CUT&Tag-seq for Olig1/2 binding at cyclin promoters, H3K4me3 ChIP, tumor proliferation assays |
Genes |
Medium |
40428395
|