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FLASH GENE
Symbol OLIG2 contributors: shn/mct - updated : 30-01-2024
HGNC name oligodendrocyte lineage transcription factor 2
HGNC id 9398
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • in the N-terminus a triple serine motif phosphorylated in cycling neural progenitors but not in their differentiated progeny
  • helix-loop-helix (HLH) DNA binding domain
  • conjugated
    HOMOLOGY
    interspecies ortholog to Olig 2, Rattus norvegicus
    ortholog to Olig 2, Mus musculus
    ortholog to olig2, danio rerio
    ortholog to OLIG2, Pan troglodytes
    Homologene
    FAMILY
  • basic helix loop helix (BHLH) family of transcription family
  • CATEGORY transcription factor
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm
    intracellular,nucleus,nucleoplasm
    intracellular,nucleus,chromatin/chromosome
    basic FUNCTION
  • plays in cooperation with Neurogenin2 vital roles in the coordinated induction of pan-neuronal and subtype-specific properties of motoneurons
  • required for oligodendrocytes and motor neuron specification in the spinal cord
  • controlling the development of neural crest cells, astrocytes and oligodendrocytes, three neuroectodermal-derived cells
  • plays critical roles in oligodendrocyte and motor neuron development
  • export of OLIG2, stimulated AKT, by from the nucleus of neural stem cell is essential for the astrocyte differentiation
  • required for the production of motor neurons and oligodendrocytes
  • repressor of neurogenesis in cells reacting to brain injury and open innovative perspectives toward evoking endogenous neuronal repair
  • having repressor function, both sufficient and necessary to prevent neuronal differentiation and to direct subventricular zone progenitors toward astrocytic and oligodendrocytic fates
  • required for proliferation of neural progenitors and for glioma formation
  • playing a crucial role in white matter astrocyte development, but not in the cortical gray matter astrocytes
  • role in gliogenesis in the dorsal pallium
  • play a role in ventral telencephalic neurogenesis
  • marks a subpopulation of retinal progenitor cells (RPCs) that are biased toward the production of postmitotic progeny
  • required for oligodendrocyte specification and differentiation
  • has the ability to permeate the cell membrane without the addition of a protein transduction domain (PTD), similar to other basic helix-loop-helix transcription factors such as MYOD1 and NEUROD2
  • OLIG2 itself had a transduction ability similar to other bHLH transcription factors
  • functions as a prepatterning factor to direct SMARCA4 to oligodendrocyte-specific enhancers
  • basic helix-loop-helix transcription factor necessary for oligodendroglial development and expressed continuously throughout the lineage
  • is involved in correct formation of the prethalamus, which leads to exclusion of the EPHA3-expressing region and is crucial for proper thalamocortical axons (TCAs) formation
  • plays a pivotal role in glioma development
  • plays a crucial role in the neurogenesis of both spinal cord and brain
  • OLIG2 is an onco-requisite factor in diffuse intrinsic pontine glioma (DIPG)
  • OLIG2-lineage astrocytes are likely involved in inhibitory neuronal transmission
  • novel function of OLIG2 in the periphery nervous system to regulate the terminal differentiation and maturation of olfactory sensory neurons
  • is an important transcription factor essential for the specification and differentiation of oligodendrocytes as well as astrocytes and neurons during developmental stages
  • functional roles of OLIG1 and OLIG2 in directing neuronal and glial formation during different stages in development
  • is a transcription factor that activates the expression of myelin-associated genes in the oligodendrocyte-lineage cells
  • OLIG2 is likely essential for anterior commissure formation, likely by regulating multiple biological processes
  • CELLULAR PROCESS nucleotide, transcription
    PHYSIOLOGICAL PROCESS development , nervous system , neurogenesis
    PATHWAY
    metabolism
    signaling
    a component
  • likely phosphorylated OLIG2 proteins form stable homodimers, whereas unphosphorylated OLIG2 prefers to form heterodimers with other bHLH proteins such as NEUROG2
  • OLIG2-SETDB1 complex can mediate transcriptional repression in oligodendrocytes progenitor cells (OPCs), affecting myelination
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • NK2 homeobox 2, Nkx2.2
  • SRY (sex determining region Y)-box 10, SOX10 and SOXE
  • NEUROG2 to modulate gene expression in motor neuron progenitor cells
  • ID2 (inhibited posttranslationally through the interaction with ID2)
  • SMARCA4 is an integral component of the transcriptional control of myelination via interaction with OLIG2 at the onset of oligodendrocyte progenitor cells differentiation
  • stage-specific regulatory role for OLIG2, mediated by OLIG1 that conveys opposing functions on the differentiation and maturation of oligodendrocytes
  • LGR5 is regulated by OLIG2, which is important for both neurogenesis and stem-like cells in glioblastoma (GSCs) maintenance
  • TAF9B binds to both promoters and distal enhancers of neuronal genes, partially co-localizing at binding sites of OLIG2, a key activator of motor neuron differentiation
  • PROX1 is a transcription repressor and downstream target of proneural genes, that suppresses OLIG2 expression and therefore controls ventral spinal cord patterning
  • SEH1L regulates oligodendrocyte progenitor cells (OPCs) differentiation by assembling OLIG2 and BRD7 into a transcription complex at nuclear periphery
  • WNT signaling suppresses oligodendrogenesis via NEUROG2-dependent direct inhibition of OLIG2 expression
  • cell & other
    REGULATION
    Other phosphorylation regulates OLIG2 cofactor choice and the motor neuron-oligodendrocyte fate switch
    proliferative function of OLIG2 is controlled by developmentally regulated phosphorylation of a conserved triple serine motif within the N-terminal domain
    OLIG2 SUMOylation enhances its genetic targeting ability, which in turn occludes TP53 recruitment to CDKN1A promoter for DNA-damage responses
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral       gain of function
    activated in T cell lymphoblastic leukemia with t(14;21) (q11.2;q22)
    constitutional     --over  
    acute and chronic brain injury
    tumoral     --low  
    may be related to the malignant behavior of human glioblastoma
    tumoral     --over  
    in oligodendroglial tumors
    constitutional   amplification    
    Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome
    constitutional     --over  
    over-expression inhibits neural progenitor proliferation through changes in potassium channel activity, thereby contributing to the reduced neuronal numbers and brain size in Down syndrome
    constitutional   deletion    
    in the cerebellum, deletion of both OLIG2 and OLIG1 results in impaired genesis of Purkinje cells (PCs) and Pax2(+) interneurons
    tumoral     --over  
    in diffuse intrinsic pontine glioma (DIPG)
    Susceptibility to schizophrenia
    Variant & Polymorphism SNP SNP rs762178 in OLIG2 seems to be a potential candidate in altering risk for schizophrenia in the Chinese Han population
    Candidate gene
    Marker
  • a molecular marker for human glial brain tumors
  • a marker for the diagnosis of oligodendroglial tumours
  • Therapy target
    SystemTypeDisorderPubmed
    cancerbrain 
    likely target gene as novel candidates in diffuse intrinsic pontine glioma (DIPG) therapy
    ANIMAL & CELL MODELS
  • in Olig1(-/-)2(-/-) double-mutant mice motoneurons are largely eliminated, and oligodendrocyte differentiation is abolished
  • mice lacking Olig2 function demonstrates a failure of NG2 cell development at embryonic and perinatal stages
  • in Olig2 deficient mouse, astrocyte development was retarded in the dorsal neocortex, but not in the basal forebrain
  • Olig2 is triplicated and overexpressed in the Ts65Dn mouse (mouse models of Down syndrome) forebrain displaying cognitive deficits