KEY POINTS * The basic helix–loop–helix transcription factors oligodendrocyte transcription factor 1 (OLIG1) and OLIG2 are structurally related within their DNA targeting domains and, to a

first approximation, are coordinately expressed during development. * Notwithstanding similarities in their protein structure and expression pattern, OLIG1 and OLIG2 have non-overlapping

functions during development and in the postnatal brain. * _Olig2_-null mice have a striking developmental phenotype involving total loss of motor neurons and near-complete loss of

oligodendrocyte progenitors. * The developmental phenotype of _Olig1_-null mice is more nuanced and largely confined to the oligodendrocyte lineage. However, OLIG1 cooperates with OLIG2 in

proteins. ABSTRACT The basic helix–loop–helix transcription factors oligodendrocyte transcription factor 1 (OLIG1) and OLIG2 are structurally similar and, to a first approximation,

coordinately expressed in the developing CNS and postnatal brain. Despite these similarities, it was apparent from early on after their discovery that OLIG1 and OLIG2 have non-overlapping

developmental functions in patterning, neuron subtype specification and the formation of oligodendrocytes. Here, we summarize more recent insights into the separate roles of these

transcription factors in the postnatal brain during repair processes and in neurological disease states, including multiple sclerosis and malignant glioma. We discuss how the unique

functions of OLIG1 and OLIG2 may reflect their distinct genetic targets, co-regulator proteins and/or post-translational modifications. Access through your institution Buy or subscribe This

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TRANSCRIPTOMIC REVEALS MOLECULAR DIVERSITY AND DEVELOPMENTAL HETEROGENEITY OF HUMAN STEM CELL-DERIVED OLIGODENDROCYTE LINEAGE CELLS Article Open access 28 January 2021 SIRT2 PROMOTES WHITE

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(2005). Article  CAS  PubMed  Google Scholar  Download references ACKNOWLEDGEMENTS The authors gratefully acknowledge helpful conversations with W. Richardson (University College London,

UK), R. Miller (Case Western Reserve University, USA) and Y. Sun (Dana–Farber Cancer Institute, USA). Work from the authors' laboratories that is cited here was supported by grants from

the National Institutes of Health (NS047572 and NS057727 to C.D.S. and NS040511 to D.H.R.) and from the Pediatric Low-Grade Astrocytoma Foundation (grant awarded to C.D.S.). D.H.R. is

supported by the Howard Hughes Medical Institute. AUTHOR INFORMATION Author notes * Christopher M. Taylor Present address: Present address., AUTHORS AND AFFILIATIONS * Departments of

Neurobiology, Harvard Medical School and Cancer Biology, Dana–Farber Cancer Institute, 450 Brookline Avenue, Boston, 02215, Massachusetts, USA Dimphna H. Meijer, Michael F. Kane, Shwetal

Mehta, Christopher M. Taylor & Charles D. Stiles * Informatics Program, Children's Hospital Boston, 300 Longwood Avenue, Boston, 02115, Massachusetts, USA Hongye Liu * Departments

of Pediatrics and Neurological Surgery, Howard Hughes Medical Institute, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, 94143, California, USA Emily Harrington

 & David H. Rowitch * EMD Serono Research Institute, 45A Middlesex Turnpike, Billerica, 01821, Massachusetts, USA Christopher M. Taylor Authors * Dimphna H. Meijer View author

publications You can also search for this author inPubMed Google Scholar * Michael F. Kane View author publications You can also search for this author inPubMed Google Scholar * Shwetal

Mehta View author publications You can also search for this author inPubMed Google Scholar * Hongye Liu View author publications You can also search for this author inPubMed Google Scholar *

Emily Harrington View author publications You can also search for this author inPubMed Google Scholar * Christopher M. Taylor View author publications You can also search for this author

inPubMed Google Scholar * Charles D. Stiles View author publications You can also search for this author inPubMed Google Scholar * David H. Rowitch View author publications You can also

search for this author inPubMed Google Scholar CORRESPONDING AUTHORS Correspondence to Charles D. Stiles or David H. Rowitch. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no

competing financial interests. SUPPLEMENTARY INFORMATION SUPPLEMENTARY INFORMATION S1 (TABLE) (PDF 161 kb) SUPPLEMENTARY INFORMATION S2 (BOX) (PDF 159 kb) RELATED LINKS RELATED LINKS

DATABASES NCBI Gene expression omnibus database GLOSSARY * Cre-_lox_ fate-mapping This recombination procedure installs a stable marker protein (usually colorimetric, such as LacZ) into a

genetically defined cell type and all of its daughter cells. * Tumour-initiating cells In tumours with a heterogeneous cell population (such as glioblastoma), these undifferentiated

stem-like cells are thought to be responsible for propagating the tumours in serial animal transplantation protocols. * Severe combined immunodeficiency (SCID). SCID mice are used as a host

animal for transplantation experiments with human tumours. * Transit-amplifying cells Also known as type C cells, these are rapidly dividing neural progenitor cells in the subventricular

zone of postnatal brain. They are also the immediate progeny of the more slowly replicating multipotent adult neural stem cells. * Single nucleotide polymorphisms (SNPs). SNPs are DNA

sequence variations that differ among individual members of a biological species or between paired chromosomes in a single individual. * Expression profiling This procedure identifies the

gene types that are expressed in a particular cell type by processing mRNA into cDNA and then annealing the cDNA to gene sequences arrayed onto a solid surface. * SUMOylation This

post-translational modification event involves the covalent ligation of small ubiquitin-like modifier (SUMO) proteins to regulate various cellular processes. RIGHTS AND PERMISSIONS Reprints

and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Meijer, D., Kane, M., Mehta, S. _et al._ Separated at birth? The functional and molecular divergence of OLIG1 and OLIG2. _Nat Rev

Neurosci_ 13, 819–831 (2012). https://doi.org/10.1038/nrn3386 Download citation * Published: 20 November 2012 * Issue Date: December 2012 * DOI: https://doi.org/10.1038/nrn3386 SHARE THIS

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