Olig1, short for oligodendrocyte transcription factor 1, is a basic helix-loop-helix transcription factor crucial for oligodendrocyte development and myelination [2,3,5]. It is involved in pathways regulating neural cell differentiation and may interact with other factors like Sox10 to drive myelin basic protein transcription [6]. Olig1 is of great biological importance as it impacts neural cell generation and maturation during development [4]. Genetic models, especially KO/CKO mouse models, are valuable for studying its functions.

In Olig1-null neonatal mice, there was significant hypomyelination after moderate neonatal stroke, and damaged white matter tracts lacked Olig2+ oligodendrocyte precursor cells (OPCs), replaced by proliferating neuronal precursors and GABAergic interneurons, indicating that Olig1 is required for noggin-induced neonatal myelin repair [1]. In Olig1-null mice, oligodendrocyte progenitor cell commitment and oligodendrocyte differentiation were impaired in the corpus callosum, resulting in hypomyelination throughout adulthood in the brain, highlighting its role in promoting oligodendrocyte progenitor cell commitment, differentiation, and myelination in the brain [5].

In conclusion, Olig1 is essential for oligodendrocyte development, differentiation, and myelination, especially in the brain. The use of Olig1 KO/CKO mouse models has revealed its critical role in neonatal myelin repair and brain myelination processes, providing insights into related neurological diseases such as neonatal white matter injury [1,5].

References:

1. Sabo, Jennifer K, Heine, Vivi, Silbereis, John C, Levison, Steven W, Rowitch, David H. . Olig1 is required for noggin-induced neonatal myelin repair. In Annals of neurology, 81, 560-571. doi:10.1002/ana.24907. https://pubmed.ncbi.nlm.nih.gov/28253550/

2. Dai, Jinxiang, Bercury, Kathryn K, Jin, Weilin, Macklin, Wendy B. . Olig1 Acetylation and Nuclear Export Mediate Oligodendrocyte Development. In The Journal of neuroscience : the official journal of the Society for Neuroscience, 35, 15875-93. doi:10.1523/JNEUROSCI.0882-15.2015. https://pubmed.ncbi.nlm.nih.gov/26631469/

3. Meijer, Dimphna H, Kane, Michael F, Mehta, Shwetal, Stiles, Charles D, Rowitch, David H. . Separated at birth? The functional and molecular divergence of OLIG1 and OLIG2. In Nature reviews. Neuroscience, 13, 819-31. doi:10.1038/nrn3386. https://pubmed.ncbi.nlm.nih.gov/23165259/

4. Qi, Qi, Zhang, Yuxin, Shen, Lin, Lü, Hezuo, Hu, Jianguo. 2016. Olig1 expression pattern in neural cells during rat spinal cord development. In Neuropsychiatric disease and treatment, 12, 909-16. doi:10.2147/NDT.S99257. https://pubmed.ncbi.nlm.nih.gov/27143892/

5. Dai, Jinxiang, Bercury, Kathryn K, Ahrendsen, Jared T, Macklin, Wendy B. . Olig1 function is required for oligodendrocyte differentiation in the mouse brain. In The Journal of neuroscience : the official journal of the Society for Neuroscience, 35, 4386-402. doi:10.1523/JNEUROSCI.4962-14.2015. https://pubmed.ncbi.nlm.nih.gov/25762682/

6. Li, Huiliang, Lu, Yan, Smith, Hazel K, Richardson, William D. . Olig1 and Sox10 interact synergistically to drive myelin basic protein transcription in oligodendrocytes. In The Journal of neuroscience : the official journal of the Society for Neuroscience, 27, 14375-82. doi:. https://pubmed.ncbi.nlm.nih.gov/18160645/