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Neural development

Keeping a lid on alternative fates

Nature Reviews Neuroscience volume 18, page 323 (2017)Cite this article

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Understanding the mechanisms by which somatic cells can be converted to a neuronal fate in vitro may provide insight into 'normal' neuronal development. Both processes require silencing of programmes that drive alternative cell fates, but how this is achieved is poorly understood. Mall et al. now show that the transcription factor MYT1L represses multiple somatic cell lineage programmes to establish and maintain neuronal identity.

The targets of MYT1L included members of the Notch signalling pathway, such as Hes1, which encode proteins that inhibit neuronal differentiation. The authors showed that MYT1L expression overcame the inhibitory effects of Notch signalling on MEF–iN conversion. Furthermore, depletion of MYT1L in mouse embryos reduced neuronal differentiation, whereas MYT1L overexpression decreased Hes1 transcription and increased neuronal differentiation in cultured neuronal stem cells. Thus, MYT1L is also involved in overcoming the effects of negative regulators of neuronal cell fate during 'normal' development.

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References

  1. Mall, M. et al. Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates. Nature 544, 245–249 (2017)

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  1. Katherine Whalley
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Mertens, J. et al. Evaluating cell reprogramming, differentiation and conversion technologies in neuroscience. Nat. Rev. Neurosci. 17, 424–437 (2016)

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Whalley, K. Keeping a lid on alternative fates. Nat Rev Neurosci 18, 323 (2017). https://doi.org/10.1038/nrn.2017.54

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