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DOT1L promotes progenitor proliferation and primes neuronal layer identity in the developing cerebral cortex
Henriette Franz1, Alejandro Villarreal1, Stefanie Heidrich1
1Institute of Anatomy and Cell Biology, Department of Molecular Embryology, Medical Faculty, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany.
Nucleic Acids Research
|October 18, 2018
Summary
DOT1L is crucial for proper brain development. Its absence disrupts cortical layering and neuronal identity, particularly affecting upper layer neuron generation.
Area of Science:
- Neuroscience
- Developmental Biology
- Epigenetics
Background:
- Cortical development relies on precise transcriptional programs.
- The role of specific factors like DOT1L in maintaining spatio-temporal activity for cell fate and layer localization is not fully understood.
Purpose of the Study:
- To investigate the function of Dot1l in murine telencephalon development.
- To understand how DOT1L, through chromatin methylation (H3K79), influences cell cycle, progenitor differentiation, and neuronal identity.
Main Methods:
- Utilized three different mouse models with Dot1l deletion in the telencephalon.
- Analyzed cortical layering, progenitor cell populations, and gene expression patterns related to neuronal identity.
Main Results:
- Dot1l deletion causes significant cortical layering defects.
- Loss of DOT1L leads to premature differentiation and reduced progenitor numbers (SoxB1 family).
- Altered distribution of deep layer neurons (TBR1, CTIP2, SOX5) and impaired upper layer neuron transcriptional programs (Satb2, Pou3f3, Cux2, SoxC) were observed.
Conclusions:
- DOT1L is essential for balancing transcriptional programs that ensure correct neuronal composition and distribution in the six cortical layers.
- DOT1L primes upper layer identity in cortical progenitors, as its loss impairs the generation of SATB2-expressing neurons during the pre-neurogenic phase.
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