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The chromodomain protein CDYL confers forebrain identity to human cortical organoids by inhibiting neuronatin

Yaming Yang1, Bai-Rong Chen1, Xi-Chun Ye1

  • 1Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health Commission and State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.

Cell Reports
|October 8, 2024
PubMed

Insights

Chromodomain Y-like (CDYL) is vital for human brain development, controlling neural stem cell (NSC) fate. CDYL deficiency increases specific neuron types, impacting cortex development and potentially neurodevelopmental disorders.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Genetics

Background:

  • Neural stem cell (NSC) fate determination is essential for human cortex development.
  • Disruptions in gene expression networks can lead to neurodevelopmental disorders.
  • The transcriptional corepressor chromodomain Y-like (CDYL) is broadly expressed in the embryonic human cortex, but its function is not well understood.

Purpose of the Study:

  • To investigate the role of CDYL in human cortical neurogenesis and NSC fate determination.
  • To identify targets of CDYL and their influence on neuronal differentiation.
  • To compare CDYL's function across species to understand its evolutionary role.

Main Methods:

  • Utilized human cortical organoids to study neurogenesis.
  • Performed gene expression analysis to identify CDYL targets.
  • Conducted cross-species comparisons of CDYL targets between human and mouse cortex.

Main Results:

  • CDYL is critical for human cortical neurogenesis.
  • CDYL deficiency in cortical organoids results in a significant increase in gamma-aminobutyric acid (GABA)-ergic neurons.
  • Neuronatin (NNAT) was identified as a key CDYL target, influencing NSC fate commitment.

Conclusions:

  • CDYL plays a crucial role in maintaining the fate of human cortical neural stem cells.
  • Abnormal CDYL expression impacts the balance of neuronal subtypes, specifically increasing GABAergic neurons.
  • CDYL's distinct target profile suggests unique evolutionary roles in human cortex development compared to mice.
Keywords:
CP: Developmental biologyCP: Neuroscience

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