ArticleiScience2025
A human-specific, concerted repression of microcephaly genes contributes to radiation-induced growth defects in cortical organoids.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Relative biological effectiveness and neural stem cell fate in carbon ion-irradiated human brain organoids.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2026Article
- Metabolic functions for molecular chaperones and stress proteins in microcephaly.Cellular and molecular life sciences : CMLS · 2025Review
- Aberrant choroid plexus formation drives the development of treatment-related brain toxicity.Communications biology · 2025Article
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12 authors.
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Abstract
Prenatal radiation-induced DNA damage poses a significant threat to neurodevelopment, resulting in microcephaly which primarily affects the cerebral cortex. So far, mechanistic studies were done in rodents. Here, we leveraged human cortical organoids to model fetal corticogenesis. Organoids were X-irradiated with moderate or high doses at different time points. Irradiation caused a dose- and time-dependent reduction in organoid size, which was more prominent in younger organoids. This coincided with a delayed and attenuated DNA damage response (DDR) in older organoids. Besides the DDR, radiation induced premature differentiation of neural progenitor cells (NPCs). Our transcriptomic analysis demonstrated a concerted p53-E2F4/DREAM-dependent repression of primary microcephaly genes, which was independently confirmed in cultured human NPCs and neurons. This was a human-specific feature, as it was not observed in mouse embryonic brains or primary NPCs. Thus, human cortical organoids are an excellent model for DNA damage-induced microcephaly and to uncover potentially targetable human-specific pathways.
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