ArticleCell death and differentiation2022
Loss of TAF8 causes TFIID dysfunction and p53-mediated apoptotic neuronal cell death.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Novel fetal phenotype of TAF8 deficiency.European journal of human genetics : EJHG · 2025Article
- Molecular profiling of a bladder cancer with very high tumour mutational burden.Cell death discovery · 2024Article
- Alleviating hypoxia to improve cancer immunotherapy.Oncogene · 2023Review
- p63 orchestrates serine and one carbon metabolism enzymes expression in head and neck cancer.Biology direct · 2023Article
- p63: a crucial player in epithelial stemness regulation.Oncogene · 2023Review
- Programmed Cell Death Pathways in Cholangiocarcinoma: Opportunities for Targeted Therapy.Cancers · 2023Review
- The ARTS of p53-dependent mitochondrial apoptosis.Journal of molecular cell biology · 2023Review
- Gene expression in organoids: an expanding horizon.Biology direct · 2023Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
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Abstract
Mutations in genes encoding general transcription factors cause neurological disorders. Despite clinical prominence, the consequences of defects in the basal transcription machinery during brain development are unclear. We found that loss of the TATA-box binding protein-associated factor TAF8, a component of the general transcription factor TFIID, in the developing central nervous system affected the expression of many, but notably not all genes. Taf8 deletion caused apoptosis, unexpectedly restricted to forebrain regions. Nuclear levels of the transcription factor p53 were elevated in the absence of TAF8, as were the mRNAs of the pro-apoptotic p53 target genes Noxa, Puma and Bax. The cell death in Taf8 forebrain regions was completely rescued by additional loss of p53, but Taf8 and p53 brains failed to initiate a neuronal expression program. Taf8 deletion caused aberrant transcription of promoter regions and splicing anomalies. We propose that TAF8 supports the directionality of transcription and co-transcriptional splicing, and that failure of these processes causes p53-induced apoptosis of neuronal cells in the developing mouse embryo.
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