ArticleNucleic acids research2024
KDM5-mediated transcriptional activation of ribosomal protein genes alters translation efficiency to regulate mitochondrial metabolism in neurons.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- A KDM5 variant outside the catalytic Jumonji C domain disrupts demethylase activity and alters the proximity interactome.G3 (Bethesda, Md.) · 2026Article
- Reduced dosage of Kmt2d modifies Tbx1 haploinsufficiency toward phenotypes of 22q11.2DS.JCI insight · 2026Article
- Individuals with reported and novel KDM5C variants present with seizures, a feature recapitulated in a Drosophila model.Human molecular genetics · 2026Article
- Local chromatin context informs transcriptional outcomes for the histone demethylase KDM5.Epigenetics & chromatin · 2025Article
- Evidence for dual roles of histone H3 lysine 4 in antagonizing Polycomb group function and promoting target gene expression.Genes & development · 2024Article
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
Abstract
Genes encoding the KDM5 family of transcriptional regulators are disrupted in individuals with intellectual disability (ID). To understand the link between KDM5 and ID, we characterized five Drosophila strains harboring missense alleles analogous to those observed in patients. These alleles disrupted neuroanatomical development, cognition and other behaviors, and displayed a transcriptional signature characterized by the downregulation of many ribosomal protein genes. A similar transcriptional profile was observed in KDM5C knockout iPSC-induced human glutamatergic neurons, suggesting an evolutionarily conserved role for KDM5 proteins in regulating this class of gene. In Drosophila, reducing KDM5 changed neuronal ribosome composition, lowered the translation efficiency of mRNAs required for mitochondrial function, and altered mitochondrial metabolism. These data highlight the cellular consequences of altered KDM5-regulated transcriptional programs that could contribute to cognitive and behavioral phenotypes. Moreover, they suggest that KDM5 may be part of a broader network of proteins that influence cognition by regulating protein synthesis.
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Registered trials
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