Knockdown of the long non-coding RNA DNAAF3-AS1 activates the p53 pathway and remodels the H3K36me3 landscape

DNAAF3-AS1 knockdown in human dermal fibroblasts markedly reduces gene-body H3K36me3 and shifts residual H3K36me3 toward promoters, linking this chromatin remodeling to p53 pathway activation.

• Why it matters: Most long non-coding RNAs remain uncharacterized as chromatin regulators, and DNAAF3-AS1’s near-exclusive association with H3K36me3 suggested a functional role worth testing.
• What they did: Human dermal fibroblasts were treated with DNAAF3-AS1 knockdown using two independent antisense oligonucleotides, followed by H3K36me3 ChIP-seq and FANTOM6 CAGE analyses.
• The result: Knockdown activated the p53 pathway and altered differential promoter usage in p53- and apoptosis-related genes, while genes gaining gene-body H3K36me3 were enriched for apoptosis-related pathways.

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