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the claim

Specific mechanisms bind the histone code with alternative splicing

the verdict
SUPPORTED
the evidence backs this
Recorded sources
2 sources for · 0 against

Counts group repeated records of the same source within each side. They do not measure evidence strength or source independence.

Current molecular evidence demonstrates that specific histone modifications directly regulate and induce alternative splicing events through identifiable adaptor mechanisms.

The analysis

The retrieved papers provide specific empirical evidence demonstrating causal mechanisms (such as targeted CRISPR/dCas9 histone modification and adaptor protein pathways like PSIP1/SRSF1) that link histone codes to alternative splicing. Both papers directly support the claim.

Evidence for · 2
Recorded source metadata

Alexandre Segelle. The role of histone modifications in the regulation of alternative splicing during epithelial-to-mesenchymal transition. https://doi.org/10.70675/40e530e9z2e50z46e1zac0aze57debc0a189

The study uses CRISPR/dCas9 systems to directly modify specific histone marks on alternative exons, proving that these marks are sufficient to induce alternative splicing changes during epithelial-to-mesenchymal transition.

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Recorded source metadata

Yungang Xu, Weiling Zhao, Scott D. Olson, Karthik S. Prabhakara, Xiaobo Zhou. Alternative splicing links histone modifications to stem cell fate decision. 2017. https://doi.org/10.1101/181875

The paper identifies specific mechanisms, such as the PSIP1/SRSF1 adaptor linking H3K36me3 to exon skipping in PBX1, demonstrating a direct connection between histone modifications and alternative splicing.

The paper trail · every fact has a biography
first checked01 Aug 2026
judged → SUPPORTED · 7501 Aug 2026
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