AI Article Synopsis
- Long interspersed element-1 (LINE-1 or L1) makes up 17% of the human genome and is known for generating genetic variations and potentially causing diseases, yet its regulatory mechanisms and functions are not well understood.* -
- This study reveals that L1 can attract RNA polymerase II (RNA Pol II), produce L1 chimeric transcripts, and establish domain boundaries within the genome, with a nuclear protein called SAFB acting as a regulator by inhibiting the activity of active L1s.* -
- The research suggests that the formation of these domain boundaries requires transcription from L1 and that L1 has played a role in the evolution of species-specific genome organization, highlighting its significance in gene
Article Abstract
Long interspersed element-1 (LINE-1 or L1) comprises 17% of the human genome, continuously generates genetic variations, and causes disease in certain cases. However, the regulation and function of L1 remain poorly understood. Here, we uncover that L1 can enrich RNA polymerase IIs (RNA Pol IIs), express L1 chimeric transcripts, and create contact domain boundaries in human cells. This impact of L1 is restricted by a nuclear matrix protein scaffold attachment factor B (SAFB) that recognizes transcriptionally active L1s by binding L1 transcripts to inhibit RNA Pol II enrichment. Acute inhibition of RNA Pol II transcription abolishes the domain boundaries associated with L1 chimeric transcripts, indicating a transcription-dependent mechanism. Deleting L1 impairs domain boundary formation, and L1 insertions during evolution have introduced species-specific domain boundaries. Our data show that L1 can create RNA Pol II-enriched regions that alter genome organization and that SAFB regulates L1 and RNA Pol II activity to preserve gene regulation.
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| http://dx.doi.org/10.1016/j.molcel.2024.03.021 | DOI Listing |
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