lncRNA read-through regulates the BX-C insulator <i>Fub-1</i>.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 37643473.
- Also identified by DOI 10.7554/eLife.84711 and PMC identifier 10497285.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Though long non-coding RNAs (lncRNAs) represent a substantial fraction of the Pol II transcripts in multicellular animals, only a few have known functions. Here we report that the blocking activity of the Bithorax complex (BX-C) <i>Fub-1</i> boundary is segmentally regulated by its own lncRNA. The <i>Fub-1</i> boundary is located between the <i>Ultrabithorax</i> (<i>Ubx</i>) gene and the <i>bxd/pbx</i> regulatory domain, which is responsible for regulating <i>Ubx</i> expression in parasegment PS6/segment A1. <i>Fub-1</i> consists of two hypersensitive sites, <i>HS1</i> and <i>HS2. HS1</i> is an insulator while <i>HS2</i> functions primarily as an lncRNA promoter. To activate <i>Ubx</i> expression in PS6/A1, enhancers in the <i>bxd/pbx</i> domain must be able to bypass <i>Fub-1</i> blocking activity. We show that the expression of the <i>Fub-1</i> lncRNAs in PS6/A1 from the <i>HS2</i> promoter inactivates <i>Fub-1</i> insulating activity. Inactivation is due to read-through as the <i>HS2</i> promoter must be directed toward <i>HS1</i> to disrupt blocking.
Medical subject headings
- RNA, Long Noncoding
- Hypersensitivity