lncRNA read-through regulates the BX-C insulator Fub-1

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Abstract

hough 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) Fub-1 boundary is segmentally regulated by its own lncRNA. The Fub-1 boundary is located between the Ultrabithorax (Ubx) gene and the bxd/pbx regulatory domain, which is responsible for regulating Ubx expression in parasegment PS6/segment A1. Fub-1 consists of two hypersensitive sites, HS1 and HS2. HS1 is an insulator while HS2 functions primarily as a lncRNA promoter. To activate Ubx expression in PS6/A1 enhancers in the bxd/pbx domain must be able to bypass Fub-1 blocking activity. We show that expression of the Fub-1 lncRNAs in PS6/A1 from the HS2 promoter inactivates Fub-1 insulating activity. Inactivation is due to readthrough as the HS2 promoter must be directed towards HS1 to disrupt blocking.

Data availability

Sequencing data have been deposited in GEO under accession code GSE217005. The data can be accessed using the following secure token sxyxomkyjlgxvmj

The following data sets were generated

(2022) The insulating activity of the Drosophila BX-C chromatin boundary Fub-1 is parasegmentally regulated by lncRNA read-through
NCBI Gene Expression Omnibus, GSE217005.

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE217005

Article and author information

Author details

Airat Ibragimov

Department of Molecular Biology, Princeton University, Princeton, United States

For correspondence
airati@princeton.edu

Competing interests
No competing interests declared.

"This ORCID iD identifies the author of this article:" 0000-0002-5973-9147
Xin Yang Bing

Lewis Sigler Institute, Princeton University, Princeton, United States

Competing interests
Xin Yang Bing, is affiliated with BlueRock Therapeutics. The author has no other competing interests to declare..
Yulii Shidlovskii

Laboratory of Gene Expression Regulation in Development, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russian Federation

Competing interests
No competing interests declared.

"This ORCID iD identifies the author of this article:" 0000-0002-3643-9889
Michael Levine

Lewis Sigler Institute, Princeton University, Princeton, United States

Competing interests
No competing interests declared.
Pavel Georgiev

Department of the Control of Genetic Processes, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russian Federation

Competing interests
No competing interests declared.
Paul Schedl

Department of Molecular Biology, Princeton University, Princeton, United States

For correspondence
pschedl@princeton.edu

Competing interests
No competing interests declared.

"This ORCID iD identifies the author of this article:" 0000-0001-5704-2349

Funding

National Institute of General Medical Sciences (R35 GM126975)

Paul Schedl

National Institute of General Medical Sciences (R01 GM118147)

Michael Levine

Russian Science Foundation (20-14-00201)

Yulii Shidlovskii

Russian Science Foundation (19-14-00103)

Pavel Georgiev

Ministry of Science and Higher Education of the Russian Federation (075-15-2019-1661)

Pavel Georgiev

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.