ArticleNucleic acids research2016
Nascent RNA length dictates opposing effects of NusA on antitermination.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Conserved protein Seb1 that interacts with RNA polymerase II and RNA is an antipausing transcription elongation factor.RNA (New York, N.Y.) · 2025Article
- Article
- In transcription antitermination by Qλ, NusA induces refolding of Qλ to form a nozzle that extends the RNA polymerase RNA-exit channel.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Transcription complexes as RNA chaperones.Transcription · 2021Article
- Structural basis of Q-dependent antitermination.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Temporal proteomic profiling reveals changes that support Burkholderia biofilms.Pathogens and disease · 2019Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The NusA protein is a universally conserved bacterial transcription elongation factor that binds RNA polymerase (RNAP). When functioning independently, NusA enhances intrinsic termination. Paradoxically, NusA stimulates the function of the N and Q antiterminator proteins of bacteriophage λ. The mechanistic basis for NusA's functional plasticity is poorly understood. Here we uncover an effect of nascent RNA length on the ability of NusA to collaborate with Q. Ordinarily, Q engages RNAP during early elongation when it is paused at a specific site just downstream of the phage late-gene promoter. NusA facilitates this engagement process and both proteins remain associated with the transcription elongation complex (TEC) as it escapes the pause and transcribes the late genes. We show that the λ-related phage 82 Q protein (82Q) can also engage RNAP that is paused at a promoter-distal position and thus contains a nascent RNA longer than that associated with the natively positioned TEC. However, the effect of NusA in this context is antagonistic rather than stimulatory. Moreover, cleaving the long RNA associated with the promoter-distal TEC restores NusA's stimulatory effect. Our findings reveal a critical role for nascent RNA in modulating NusA's effect on 82Q-mediated antitermination, with implications for understanding NusA's functional plasticity.
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