Speaker
Description
Influenza A virus mRNAs are synthesised in the nucleus by the viral RNA-dependent RNA polymerase (FluPol). To initiate viral transcription, FluPol binds host RNA polymerase II (RNAPII). The endonuclease subunit of FluPol then cleaves nascent transcript, producing a short capped RNA fragment, which primes viral mRNA synthesis. Previous studies suggested this cap-snatching process is largely dependent on transcript level, though others reported gene-specificity. However, these studies were based on sequencing Flu mRNAs and thus limited by small 12 nt primers, which are hard to uniquely map to the human genome.
Here, we present a complimentary approach of identifying the downstream portion of the host cap-snatched transcripts using polymerase intact nascent transcript (POINT) technology. We use native immunoprecipitation of RNAPII elongation complexes to isolate associated nascent RNAs and prepare 5ʹ-end specific libraries, with reads long enough for unique mapping.
This approach allowed us to identify cap-snatching events directly from the 5′ ends of RNAPII-associated transcripts. We report a previously overlooked preference for variant spliceosomal U1 snRNAs and avoidance of the more abundant U1 snRNAs. These findings suggest that in addition to transcript abundance, other factors are regulating influenza A virus co-transcriptional cap-snatching and potentially support a model in which FluPol exhibits a higher degree of substrate specificity than previously appreciated.
| Registration ID | INF26-105 |
|---|---|
| Professional status of the speaker | Postdoc |
| Junior scientist status | No, I am not a junior scientist. |
Authors
Co-authors
External references
- 40
