AI Article Synopsis
- RNA methylation (specifically m^6A) normally suppresses the immune response of endogenous RNA, but when m^6A is lacking, it can lead to increased inflammation and cell death.
- The study reveals that noncoding RNA 7SK becomes immunostimulatory without m^6A, activating RIG-I/MAVS pathways and leading to interferon (IFN) signaling.
- Additionally, both high levels of IFN and reduced m^6A work together to form RNA G-quadruplexes (rG4), which promote necroptotic cell death through ZBP1 activation, linking m^6A changes to inflammatory responses.
Article Abstract
m A RNA methylation suppresses the immunostimulatory potential of endogenous RNA. Deficiency of m A provokes inflammatory responses and cell death, but the underlying mechanisms remain elusive. Here we showed that the noncoding RNA 7SK gains immunostimulatory potential upon m A depletion and subsequently activates the RIG-I/MAVS axis to spark interferon (IFN) signaling cascades. Concomitant excess of IFN and m A deficiency synergistically facilitate the formation of RNA G-quadruplexes (rG4) to promote ZBP1-mediated necroptotic cell death. Collectively, our findings delineate a hitherto uncharacterized mechanism that links m A dysregulation with ZBP1 activity in triggering inflammatory cell death.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11230363 | PMC |
| http://dx.doi.org/10.1101/2024.06.29.601251 | DOI Listing |
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