bioRxiv Science⌕ Search

bioRxiv · 10.1101/605063

In situ structure of rotavirus VP1 RNA-dependent RNA polymerase

Abstract

Rotaviruses, like other non-enveloped, double-strand RNA (dsRNA) viruses, package an RNA-dependent RNA polymerase (RdRp) with each duplex of their segmented genomes. Rotavirus cell entry results in loss of an outer protein layer and delivery into the cytosol of an intact, inner capsid particle (the \"double-layer particle\" or DLP). The RdRp, designated VP1, is active inside the DLP; each VP1 achieves many rounds of mRNA transcription from its associated genome segment. Previous work has shown that one VP1 molecule lies close to each fivefold axis of the icosahedrally symmetric DLP, just beneath the inner surface of its protein shell, embedded in tightly packed RNA. We have determined a high-resolution structure for the rotavirus VP1 RdRp in situ, by local reconstruction of density around individual fivefold positions. We have analyzed intact virions (\"triple-layer particles\" or TLPs), non-transcribing DLPs and transcribing DLPs. Outer layer dissociation enables the DLP to synthesize RNA, in vitro as well as in vivo, but appears not to induce any detectable structural change in the RdRp. Addition of NTPs, Mg2+, and S-adenosyl methionine, which allows active transcription, results in conformational rearrangements, in both VP1 and the DLP capsid shell protein, that allow a transcript to exit the polymerase and the particle. The position of VP1 (among the five symmetrically related alternatives) at one vertex does not correlate with its position at other vertices. This stochastic distribution of site occupancies limits long-range order in the 11-segment, dsRNA genome.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Jenni, S., Salgado, E. N., Herrmann, T., Li, Z., Grant, T., Grigorieff, N., Trapani, S., Estrozi, L. F., Harrison, S. C.. 2019-04-13. In situ structure of rotavirus VP1 RNA-dependent RNA polymerase. https://doi.org/10.1101/605063

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Physiological mapping and prediction reveal stress-responsive translation initiation landscapes

Translation initiation defines the protein output of the transcriptome, but its physiological dynamics in cells and tissues remain incompletely characterized. Here we develop TISCA2, an inhibitor-free method that captures eIF5B-associated initiating ribosomes to map translation initiation sites genome-wide. By directly identifying start sites rather than inferring translation from elongating-ribosome periodicity, TISCA2 improves the detection of short and overlapping translons. Translation of a subset of TISCA2-identified translons is supported by N-terminal proteomics and HLA-I immunopeptidomics. The arsenite-induced integrated stress response broadly redistributes start-site usage, reducing upstream initiation in favor of downstream initiation. TISCA2 further reveals tissue-specific initiation landscapes in vivo, with increased detection of downstream candidate start sites in the testis. Finally, we develop IncepTIS, a sequence-based deep learning model that predicts position-resolved and condition-dependent initiation landscapes. IncepTIS-guided optimization generates de novo mRNA 5' leaders with stress-responsive initiation patterns. Together, TISCA2 and IncepTIS provide an experimental and computational framework for mapping, predicting and engineering translation initiation in mammalian cells and tissues.

molecular biology↗

Optimal compositions of potent sliced-siRNA with DNA bases substitution and insights of Ago2 slicing actions

We have previously characterized the nucleotide compositions of single-stranded ago2-sliced small interfering RNAs (sliced-siRNA, sliRNA), a novel type of potent RNAi trigger designed based on the biogenesis mechanism of miRNA-451. sliRNAs have on par antisense mediated silencing activity but about 1000-fold reduced passenger strand activity compared to siRNA. In the current study, to further characterize sliRNAs to facilitate their in vivo application, we have investigated the effects of substituting RNA nucleotides (nts) in sliRNA with DNA nts (sliDRNAs), which will allow us to study the potential effects on their processing, maturation, and silencing activity from individual or multiple nts at different positions. Our results showed sliDRNAs have distinguished composition from siRNA with DNA nts (siDRNA), indicated that, in addition to their different biogenesis mechanisms, these two types of RNAi triggers may also have adopted additional different silencing mechanisms. Our results also revealed some mechanism related to how Ago2 executes its slicer activity and the effects on sliRNA potency by trimming and tailing during sliRNA maturation. These results have paved the way for using other chemically modified nts in sliRNAs that may enhance their in vivo stability and transportability to facilitate their in vivo applications.

molecular biology↗

Hijacking Cellular S-Acylation with Molecular Assemblies Rewires Oncogenic Signaling

KRAS-mutant cancers are generally treated by suppressing oncogenic signaling. Here, we investigated whether endogenous lipidation machinery could instead be used to spatially perturb that signaling. The thioester-bearing peptide precursor Stb-DPhe-DPhe-SAc (1) potently reduced PANC-1 cell viability and formed a palmitoylated product in treated cells. Synthetic palmitoylated 1 displayed increased assembly propensity, while fluorescent analogue 2 accumulated at the Golgi in a 2-bromopalmitate-sensitive manner. Compound 1 increased plasma-membrane-associated KRAS staining and ERK/AKT phosphorylation and induced pronounced LC3B and p62 remodeling. Inhibition of palmitoylation suppressed Golgi accumulation, attenuated the LC3B response, and rescued cell viability. These findings support a model in which cellular S-acylation drives organelle-localized molecular assembly that perturbs KRAS localization, oncogenic signaling, and associated stress responses. This work identifies endogenous lipidation machinery as a synthetic handle for spatial control of cancer signaling.

molecular biology↗