Several recent studies have demonstrated the importance of crustal corrections when inverting surface wave data to model lateral variations in mantle radial anisotropy. It has also been shown that the choice of the prior crustal model to correct the data can strongly influence the anisotropy model and potentially lead to different geodynamic interpretations. In comparing tomographic models of radial anisotropy obtained from different crustal corrections, these studies did not, however, determine quantitative model uncertainties. Nevertheless, mantle models resulting from different prior crustal corrections are statistically different only if the posterior model errors stemming from the non-uniqueness of the inverse problem are smaller than the effect of the crustal correction itself. Here, we applied a model space search approach to global fundamental and higher mode Rayleigh and Love wave phase velocity maps to determine reliable, quantitative model uncertainties on seismic velocities and radial anisotropy. The technique employed enabled us to describe the model space with a posterior probability density function, and therefore to test whether models obtained from different crustal corrections are statistically different. We thus assessed the significance of the choice of the crustal model by comparing the posterior model errors to the differences in mantle structure resulting from different crustal corrections. We tested prior crustal models CRUST2.0, CRUST1.0 and 3SMAC. Our study shows that the use of prior crustal corrections from different crustal models yields significant discrepancies in mantle velocities around 50 km depth and in radialanisotropy down to 100 km. The impact of the crustal correction on radial anisotropy can extend down to 250 km in some locations. We found that choosing 3SMAC instead of the other crustal models has a stronger influence on the mantle model, but that CRUST1.0 and CRUST2.0 yield statistically identical anisotropy models at all depths, except at a few grid cells. Importantly, the effect of the crustal model is most significant in continental regions and not so much beneath oceans, which has important consequences for determining the depth of continental roots. Our results therefore suggest that improving constraints on crustal structure in continents is essential for our understanding of continent formation. Our work also demonstrates that the prior crustal model does not significantly affect radial anisotropy and velocities at depths greater than 100 km. This implies that if geodynamic interpretations of radial anisotropy below 100 km depth were to account for tomographic model uncertainties, they would not depend on the choice of the prior crustal model. It is therefore important for geodynamicists and seismologists to work in concert and to put effort into determining quantitative tomographic model uncertainties before interpreting the results. Our results also caution against the use of 3SMAC to correct surface wave data for studies of the continental lithosphere and suggest that the solid Earth community would benefit from putting some efforts towards building a revised 3SMAC. The discrepancies between mantle models built based on 3SMAC crustal corrections and those based on CRUST1.0 or CRUST2.0 should also help shed light on the validity of the geodynamical assumptions made in the construction of models like 3SMAC.

The boundary between the lithosphere and asthenosphere is associated with a plate-wide high seismic velocity “lid” overlying lowered velocities, consistent with thermal models. Seismic body waves also intermittently detect a sharp velocity reduction at similar depths, the Gutenberg (G) discontinuity, which cannot be explained by temperature alone. We compared an anisotropic tomography model with detections of the G to evaluate their context and relation to the lithosphere-asthenosphere boundary (LAB). We find that the G is primarily associated with vertical changes in azimuthal anisotropy and lies above a thermally controlled LAB, implying the two are not equivalent interfaces. The origin of the G is a result of frozen-in lithospheric structures, regional compositional variations of the mantle, or dynamically perturbed LAB.

The boundary between the lithosphere and asthenosphere is associated with a platewide high-seismic velocity "lid" overlying lowered velocities, consistent with thermal models. Seismic body waves also intermittently detect a sharp velocity reduction at similar depths, the Gutenberg (G) discontinuity, which cannot be explained by temperature alone. We compared an anisotropic tomography model with detections of the G to evaluate their context and relation to the lithosphere-asthenosphere boundary (LAB). We find that the G is primarily associated with vertical changes in azimuthal anisotropy and lies above a thermally controlled LAB, implying that the two are not equivalent interfaces. The origin of the G is a result of frozen-in lithospheric structures, regional compositional variations of the mantle, or dynamically perturbed LAB.

RNA helicases are a class of enzymes that unwind RNA duplexes in vitro but whose cellular functions are largely enigmatic. Here, we provide evidence that the DEAD-box protein Dbp2 remodels RNA-protein complex (RNP) structure to facilitate efficient termination of transcription in Saccharomyces cerevisiae via the Nrd1-Nab3-Sen1 (NNS) complex. First, we find that loss of DBP2 results in RNA polymerase II accumulation at the 3' ends of small nucleolar RNAs and a subset of mRNAs. In addition, Dbp2 associates with RNA sequence motifs and regions bound by Nrd1 and can promote its recruitment to NNS-targeted regions. Using Structure-seq, we find altered RNA/RNP structures in dbp2∆ cells that correlate with inefficient termination. We also show a positive correlation between the stability of structures in the 3' ends and a requirement for Dbp2 in termination. Taken together, these studies provide a role for RNA remodeling by Dbp2 and further suggests a mechanism whereby RNA structure is exploited for gene regulation.

Volatile organic compounds (VOCs) emanating from humans have the potential to revolutionize non-invasive diagnostics. Yet, little is known about how these compounds are generated by complex biological systems, and even less is known about how these compounds are reflective of a particular physiological state. In this proof-of-concept study, we examined VOCs produced directly at the cellular level from B lymphoblastoid cells upon infection with three live influenza virus subtypes: H9N2 (avian), H6N2 (avian), and H1N1 (human). Using a single cell line helped to alleviate some of the complexity and variability when studying VOC production by an entire organism, and it allowed us to discern marked differences in VOC production upon infection of the cells. The patterns of VOCs produced in response to infection were unique for each virus subtype, while several other non-specific VOCs were produced after infections with all three strains. Also, there was a specific time course of VOC release post infection. Among emitted VOCs, production of esters and other oxygenated compounds was particularly notable, and these may be attributed to increased oxidative stress resulting from infection. Elucidating VOC signatures that result from the host cells response to infection may yield an avenue for non-invasive diagnostics and therapy of influenza and other viral infections.