Rapid localized flank inflation and implications for potential slope instability at Tungurahua volcano, Ecuador

This is the final version. Available on open access from Elsevier via the DOI in this recordHigh rates of volcano surface deformation can be indicative of a forthcoming eruption, but can also relate to slope instability and possible flank collapse. Tungurahua volcano, Ecuador, has been persistently active since 1999 and has previously experienced catastrophic flank failures. During the ongoing eruptive activity, significant surface deformation has been observed, with the highest rates contained within the amphitheatre-shaped scar from the 3000-year-old failure on the west flank However, the cause of this asymmetric deformation and how it might relate to slope stability has not been assessed. Here, for the first time, we present a range of models to test physical processes that might produce asymmetric deformation, which are then applied to slope stability. Our models are informed by InSAR measurements of a deformation episode in November 2015, which show a maximum displacement of ~3.5 cm over a period of ~3 weeks, during which time the volcano also experienced multiple explosions and heightened seismicity. Asymmetric flank material properties, from the rebuilding of the cone, cannot explain the full magnitude and spatial footprint of the observed west flank deformation. The inflation is inferred to be primarily caused by shallow, short35 term, pre-eruptive magma storage that preferentially exploits the 3 ka flank collapse surface. Shallow and rapid pressurization from this inclined deformation source can generate shear stress along the collapse surface, which increases with greater volumes of magma. This may contribute to slope instability during future unrest episodes and promote flank failure, with general application to other volcanoes worldwide displaying asymmetric deformation patterns.Royal SocietyNatural Environment Research Council (NERC)Economic and Social Research Council (ESRC

A quantitative modular modeling approach reveals the effects of different A20 feedback implementations for the NF-κB signaling dynamics

Signaling pathways involve complex molecular interactions and are controled by non-linear regulatory mechanisms. If details of regulatory mechanisms are not fully elucidated, they can be implemented by different, equally reasonable mathematical representations in computational models. The study presented here focusses on NF-κB signaling, which is regulated by negative feedbacks via IκBα and A20. A20 inhibits NF-κB activation indirectly through interference with proteins that transduce the signal from the TNF receptor complex to activate the IκB kinase (IKK) complex. A number of pathway models has been developed implementing the A20 effect in different ways. We here focus on the question how different A20 feedback implementations impact the dynamics of NF-κB. To this end, we develop a modular modeling approach that allows combining previously published A20 modules with a common pathway core module. The resulting models are fitted to a published comprehensive experimental data set and therefore show quantitatively comparable NF-κB dynamics. Based on defined measures for the initial and long-term behavior we analyze the effects of a wide range of changes in the A20 feedback strength, the IκBα feedback strength and the TNFα stimulation strength on NF-κB dynamics. This shows similarities between the models but also model-specific differences. In particular, the A20 feedback strength and the TNFα stimulation strength affect initial and long-term NF-κB concentrations differently in the analyzed models. We validated our model predictions experimentally by varying TNFα concentrations applied to HeLa cells. These time course data indicate that only one of the A20 feedback models appropriately describes the impact of A20 on the NF-κB dynamics in this cell type

RC3H1 post-transcriptionally regulates A20 mRNA and modulates the activity of the IKK/NF-kappa B pathway

The RNA-binding protein RC3H1 (also known as ROQUIN) promotes TNF alpha mRNA decay via a 3'UTR constitutive decay element (CDE). Here we applied PAR-CLIP to human RC3H1 to identify similar to 3, 800 mRNA targets with 416, 000 binding sites. A large number of sites are distinct from the consensus CDE and revealed a structure-sequence motif with U-rich sequences embedded in hairpins. RC3H1 binds preferentially short-lived and DNA damage-induced mRNAs, indicating a role of this RNA-binding protein in the post-transcriptional regulation of the DNA damage response. Intriguingly, RC3H1 affects expression of the NF-kappa B pathway regulators such as I kappa B alpha and A20. RC3H1 uses ROQ and Zn-finger domains to contact a binding site in the A20 30UTR, demonstrating a not yet recognized mode of RC3H1 binding. Knockdown of RC3H1 resulted in increased A20 protein expression, thereby interfering with I kappa B kinase and NF-kappa B activities, demonstrating that RC3H1 can modulate the activity of the IKK/NF-kappa B pathway

Understanding cyclic seismicity and ground deformation patterns at volcanoes: intriguing lessons from Tungurahua volcano, Ecuador

Cyclic seismicity and ground deformation patterns are observed on many volcanoes worldwide where seismic swarms and the tilt of the volcanic flanks provide sensitive tools to assess the state of volcanic activity. Ground deformation at active volcanoes is often interpreted as pressure changes in a magmatic reservoir, and tilt is simply translated accordingly into inflation and deflation of such a reservoir. Tilt data recorded by an instrument in the summit area of Tungurahua volcano in Ecuador, however, show an intriguing and unexpected behaviour on several occasions: prior to a Vulcanian explosion when a pressurisation of the system would be expected, the tilt signal declines significantly, hence indicating depressurisation. At the same time, seismicity increases drastically. Envisaging that such a pattern could carry the potential to forecast Vulcanian explosions on Tungurahua, we use numerical modelling and reproduce the observed tilt patterns in both space and time. We demonstrate that the tilt signal can be more easily explained as caused by shear stress due to viscous flow resistance, rather than by pressurization of the magmatic plumbing system. In general, our numerical models prove that if magma shear viscosity and ascent rate are high enough, the resulting shear stress is sufficient to generate a tilt signal as observed on Tungurahua. Furthermore, we address the interdependence of tilt and seismicity through shear stress partitioning and suggest that a joint interpretation of tilt and seismicity can shed new light on the eruption potential of silicic volcanoes