Highly variable magmatic accretion at the ultraslow-spreading Gakkel Ridge.

Crustal accretion at mid-ocean ridges governs the creation and evolution of the oceanic lithosphere. Generally accepted models1-4 of passive mantle upwelling and melting predict notably decreased crustal thickness at a spreading rate of less than 20 mm year-1. We conducted the first, to our knowledge, high-resolution ocean-bottom seismometer (OBS) experiment at the Gakkel Ridge in the Arctic Ocean and imaged the crustal structure of the slowest-spreading ridge on the Earth. Unexpectedly, we find that crustal thickness ranges between 3.3 km and 8.9 km along the ridge axis and it increased from about 4.5 km to about 7.5 km over the past 5 Myr in an across-axis profile. The highly variable crustal thickness and relatively large average value does not align with the prediction of passive mantle upwelling models. Instead, it can be explained by a model of buoyant active mantle flow driven by thermal and compositional density changes owing to melt extraction. The influence of active versus passive upwelling is predicted to increase with decreasing spreading rate. The process of active mantle upwelling is anticipated to be primarily influenced by mantle temperature and composition. This implies that the observed variability in crustal accretion, which includes notably varied crustal thickness, is probably an inherent characteristic of ultraslow-spreading ridges.

Extensional tectonics and two-stage crustal accretion at oceanic transform faults.

Oceanic transform faults are seismically and tectonically active plate boundaries1 that leave scars-known as fracture zones-on oceanic plates that can cross entire ocean basins2. Current descriptions of plate tectonics assume transform faults to be conservative two-dimensional strike-slip boundaries1,3, at which lithosphere is neither created nor destroyed and along which the lithosphere cools and deepens as a function of the age of the plate4. However, a recent compilation of high-resolution multibeam bathymetric data from 41 oceanic transform faults and their associated fracture zones that covers all possible spreading rates shows that this assumption is incorrect. Here we show that the seafloor along transform faults is systemically deeper (by up to 1.6 kilometres) than their associated fracture zones, in contrast to expectations based on plate-cooling arguments. Accretion at intersections between oceanic ridges and transform faults seems to be strongly asymmetric: the outside corners of the intersections show shallower relief and more extensive magmatism, whereas the inside corners have deep nodal basins and seem to be magmatically starved. Three-dimensional viscoplastic numerical models show that plastic-shear failure within the deformation zone around the transform fault results in the plate boundary experiencing increasingly oblique shear at increasing depths below the seafloor. This results in extension around the inside corner, which thins the crust and lithosphere at the transform fault and is linked to deepening of the seafloor along the transform fault. Bathymetric data suggest that the thinned transform-fault crust is augmented by a second stage of magmatism as the transform fault intersects the opposing ridge axis. This makes accretion at transform-fault systems a two-stage process, fundamentally different from accretion elsewhere along mid-ocean ridges.

Gondwanan flood basalts linked seismically to plume-induced lithosphere instability.

Delamination of the continental lithospheric mantle is well recorded beneath several continents. However, the fate of the removed continental lithosphere has been rarely noted, unlike subducted slabs reasonably well imaged in the upper and mid mantle. Beneath former Gondwana, recent seismic tomographic models indicate the presence of at least 5 horizontal fast-wavespeed anomalies at ~600 km depths that do not appear to be related to slab subduction, including fast structures in locations consistent with delamination associated with the Paraná Flood Basalt event at ~134 Ma and the Deccan Traps event at ~66 Ma. These fast-wavespeed anomalies often lie above broad slow seismic wavespeed trunks at 500 to 700 km depths beneath former Gondwana, with slow wavespeed anomalies branching around them. Numerical experiments indicate that delaminated lithosphere tends to stagnate in the transition zone and mid-mantle above a mantle plume where it shapes subsequent plume upwelling. For hot plumes, the melt volume generated during plume-influenced delamination can easily reach ~2 to 4 × 106 km3, consistent with the basalt eruption volume at the Deccan Traps. This seismic and numerical evidence suggests that observed high-wavespeed mid-mantle anomalies beneath the locations of former flood basalts are delaminated fragments of former continental lithosphere, and that lithospheric delamination events in the presence of subcontinental plumes induced several of the continental flood basalts associated with the multiple breakup stages of Gondwanaland. Continued upwelling in these plumes can also have entrained subcontinental lithosphere in the mid-mantle to bring its distinctive geochemical signal to the modern mid-ocean spreading centers that surround southern and western Africa.

Transmogrification of ocean into continent: implications for continental evolution.

When continents collide, the typical embayments and protrusions along their rifted margins make it likely that fragments of seafloor will be trapped within the growing orogenic belt. These trapped seafloor fragments become preferential depocenters for marine and terrestrial sedimentation. After ∼0.5 Gy, the high radioactivity of their thick terrigenous sediment pile converts former seafloor into a unique form of continental crust and underlying lithosphere. We call this process transmogrification. Initially strong and low-lying basins that act as mechanically stronger blocks in the collisional orogeny will eventually warm, weaken, and thermoisostatically rise and will eventually transform into preferred sites for future continental rifting. In modern Asia, transmogrifying basins have induced the characteristic paired-mountain belt geomorphology associated with the assembly of this supercontinent, for example, the Himalaya/Tibet + Tian Shan surrounding the Tarim Basin that has greatly strengthened the East Asian Monsoon. The time-dependent temperature, uplift, and strength changes associated with transmogrification are relevant for improving our understanding of continental evolution, basin modeling, paleoclimate studies, and natural resources prospection.

Seismic constraints and geodynamic implications of differential lithosphere-asthenosphere flow revealed in East Asia.

During the last 50 Ma, the East Asian continent has been a zone of massive continental collision and lithospheric deformation. While the consequences of this for Asian surface and lithospheric deformation have been intensively studied over the past 4 decades, the relationships between lithospheric deformation and underlying asthenospheric flow have been more difficult to constrain. Here we present a high resolution 3-D azimuthal anisotropy model for the northeastern Tibetan Plateau and its eastward continuation based on surface-wave tomography and shear-wave splitting measurements. This model shows that eastward lateral flow of asthenosphere beneath the northeastern Tibetan Plateau is being blocked by thick Ordos and Sichuan cratonic keels. The damming effect of these keels induces flow to first rotate around the Ordos keel and then transition into strong east-west flow beneath the thinner lithosphere that forms the lithospheric suture between the two cratonic keels. We further find that asthenosphere flow directions can differ from those of overlying lithosphere, with the asthenosphere neither being passively dragged by overlying lithosphere, nor being able to drag the overlying plate to mimic its subsurface flow. Finally, the region of eastward-channeled asthenospheric flow from Tibet underlies a belt of stronger intracontinental deformation in eastern China.

Causes and consequences of asymmetric lateral plume flow during South Atlantic rifting.

Volcanic rifted margins are typically associated with a thick magmatic layer of seaward dipping reflectors and anomalous regional uplift. This is conventionally interpreted as due to melting of an arriving mantle plume head at the onset of rifting. However, seaward dipping reflectors and uplift are sometimes asymmetrically distributed with respect to the subsequent plume track. Here we investigate if these asymmetries are induced by preexisting lateral variations in the thickness of continental lithosphere and/or lithospheric stretching rates, variations that promote lateral sublithospheric flow of plume material below only one arm of the extending rift. Using three-dimensional numerical experiments, we find that South Atlantic rifting is predicted to develop a strong southward asymmetry in its distribution of seaward dipping reflectors and associated anomalous relief with respect to the Tristan Plume that "drove" this volcanic rifted margin, and that the region where plume material drains into the rift should experience long-lived uplift during rifting-both as observed. We conclude that a mantle plume is still needed to source the anomalously hot sublithospheric material that generates a volcanic rifted margin, but lateral along-rift flow from this plume, not a broad starting plume head, is what controls when and where a volcanic rifted margin will form.

Shiga toxin sub-type 2a increases the efficiency of Escherichia coli O157 transmission between animals and restricts epithelial regeneration in bovine enteroids.

Specific Escherichia coli isolates lysogenised with prophages that express Shiga toxin (Stx) can be a threat to human health, with cattle being an important natural reservoir. In many countries the most severe pathology is associated with enterohaemorrhagic E. coli (EHEC) serogroups that express Stx subtype 2a. In the United Kingdom, phage type (PT) 21/28 O157 strains have emerged as the predominant cause of life-threatening EHEC infections and this phage type commonly encodes both Stx2a and Stx2c toxin types. PT21/28 is also epidemiologically linked to super-shedding (>103 cfu/g of faeces) which is significant for inter-animal transmission and human infection as demonstrated using modelling studies. We demonstrate that Stx2a is the main toxin produced by stx2a+/stx2c+ PT21/28 strains induced with mitomycin C and this is associated with more rapid induction of gene expression from the Stx2a-encoding prophage compared to that from the Stx2c-encoding prophage. Bacterial supernatants containing either Stx2a and/or Stx2c were demonstrated to restrict growth of bovine gastrointestinal organoids with no restriction when toxin production was not induced or prevented by mutation. Isogenic strains that differed in their capacity to produce Stx2a were selected for experimental oral colonisation of calves to assess the significance of Stx2a for both super-shedding and transmission between animals. Restoration of Stx2a expression in a PT21/28 background significantly increased animal-to-animal transmission and the number of sentinel animals that became super-shedders. We propose that while both Stx2a and Stx2c can restrict regeneration of the epithelium, it is the relatively rapid and higher levels of Stx2a induction, compared to Stx2c, that have contributed to the successful emergence of Stx2a+ E. coli isolates in cattle in the last 40 years. We propose a model in which Stx2a enhances E. coli O157 colonisation of in-contact animals by restricting regeneration and turnover of the colonised gastrointestinal epithelium.

Metabolic acidosis in a lactating woman induced by a deliberate ketogenic diet.

ABSTRACT: This article describes a rare case of lactation ketoacidosis in a patient who started a ketogenic diet while nursing an infant and toddler. The patient presented to the ED with a history of nausea, vomiting, and postural dizziness, and was found to have a significant metabolic acidosis and elevated lipase level. The metabolic changes induced in this patient could occur in anyone with high metabolic demands who also is on a strict ketogenic diet. The case highlights the importance of a dietary history in patients with unexplained metabolic derangements.

Hybrid shallow on-axis and deep off-axis hydrothermal circulation at fast-spreading ridges.

Hydrothermal flow at oceanic spreading centres accounts for about ten per cent of all heat flux in the oceans and controls the thermal structure of young oceanic plates. It also influences ocean and crustal chemistry, provides a basis for chemosynthetic ecosystems, and has formed massive sulphide ore deposits throughout Earth's history. Despite this, how and under what conditions heat is extracted, in particular from the lower crust, remains largely unclear. Here we present high-resolution, whole-crust, two- and three-dimensional simulations of hydrothermal flow beneath fast-spreading ridges that predict the existence of two interacting flow components, controlled by different physical mechanisms, that merge above the melt lens to feed ridge-centred vent sites. Shallow on-axis flow structures develop owing to the thermodynamic properties of water, whereas deeper off-axis flow is strongly shaped by crustal permeability, particularly the brittle-ductile transition. About 60 per cent of the discharging fluid mass is replenished on-axis by warm (up to 300 degrees Celsius) recharge flow surrounding the hot thermal plumes, and the remaining 40 per cent or so occurs as colder and broader recharge up to several kilometres away from the axis that feeds hot (500-700 degrees Celsius) deep-rooted off-axis flow towards the ridge. Despite its lower contribution to the total mass flux, this deep off-axis flow carries about 70 per cent of the thermal energy released at the ridge axis. This combination of two flow components explains the seismically determined thermal structure of the crust and reconciles previously incompatible models favouring either shallower on-axis or deeper off-axis hydrothermal circulation.

Symposium: Reflections Before, During, and Beyond COVID-19: Reflections on a Secular Age: Dharmasastric and Confucian Social Orderings.

The modern world is often described as highly secularized. This secularization can distort our view of the past, and also of societies in which secularization holds less sway than in other places. In this essay, I examine Confucianism and Dharmasastra as two paradigms for the study of pre-secular or non-secular societies, comparing and contrasting Confucian and Hindu societies while comparing and contrasting both with the current, "secular age".

Sustained translational repression by eIF2α-P mediates prion neurodegeneration.

The mechanisms leading to neuronal death in neurodegenerative disease are poorly understood. Many of these disorders, including Alzheimer's, Parkinson's and prion diseases, are associated with the accumulation of misfolded disease-specific proteins. The unfolded protein response is a protective cellular mechanism triggered by rising levels of misfolded proteins. One arm of this pathway results in the transient shutdown of protein translation, through phosphorylation of the α-subunit of eukaryotic translation initiation factor, eIF2. Activation of the unfolded protein response and/or increased eIF2α-P levels are seen in patients with Alzheimer's, Parkinson's and prion diseases, but how this links to neurodegeneration is unknown. Here we show that accumulation of prion protein during prion replication causes persistent translational repression of global protein synthesis by eIF2α-P, associated with synaptic failure and neuronal loss in prion-diseased mice. Further, we show that promoting translational recovery in hippocampi of prion-infected mice is neuroprotective. Overexpression of GADD34, a specific eIF2α-P phosphatase, as well as reduction of levels of prion protein by lentivirally mediated RNA interference, reduced eIF2α-P levels. As a result, both approaches restored vital translation rates during prion disease, rescuing synaptic deficits and neuronal loss, thereby significantly increasing survival. In contrast, salubrinal, an inhibitor of eIF2α-P dephosphorylation, increased eIF2α-P levels, exacerbating neurotoxicity and significantly reducing survival in prion-diseased mice. Given the prevalence of protein misfolding and activation of the unfolded protein response in several neurodegenerative diseases, our results suggest that manipulation of common pathways such as translational control, rather than disease-specific approaches, may lead to new therapies preventing synaptic failure and neuronal loss across the spectrum of these disorders.

Global Regulator of Virulence A (GrvA) Coordinates Expression of Discrete Pathogenic Mechanisms in Enterohemorrhagic Escherichia coli through Interactions with GadW-GadE.

UNLABELLED: Global regulator of virulence A (GrvA) is a ToxR-family transcriptional regulator that activates locus of enterocyte effacement (LEE)-dependent adherence in enterohemorrhagic Escherichia coli (EHEC). LEE activation by GrvA requires the Rcs phosphorelay response regulator RcsB and is sensitive to physiologically relevant concentrations of bicarbonate, a known stimulant of virulence systems in intestinal pathogens. This study determines the genomic scale of GrvA-dependent regulation and uncovers details of the molecular mechanism underlying GrvA-dependent regulation of pathogenic mechanisms in EHEC. In a grvA-null background of EHEC strain TW14359, RNA sequencing analysis revealed the altered expression of over 700 genes, including the downregulation of LEE- and non-LEE-encoded effectors and the upregulation of genes for glutamate-dependent acid resistance (GDAR). Upregulation of GDAR genes corresponded with a marked increase in acid resistance. GrvA-dependent regulation of GDAR and the LEE required gadE, the central activator of GDAR genes and a direct repressor of the LEE. Control of gadE by GrvA was further determined to occur through downregulation of the gadE activator GadW. This interaction of GrvA with GadW-GadE represses the acid resistance phenotype, while it concomitantly activates the LEE-dependent adherence and secretion of immune subversion effectors. The results of this study significantly broaden the scope of GrvA-dependent regulation and its role in EHEC pathogenesis. IMPORTANCE: Enterohemorrhagic Escherichia coli (EHEC) is an intestinal human pathogen causing acute hemorrhagic colitis and life-threatening hemolytic-uremic syndrome. For successful transmission and gut colonization, EHEC relies on the glutamate-dependent acid resistance (GDAR) system and a type III secretion apparatus, encoded on the LEE pathogenicity island. This study investigates the mechanism whereby the DNA-binding regulator GrvA coordinates activation of the LEE with repression of GDAR. Investigating how these systems are regulated leads to an understanding of pathogenic behavior and novel strategies aimed at disease prevention and control.

The role for TolA in enterohemorrhagic Escherichia coli pathogenesis and virulence gene transcription.

Loss of the periplasm spanning protein TolA in Escherichia coli leads to activation of the Rcs phosphorelay, and is required for full virulence in Gram-negative pathogens such as Salmonella enterica and Dickeya dadantii. This study explores the role for TolA in the pathogenesis of enterohemorrhagic E. coli (EHEC) and the effect of its mutation on the transcription of key EHEC virulence genes controlled by Rcs phosphorelay, including the type III secretion system (T3SS) (espA and tir), the E. coli common pilus (ecpA), and motility (fliC). Promoter activity for T3SS regulator ler was substantially higher following inactivation of tolA, and corresponded with a similar elevation in espA and tir transcription. Likewise, ecpA transcription was increased in EHECΔtolA. Conversely, and in-line with previous studies, inactivation of tolA resulted in complete loss of motility and decreased fliC transcription. For all genes examined, altered transcription observed for EHECΔtolA was dependent on the outer-membrane lipoprotein RcsF. Despite elevated virulence gene transcription, in tolA deleted strains virulence of EHEC in the Galleria mellonella wax worm model was substantially attenuated in a manner at least partly dependent on RcsF, and adherence to cultured HT-29 colonic epithelial cells was markedly reduced. The results of this study broaden the role for TolA in EHEC pathogenesis, and suggest that significant outer-membrane perturbations are able to promote transcription of important EHEC adherence factors.

Near-isothermal conditions in the middle and lower crust induced by melt migration.

The thermal structure of the crust strongly influences deformation, metamorphism and plutonism. Models for the geothermal gradient in stable crust predict a steady increase of temperature with depth. This thermal structure, however, is incompatible with observations from high-temperature metamorphic terranes exhumed in orogens. Global compilations of peak conditions in high-temperature metamorphic terranes define relatively narrow ranges of peak temperatures over a wide range in pressure, for both isothermal decompression and isobaric cooling paths. Here we develop simple one-dimensional thermal models that include the effects of melt migration. These models show that long-lived plutonism results in a quasi-steady-state geotherm with a rapid temperature increase in the upper crust and nearly isothermal conditions in the middle and lower crust. The models also predict that the upward advection of heat by melt generates granulite facies metamorphism, and widespread andalusite-sillimanite metamorphism in the upper crust. Once the quasi-steady-state thermal profile is reached, the middle and lower crust are greatly weakened due to high temperatures and anatectic conditions, thus setting the stage for gravitational collapse, exhumation and isothermal decompression after the onset of plutonism. Near-isothermal conditions in the middle and lower crust result from the thermal buffering effect of dehydration melting reactions that, in part, control the shape of the geotherm.

RcsB determines the locus of enterocyte effacement (LEE) expression and adherence phenotype of Escherichia coli O157 : H7 spinach outbreak strain TW14359 and coordinates bicarbonate-dependent LEE activation with repression of motility.

The 2006 US spinach outbreak of Escherichia coli O157 : H7, characterized by unusually severe disease, has been attributed to a strain (TW14359) with enhanced pathogenic potential, including elevated virulence gene expression, robust adherence and the presence of novel virulence factors. This study proposes a mechanism for the unique virulence expression and adherence phenotype of this strain, and further expands the role for regulator RcsB in control of the E. coli locus of enterocyte effacement (LEE) pathogenicity island. Proteomic analysis of TW14359 revealed a virulence proteome consistent with previous transcriptome studies that included elevated levels of the LEE regulatory protein Ler and type III secretion system (T3SS) proteins, secreted T3SS effectors and Shiga toxin 2. Basal levels of the LEE activator and Rcs phosphorelay response regulator, RcsB, were increased in strain TW14359 relative to O157 : H7 strain Sakai. Deletion of rcsB eliminated inherent differences between these strains in ler expression, and in T3SS-dependent adherence. A reciprocating regulatory pathway involving RcsB and LEE-encoded activator GrlA was identified and predicted to co-ordinate LEE activation with repression of the flhDC flagellar regulator and motility. Overexpression of grlA was shown to increase RcsB levels, but did not alter expression from promoters driving rcsB transcription. Expression of rcsDB and RcsB was determined to increase in response to physiological levels of bicarbonate, and bicarbonate-dependent stimulation of the LEE was shown to be dependent on an intact Rcs system and ler activator grvA. The results of this study significantly broaden the role for RcsB in enterohaemorrhagic E. coli virulence regulation.

W. Jason Morgan (1935-2023).

Discoverer of plate tectonics and mantle plumes.

Modelling Cancer Metastasis in Drosophila melanogaster.

Cancer metastasis, the process by which tumour cells spread throughout the body and form secondary tumours at distant sites, is the leading cause of cancer-related deaths. The metastatic cascade is a highly complex process encompassing initial dissemination from the primary tumour, travel through the blood stream or lymphatic system, and the colonisation of distant organs. However, the factors enabling cells to survive this stressful process and adapt to new microenvironments are not fully characterised. Drosophila have proven a powerful system in which to study this process, despite important caveats such as their open circulatory system and lack of adaptive immune system. Historically, larvae have been used to model cancer due to the presence of pools of proliferating cells in which tumours can be induced, and transplanting these larval tumours into adult hosts has enabled tumour growth to be monitored over longer periods. More recently, thanks largely to the discovery that there are stem cells in the adult midgut, adult models have been developed. We focus this review on the development of different Drosophila models of metastasis and how they have contributed to our understanding of important factors determining metastatic potential, including signalling pathways, the immune system and the microenvironment.

New constraints on Cenozoic subduction between India and Tibet.

The type of lithosphere subducted between India and Tibet since the Paleocene remains controversial; it has been suggested to be either entirely continental, oceanic, or a mixture of the two. As the subduction history of this lost lithosphere strongly shaped Tibetan intraplate tectonism, we attempt to further constrain its nature and density structure with numerical models that aim to reproduce the observed history of magmatism and crustal thickening in addition to present-day plateau properties between 83°E and 88°E. By matching time-evolving geological patterns, here we show that Tibetan tectonism away from the Himalayan syntaxis is consistent with the initial indentation of a craton-like terrane at 55 ± 5 Ma, followed by a buoyant tectonic plate with a thin crust, e.g., a broad continental margin (Himalandia). This new geodynamic scenario can explain the seemingly contradictory observations that had led to competing hypotheses like the subduction of Greater India versus largely oceanic subduction prior to Indian indentation.

Mechanism of progressive broad deformation from oceanic transform valley to off-transform faulting and rifting.

Oceanic transform faults (TFs) are commonly viewed as single, narrow strike-slip seismic faults that offset two mid-ocean ridge segments. However, broad zones of complex deformation are ubiquitous at TFs. Here, we propose a new conceptual model for the progressive deformation within broad zones at oceanic TFs through detailed morphological, seismic, and stress analyses. We argue that, under across-transform extension due to a change in plate motion, plate deformation occurs first along high-angle transtensional faults (TTFs) within the transform valleys. Off-transform normal faults (ONFs) form when across-transform deviatoric extensional stresses exceed the yield strength of the adjacent oceanic lithosphere. With further extension, these normal faults can develop into off-transform rift zones (ORZs), some of which can further develop into transform plate boundaries. We illustrate that such progressive complex deformation is an inherent feature of oceanic TFs. The new conceptual model provides a unifying theory to explain the observed broad deformation at global transform systems.

A strength inversion origin for non-volcanic tremor.

Non-volcanic tremor is a particularly enigmatic form of seismic activity. In its most studied subduction zone setting, tremor typically occurs within the plate interface at or near the shallow and deep edges of the interseismically locked zone. Detailed seismic observations have shown that tremor is composed of repeating small low-frequency earthquakes, often accompanied by very-low-frequency earthquakes, all involving shear failure and slip. However, low-frequency earthquakes and very-low-frequency earthquakes within each cluster show nearly constant source durations for all observed magnitudes, which implies characteristic tremor sub-event sources of near-constant size. Here we integrate geological observations and geomechanical lab measurements on heterogeneous rock assemblages representative of the shallow tremor region offshore the Middle America Trench with numerical simulations to demonstrate that these tremor events are consistent with the seismic failure of relatively weaker blocks within a stronger matrix. In these subducting rocks, hydrothermalism has led to a strength-inversion from a weak matrix with relatively stronger blocks to a stronger matrix with embedded relatively weaker blocks. Tremor naturally occurs as the now-weaker blocks fail seismically while their surrounding matrix has not yet reached a state of general seismic failure.