Pervasive deformation of an oceanic plate and relationship to large >Mw 8 intraplate earthquakes: The northern Wharton Basin, Indian Ocean

Large-magnitude intraplate earthquakes within the ocean basins are not well understood. The Mw 8.6 and Mw 8.2 strike-slip intraplate earthquakes on 11 April 2012, while clearly occurring in the equatorial Indian Ocean diffuse plate boundary zone, are a case in point, with disagreement on the nature of the focal mechanisms and the faults that ruptured. We use bathymetric and seismic reflection data from the rupture area of the earthquakes in the northern Wharton Basin to demonstrate pervasive brittle deformation between the Ninetyeast Ridge and the Sunda subduction zone. In addition to evidence of recent strike-slip deformation along approximately north-south–trending fossil fracture zones, we identify a new type of deformation structure in the Indian Ocean: conjugate Riedel shears limited to the sediment section and oriented oblique to the north-south fracture zones. The Riedel shears developed in the Miocene, at a similar time to the onset of diffuse deformation in the central Indian Ocean. However, left-lateral strike-slip reactivation of existing fracture zones started earlier, in the Paleocene to early Eocene, and compartmentalizes the Wharton Basin. Modeled rupture during the 11 April 2012 intraplate earthquakes is consistent with the location of two reactivated, closely spaced, approximately north-south–trending fracture zones. However, we find no evidence for WNW-ESE–trending faults in the shallow crust, which is at variance with most of the earthquake fault models

Probing the mechanisms of electron capture dissociation mass spectrometry with nitrated peptides

Previously we have shown that the presence of 3-nitrotyrosine within a peptide sequence severely depletes the peptide backbone fragments typically observed following electron capture dissociation (ECD) mass spectrometry. Instead, ECD of nitrated peptides is characterised by abundant losses of small neutrals (hydroxyl radicals, water and ammonia). Here, we investigate the origin of ammonia loss by comparing the ECD behaviour of lysine- and arginine-containing nitrated peptides, and their N-acetylated counterparts, and nitrated peptides containing no basic amino acid residues. The results reveal that ammonia loss derives from the N-terminus of the peptides, however, the key finding of this work is the insight provided into the hierarchy of various proposed ECD mechanisms: the Utah-Washington mechanism, the electron predator mechanism and the Oslo mechanism

Neotectonics of the Owen Fracture Zone (NW Indian Ocean): structural evolution of an oceanic strike-slip plate boundary

International audienceThe Owen Fracture Zone is a 800 km-long fault system that accommodates the dextral strike-slip motion between India and Arabia plates. Because of slow pelagic sedimentation rates that preserve the seafloor expression of the fault since the Early Pliocene, the fault is clearly observed on bathymetric data. It is made up of a series of fault segments separated by releasing and restraining bends, including a major pull-apart basin at latitude 20°N. Some distal turbiditic channels from the Indus deep-sea fan overlap the fault system and are disturbed by its activity, thus providing landmarks to date successive stages of fault activity and structural evolution of the Owen Fracture Zone from Pliocene to Present. We determine the durability of relay structures and the timing of their evolution along the principal displacement zone, from their inception to their extinction. We observe subsidence migration in the 20°N basin, and alternate activation of fault splays in the vicinity of the Qalhat seamount. The present-day Owen Fracture Zone is the latest stage of structural evolution of the 20-Myr-old strike-slip fault system buried under Indus turbiditic deposits whose activity started at the eastern foot of the Owen Ridge when the Gulf of Aden opened. The evolution of the Owen Fracture Zone since 3-6 Myr reflects a steady state plate motion between Arabia and India, such as inferred by kinematics for the last 20 Myr period. The structural evolution of the Owen Fracture Zone since 20 Myr- including fault segments propagation and migration, pull-apart basin opening and extinction - seems to be characterized by a progressive reorganisation of the fault system, and does not require any major kinematics change

In-situ evidence for dextral active motion at the Arabia-India plate boundary

International audienceThe Arabia-India plate boundary--also called theOwen fracture zone--is perhaps the least-known boundary among large tectonic plates1-6. Although it was identified early on as an example of a transform fault converting the divergent motion along the Carlsberg Ridge to convergent motion in the Himalayas7, its structure and rate of motion remains poorly constrained. Here we present the first direct evidence for active dextral strike-slip motion along this fault, based on seafloor multibeam mapping of the Arabia-India-Somalia triple junction in the northwest Indian Ocean. There is evidence for 12km of apparent strike-slip motion along the mapped segment of the Owen fracture zone, which is terminated to the south by a 50-km-wide pull-apart basin bounded by active faults. By evaluating these new constraints within the context of geodetic models of global plate motions, we determine a robust angular velocity for the Arabian plate relative to the Indian plate that predicts 2-4mmyr−1 dextral motion along the Owen fracture zone. This transformfault was probably initiated around 8 million years ago in response to a regional reorganization of plate velocities and directions8-11, which induced a change in configuration of the triple junction. Infrequent earthquakes of magnitude 7 and greater may occur along the Arabia-India plate boundary, unless deformation is in the formof aseismic creep

Hydrogen Bonding Constrains Free Radical Reaction Dynamics at Serine and Threonine Residues in Peptides

Free radical-initiated peptide sequencing (FRIPS) mass spectrometry derives advantage from the introduction of highly selective low-energy dissociation pathways in target peptides. An acetyl radical, formed at the peptide N-terminus via collisional activation and subsequent dissociation of a covalently attached radical precursor, abstracts a hydrogen atom from diverse sites on the peptide, yielding sequence information through backbone cleavage as well as side-chain loss. Unique free-radical-initiated dissociation pathways observed at serine and threonine residues lead to cleavage of the neighboring N-terminal C_α–C or N–C_α bond rather than the typical Cα–C bond cleavage observed with other amino acids. These reactions were investigated by FRIPS of model peptides of the form AARAAAXAA, where X is the amino acid of interest. In combination with density functional theory (DFT) calculations, the experiments indicate the strong influence of hydrogen bonding at serine or threonine on the observed free radical chemistry. Hydrogen bonding of the side-chain hydroxyl group with a backbone carbonyl oxygen aligns the singly occupied π orbital on the β-carbon and the N–C_α bond, leading to low-barrier β-cleavage of the N–C_α bond. Interaction with the N-terminal carbonyl favors a hydrogen-atom transfer process to yield stable c and z• ions, whereas C-terminal interaction leads to effective cleavage of the C_α–C bond through rapid loss of isocyanic acid. Dissociation of the C_α–C bond may also occur via water loss followed by β-cleavage from a nitrogen-centered radical. These competitive dissociation pathways from a single residue illustrate the sensitivity of gas-phase free radical chemistry to subtle factors such as hydrogen bonding that affect the potential energy surface for these low-barrier processes

Genome Wide Expression Profiling Reveals Suppression of Host Defence Responses during Colonisation by Neisseria meningitides but not N. lactamica

Both Neisseria meningitidis and the closely related bacterium Neisseria lactamica colonise human nasopharyngeal mucosal surface, but only N. meningitidis invades the bloodstream to cause potentially life-threatening meningitis and septicaemia. We have hypothesised that the two neisserial species differentially modulate host respiratory epithelial cell gene expression reflecting their disease potential. Confluent monolayers of 16HBE14 human bronchial epithelial cells were exposed to live and/or dead N. meningitidis (including capsule and pili mutants) and N. lactamica, and their transcriptomes were compared using whole genome microarrays. Changes in expression of selected genes were subsequently validated using Q-RT-PCR and ELISAs. Live N. meningitidis and N. lactamica induced genes involved in host energy production processes suggesting that both bacterial species utilise host resources. N. meningitidis infection was associated with down-regulation of host defence genes. N. lactamica, relative to N. meningitidis, initiates up-regulation of proinflammatory genes. Bacterial secreted proteins alone induced some of the changes observed. The results suggest N. meningitidis and N. lactamica differentially regulate host respiratory epithelial cell gene expression through colonisation and/or protein secretion, and that this may contribute to subsequent clinical outcomes associated with these bacteria