Late Cretaceous to Recent Deformation Related to Inherited Structures and Subsequent Compression within the Persian Gulf: A 2D Seismic Case Study

The Persian Gulf is part of an asymmetric foreland basin related to the Zagros Orogen. Few published studies of this basin and associated onshore areas include seismic reflection data. We present a seismic-stratigraphic interpretation based on marine 2D seismic data, which reveals the presence of two types of compressional structures within the basin: (1) faulted domes related to salt movement and the offshore trace of a NNE–SSW-trending dextral basement fault (the Kazerun Fault); (2) long-wavelength (16 km), low-amplitude (60 ms two-way travel time) folds relating to the advancing deformation front associated with the orogen. Thinning of age-constrained stratal units across structures related to the offshore trace of the Kazerun Fault implies a distinct pulse of uplift on this fault during the Maastrichtian. The geometry of growth strata across other intra-basin structures suggests a second, later stage of deformation, which began in the Middle Miocene. Thickening and folding of post-Middle Miocene stratal units towards the NE (i.e. towards the Zagros Orogen) is interpreted to reflect rapid loading, subsidence and compression related to southwestwards advance of the orogen. The results of this study have implications for the interaction between pre-existing structures and later compressional events both within the Persian Gulf and elsewhere

Late Cretaceous to Recent Deformation Related to Inherited Structures and Subsequent Compression within the Persian Gulf: A 2D Seismic Case Study

The Persian Gulf is part of an asymmetric foreland basin related to the Zagros Orogen. Few published studies of this basin and associated onshore areas include seismic reflection data. We present a seismic-stratigraphic interpretation based on marine 2D seismic data, which reveals the presence of two types of compressional structures within the basin: (1) faulted domes related to salt movement and the offshore trace of a NNE–SSW-trending dextral basement fault (the Kazerun Fault); (2) long-wavelength (16 km), low-amplitude (60 ms two-way travel time) folds relating to the advancing deformation front associated with the orogen. Thinning of age-constrained stratal units across structures related to the offshore trace of the Kazerun Fault implies a distinct pulse of uplift on this fault during the Maastrichtian. The geometry of growth strata across other intra-basin structures suggests a second, later stage of deformation, which began in the Middle Miocene. Thickening and folding of post-Middle Miocene stratal units towards the NE (i.e. towards the Zagros Orogen) is interpreted to reflect rapid loading, subsidence and compression related to southwestwards advance of the orogen. The results of this study have implications for the interaction between pre-existing structures and later compressional events both within the Persian Gulf and elsewhere

Surficial fractures in the Navajo sandstone, south-western USA: the roles of thermal cycles, rainstorms, granular disintegration, and iterative cracking

Deep (\u3e 5 m) sheeting fractures in the Navajo sandstone are evident at numerous sites in southern Utah and derive from tectonic stresses. Strong diurnal thermal cycles are, however, the likely triggers for shallow (\u3c 0.3 m) sheeting fractures. Data from subsurface thermal sensors reveal that large temperature differences between sensors at 2 and 15 cm depth on clear summer afternoons are as great as those that trigger sheeting fractures in exposed California granite. Extensive polygonal patterns in the Navajo sandstone are composed of surface-perpendicular fractures and were produced by contractile stresses. Numerous studies have shown that porewater diminishes the tensile strength of sandstone. Based on our thermal records, we propose that cooling during monsoonal rainstorms triggers polygonal fracturing of temporarily weakened rock. On steep outcrops, polygonal patterns are rectilinear and orthogonal, with T-vertices. Lower-angle slopes host hexagonal patterns (defined by the dominance of Y-vertices). Intermediate patterns with rectangles and hexagons of similar scale are common. We posit that outcropping fractures are advancing downward by iterative steps, and that hexagons on sandstone surfaces (like prismatic columns of basalt) have evolved from ancestral orthogonal polygons of similar scale. In lava flows, fractures elongate intermittently as they follow a steep thermal gradient (the source of stress) as it rapidly moves through the rock mass. In our model, a steep, surficial thermal gradient descends through unfractured sandstone, but at the slow pace of granular disintegration. Through time, as the friable rock on stable slopes erodes, iterative cracking advances into new space. Hexagonal patterns form as new fractures, imperfectly guided by the older ones, propagate in new directions, and vertices drift into a configuration that minimizes the ratio of fracture length to polygon area

Strain analysis of a seismically imaged mass‐transport complex, offshore Uruguay

Strain style, magnitude and distribution within mass‐transport complexes (MTCs) are important for understanding the process evolution of submarine mass flows and for estimating their runout distances. Structural restoration and quantification of strain in gravitationally driven passive margins have been shown to approximately balance between updip extensional and downdip contractional domains; such an exercise has not yet been attempted for MTCs. We here interpret and structurally restore a shallowly buried (c. 1,500 mbsf) and well‐imaged MTC, offshore Uruguay using a high‐resolution (12.5 m vertical and 15 × 12.5 m horizontal resolution) three‐dimensional seismic‐reflection survey. This allows us to characterise and quantify vertical and lateral strain distribution within the deposit. Detailed seismic mapping and attribute analysis shows that the MTC is characterised by a complicated array of kinematic indicators, which vary spatially in style and concentration. Seismic‐attribute extractions reveal several previously undocumented fabrics preserved in the MTC, including internal shearing in the form of sub‐orthogonal shear zones, and fold‐thrust systems within the basal shear zone beneath rafted‐blocks. These features suggest multiple transport directions and phases of flow during emplacement. The MTC is characterised by a broadly tripartite strain distribution, with extensional (e.g. normal faults), translational and contractional (e.g. folds and thrusts) domains, along with a radial frontally emergent zone. We also show how strain is preferentially concentrated around intra‐MTC rafted‐blocks due to their kinematic interactions with the underlying basal shear zone. Overall, and even when volume loss within the frontally emergent zone is included, a strain deficit between the extensional and contractional domains (c. 3%–14%) is calculated. We attribute this to a combination of distributed, sub‐seismic, ‘cryptic’ strain, likely related to de‐watering, grain‐scale deformation and related changes in bulk sediment volume. This work has implications for assessing MTCs strain distribution and provides a practical approach for evaluating structural interpretations within such deposits

C9ORF72 interaction with cofilin modulates actin dynamics in motor neurons.

Intronic hexanucleotide expansions in C9ORF72 are common in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, but it is unknown whether loss of function, toxicity by the expanded RNA or dipeptides from non-ATG-initiated translation are responsible for the pathophysiology. We determined the interactome of C9ORF72 in motor neurons and found that C9ORF72 was present in a complex with cofilin and other actin binding proteins. Phosphorylation of cofilin was enhanced in C9ORF72-depleted motor neurons, in patient-derived lymphoblastoid cells, induced pluripotent stem cell-derived motor neurons and post-mortem brain samples from ALS patients. C9ORF72 modulates the activity of the small GTPases Arf6 and Rac1, resulting in enhanced activity of LIM-kinases 1 and 2 (LIMK1/2). This results in reduced axonal actin dynamics in C9ORF72-depleted motor neurons. Dominant negative Arf6 rescues this defect, suggesting that C9ORF72 acts as a modulator of small GTPases in a pathway that regulates axonal actin dynamics

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

C9orf72-mediated ALS and FTD: multiple pathways to disease

The discovery that repeat expansions in the C9orf72 gene are a frequent cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) has revolutionized our understanding of these diseases. Substantial headway has been made in characterizing C9orf72-mediated disease and unravelling its underlying aetiopathogenesis. Three main disease mechanisms have been proposed: loss of function of the C9orf72 protein and toxic gain of function from C9orf72 repeat RNA or from dipeptide repeat proteins produced by repeat-associated non-ATG translation. Several downstream processes across a range of cellular functions have also been implicated. In this article, we review the pathological and mechanistic features of C9orf72-associated FTD and ALS (collectively termed C9FTD/ALS), the model systems used to study these conditions, and the probable initiators of downstream disease mechanisms. We suggest that a combination of upstream mechanisms involving both loss and gain of function and downstream cellular pathways involving both cell-autonomous and non-cell-autonomous effects contributes to disease progression