Deep seismic structure across the southernmost Mariana trench: Implications for arc rifting and plate hydration

Author Posting. © American Geophysical Union, 2019. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research-Solid Earth 124(5), (2019): 4710-4727, doi:10.1029/2018JB017080.The southernmost Mariana margin lacks a mature island arc and thus differs significantly from the central‐north Mariana and Izu‐Bonin margins. This paper presents a new P wave velocity model of the crust and uppermost mantle structure based on a 349‐km‐long profile of wide‐angle reflection/refraction data. The active source seismic experiment was conducted from the subducting Pacific plate to the overriding Philippine plate, passing through the Challenger Deep. The subducting plate has an average crustal thickness of ~6.0 km with Vp of 7.0 ± 0.2 km/s at the base of the crust and low values of only 5.5–6.9 km/s near the trench axis. The uppermost mantle of the subducting plate is characterized by low velocities of 7.0–7.3 km/s. The overriding plate has a maximum crustal thickness of ~18 km beneath the forearc with Vp of ~7.4 km/s at the crustal bottom and 7.5–7.8 km/s in the uppermost mantle. A zone of slight velocity reduction is imaged beneath the Southwest Mariana Rift that is undergoing active rifting. The observed significant velocity reduction in a near‐trench crustal zone of ~20–30 km in the subducting plate is interpreted as a result of faulting‐induced porosity changes and fracture‐filling fluids. The velocity reduction in the uppermost mantle of both subducting and overriding plates is interpreted as mantle serpentinization with fluid sources from dehydration of the subducting plate and/or fluid penetration along faults.Data acquisition and sample collections were supported by the Mariana Trench Initiative of the Chinese Academy of Sciences (CAS). We are grateful to the science parties and crews of R/V Shiyan 3 of the South China Sea Institute of Oceanology, CAS, for contributions to data acquisition. Constructive reviews by Robert Stern, Martha Savage, and anonymous reviewers significantly improved the manuscript. We thank Gaohua Zhu, Fan Zhang, Chunfeng Li, Zhen Sun, Zhi Wang, and Minghui Zhao for helpful discussion. The bathymetric maps were plotted using GMT (Wessel & Smith, 1995). Digital files of the velocity models and selected raw data are deposited and accessible online (at https://pan.baidu.com/s/1AbDJOgLZhYn1C‐3sg7S9Xw). This work was supported by the Strategic Priority Program of CAS (XDA13010101), CAS (Y4SL021001, QYZDY‐SSW‐DQC005, and 133244KYSB20180029), Key Laboratory of Ocean and Marginal Sea Geology, CAS (OMG18‐03), National Natural Science Foundation of China (41890813, 41676042, U1701641, 91628301, 41576041, and U1606401), and HKSAR Research Grant Council grants (14313816).2019-10-0

Regulation of tumor suppressor PDCD4 by novel protein kinase C isoforms

AbstractTransforming growth factor-β1 (TGF-β1) induces apoptosis in normal hepatocytes and hepatoma cells. PDCD4 is involved in TGF-β1-induced apoptosis via the Smad pathway. The tumor promoter 12-O-tetradecanoylphorbor-13-acetate (TPA), a protein kinase C stimulator, inhibits TGF-β1-induced apoptosis. However, the mechanisms of TPA action on PDCD4 expression remain to be elucidated. Therefore. the regulatory mechanism of PDCD4 expression by PKC was investigated. The treatment of the human hepatoma cell line, Huh7 with TPA suppressed PDCD4 protein expression and TGF-β1 failed to increase the PDCD4 protein expression. PKC inhibitors Ro-31-8425 or bisindolylmaleimide-1-hydrocholoride (pan-PKC inhibitors) and rottlerin (PKCδ inhibitor), but not Go6976 (PKCα inhibitor), enhanced the induction of PDCD4 protein by TGF-β1. Furthermore, siRNA-mediated knockdown of PKCδ and ε, but not PKCα, augmented the TGF-β1-stimulated PDCD4 protein expression. However, TPA or pan-PKC inhibitor did not alter the PDCD4 mRNA expression either under basal- and TGF-β1-treated conditions. The down-regulation of PDCD4 by TPA was restored by treatment with the proteasome inhibitor MG132. These data suggest that two isoforms of PKCs are involved in the regulation of the PDCD4 protein expression related to the proteasomal degradation pathway

Along-strike segmentation of the South China Sea margin imposed by inherited pre-rift basement structures

Multibeam bathymetric, seismic and borehole data are used to investigate a large-scale strike-slip structure, the Baiyun-Liwan Fault Zone, in the northern South China Sea. This fault zone comprises NW- to NE-striking faults and negative flower structures that were generated by oblique extensional displacement. Notably, the interpreted data reveals that the Baiyun-Liwan Fault Zone was active during the Cenozoic, recording intense magmatism, and accommodating significant intraplate deformation during progressive continental rifting and ocean spreading. It bounds two distinct crustal segments and played a significant role in segmenting the northern margin of the South China Sea. The geometry of faults and strata within the Baiyun-Liwan Fault Zone also controlled local sediment routing and depocentre evolution during the Cenozoic. As basement and syn-rift structures change markedly across the Baiyun-Liwan Fault Zone, we propose this structure to be inherited from a lithospheric-scale fault zone separating the Mesozoic arc from forearc-related terrains. We therefore stress the importance of pre-existing structures in the development of rifted margins, with the example provided by the Baiyun-Liwan Fault Zone having profound implications for palaeogeographic reconstructions in the South China Sea. At present, the Baiyun-Liwan Fault Zone is incised by the Pearl River Canyon and eroded by recurrent submarine landslides, forming a major area of sediment bypass towards the abyssal plain

PDCD4 Knockdown Induces Senescence in Hepatoma Cells by Up-Regulating the p21 Expression

While the over-expression of tumor suppressor programmed cell death 4 (PDCD4) induces apoptosis, it was recently shown that PDCD4 knockdown also induced apoptosis. In this study, we examined the cell cycle regulators whose activation is affected by PDCD4 knockdown to investigate the contribution of PDCD4 to cell cycle regulation in three types of hepatoma cells: HepG2, Huh7 (mutant p53 and p16-deficient), and Hep3B (p53- and Rb-deficient). PDCD4 knockdown suppressed cell growth in all three cell lines by inhibiting Rb phosphorylation via down-regulating the expression of Rb itself and CDKs, which phosphorylate Rb, and up-regulating the expression of the CDK inhibitor p21 through a p53-independent pathway. We also found that apoptosis was induced in a p53-dependent manner in PDCD4 knockdown HepG2 cells (p53+), although the mechanism of cell death in PDCD4 knockdown Hep3B cells (p53-) was different. Furthermore, PDCD4 knockdown induced cellular senescence characterized by β-galactosidase staining, and p21 knockdown rescued the senescence and cell death as well as the inhibition of Rb phosphorylation induced by PDCD4 knockdown. Thus, PDCD4 is an important cell cycle regulator of hepatoma cells and may be a promising therapeutic target for the treatment of hepatocellular carcinoma

Simple and sensitive determination of nucleic acid by Rayleigh light scattering technique with methyl green-CTMAB

1121-1123A method is presented for the determination of nucleic acid, based on the enhancement of Rayleigh light scattering (RLS) of methyl green (MG)-CTMAB in the pH range 6.9-7.2 at 414.0 nm. The enhanced intensity of RLS is proportional to the concentration of nucleic acid in the range 2.5×10-8-2.0×10-6g/ml for calf thymus (ct)DNA, 2.5×10-8-2.0×10-6g/ml  for fish sperm (fs)DNA, 7.5×10-8-2.0×10-6g/ml for yeast (y)RNA. The detection limits (3σ) are 7.8, 2.6, 9.9 ng/ml for ctDNA, fsDNA and yRNA respectively. Besides its high sensitivity, it has some other advantages: simplicity of operation, commonality of spectrometer and reagents, good stability of chemical system and reproducibility. The procedure has been successfully applied to the determination of nucleic acid in synthetic samples

Travel-Time Inversion Method of Converted Shear Waves Using RayInvr Algorithm

The detailed studies of converted S-waves recorded on the Ocean Bottom Seismometer (OBS) can provide evidence for constraining lithology and geophysical properties. However, the research of converted S-waves remains a weakness, especially the S-waves’ inversion. In this study, we applied a travel-time inversion method of converted S-waves to obtain the crustal S-wave velocity along the profile NS5. The velocities of the crust are determined by the following four aspects: (1) modelling the P-wave velocity, (2) constrained sediments Vp/Vs ratios and S-wave velocity using PPS phases, (3) the correction of PSS phases’ travel-time, and (4) appropriate parameters and initial model are selected for inversion. Our results show that the vs. and Vp/Vs of the crust are 3.0–4.4 km/s and 1.71–1.80, respectively. The inversion model has a similar trend in velocity and Vp/Vs ratios with the forward model, due to a small difference with ∆Vs of 0.1 km/s and ∆Vp/Vs of 0.03 between two models. In addition, the high-resolution inversion model has revealed many details of the crustal structures, including magma conduits, which further supports our method as feasible

Degradation of the Tumor Suppressor PDCD4 Is Impaired by the Suppression of p62/SQSTM1 and Autophagy

PDCD4 (programmed cell death 4) is a tumor suppressor that plays a crucial role in multiple cellular functions, such as the control of protein synthesis and transcriptional control of some genes, the inhibition of cancer invasion and metastasis. The expression of this protein is controlled by synthesis, such as via transcription and translation, and degradation by the ubiquitin-proteasome system. The mitogens, known as tumor promotors, EGF (epidermal growth factor) and TPA (12-O-tetradecanoylphorbol-13-acetate) stimulate the degradation of PDCD4 protein. However, the whole picture of PDCD4 degradation mechanisms is still unclear, we therefore investigated the relationship between PDCD4 and autophagy. The proteasome inhibitor MG132 and the autophagy inhibitor bafilomycin A1 were found to upregulate the PDCD4 levels. PDCD4 protein levels increased synergistically in the presence of both inhibitors. Knockdown of p62/SQSTM1 (sequestosome-1), a polyubiquitin binding partner, also upregulated the PDCD4 levels. P62 and LC3 (microtubule-associated protein 1A/1B-light chain 3)-II were co-immunoprecipitated by an anti-PDCD4 antibody. Colocalization particles of PDCD4, p62 and the autophagosome marker LC3 were observed and the colocalization areas increased in the presence of autophagy and/or proteasome inhibitor(s) in Huh7 cells. In ATG (autophagy related) 5-deficient Huh7 cells in which autophagy was impaired, the PDCD4 levels were increased at the basal levels and upregulated in the presence of autophagy inhibitors. Based on the above findings, we concluded that after phosphorylation in the degron and ubiquitination, PDCD4 is degraded by both the proteasome and autophagy systems