The 2015 Fillmore Earthquake Swarm and Possible Crustal Deformation Mechanisms near the Bottom of the Eastern Ventura Basin, California

The 2015 Fillmore swarm occurred about 6 km west of the city of Fillmore in Ventura, California, and was located beneath the eastern part of the actively subsiding Ventura basin at depths from 11.8 to 13.8 km, similar to two previous swarms in the area. Template‐matching event detection showed that it started on 5 July 2015 at 2:21 UTC with an M ∼1.0 earthquake. The swarm exhibited unusual episodic spatial and temporal migrations and unusual diversity in the nodal planes of the focal mechanisms as compared to the simple hypocenter‐defined plane. It was also noteworthy because it consisted of >1400 events of M ≥ 0.0, with M 2.8 being the largest event. We suggest that fluids released by metamorphic dehydration processes, migration of fluids along a detachment zone, and cascading asperity failures caused this prolific earthquake swarm, but other mechanisms (such as simple mainshock–aftershock stress triggering or a regional aseismic creep event) are less likely. Dilatant strengthening may be a mechanism that causes the temporal decay of the swarm as pore‐pressure drop increased the effective normal stress, and counteracted the instability driving the swarm

Airborne lidar detection and characterization of internal waves in a shallow fjord

A dual-polarization lidar and photography are used to sense internal waves in West Sound, Orcas Island, Washington, from a small aircraft. The airborne lidar detected a thin plankton layer at the bottom of the upper layer of the water, and this signal provides the depth of the upper layer, amplitude of the internal waves, and the propagation speed. The lidar is most effective when the polarization filter on the receiver is orthogonal to the transmitted light, but this does not depend significantly on whether the transmitted light is linearly or circularly polarized. The depolarization is greater with circular polarization, and our results are consistent with a single parameter Mueller scattering matrix. Photographs of the surface manifestation of the internal waves clearly show the propagation direction and width of the phase fronts of the internal waves, even though the contrast is low (2%). Combined with the lidar profile, the total energy of the internal wave packet was estimated to be 9 MJ

Male alternative reproductive tactics and associated evolution of anatomical characteristics in loliginid squid

© The Author(s), 2019. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Marian, J. E. A. R., Apostólico, L. H., Chiao, C. C., Hanlon, R. T., Hirohashi, N., Iwata, Y., Mather, J., Sato, N., & Shaw, P. W. Male alternative reproductive tactics and associated evolution of anatomical characteristics in loliginid squid. Frontiers in Physiology, 10, (2019): 1281, doi: 10.3389/fphys.2019.01281.Loliginid squids provide a unique model system to explore male alternative reproductive tactics (ARTs) and their linkage to size, behavioral decision making, and possibly age. Large individuals fight one another and the winners form temporary consortships with females, while smaller individuals do not engage in male-male agonistic bouts but use various sneaker tactics to obtain matings, each with varying mating and fertilization success. There is substantial behavioral flexibility in most species, as smaller males can facultatively switch to the alternative consort behaviors as the behavioral context changes. These forms of ARTs can involve different: mating posture; site of spermatophore deposition; fertilization success; and sperm traits. Most of the traits of male dimorphism (both anatomical and behavioral) are consistent with traditional sexual selection theory, while others have unique features that may have evolved in response to the fertilization environment faced by each temporary or permanent male morph.JM acknowledges the funding provided by FAPESP (São Paulo Research Foundation – proc. 2013/02653-1, 2014/11008-5, 2015/15447-6, 2017/16182-1, and 2018/19180-2), CNPq (National Council for Scientific and Technological Development – proc. 477233/2013–9), and CAPES (Coordination for the Improvement of Higher Education Personnel – Finance Code 001)

Strong ecological but weak evolutionary effects of elevated CO2 on a recombinant inbred population of Arabidopsis thaliana

Summary • Increases in atmospheric CO 2 concentration have an impact on plant communities by influencing plant growth and morphology, species interactions, and ecosystem processes. These ecological effects may be accompanied by evolutionary change if elevated CO 2 (eCO 2 ) alters patterns of natural selection or expression of genetic variation. • Here, a statistically powerful quantitative genetic experiment and manipulations of CO 2 concentrations in a field setting were used to investigate how eCO 2 impacts patterns of selection on ecologically important traits in Arabidopsis thaliana ; heritabilities, which influence the rate of response to selection; and genetic covariances between traits, which may constrain responses to selection. • CO 2 had strong phenotypic effects; plants grown in eCO 2 were taller and produced more biomass and fruits. Also, significant directional selection was observed on many traits and significant genetic variation was observed for all traits. However, no evolutionary effect of eCO 2 was detected; patterns of selection, heritabilities and genetic correlations corresponded closely in ambient and elevated CO 2 environments. • The data suggest that patterns of natural selection and the quantitative genetic parameters of this A. thaliana population are robust to increases in CO 2 concentration and that responses to eCO 2 will be primarily ecological

The 2015 Fillmore Earthquake Swarm and Possible Crustal Deformation Mechanisms near the Bottom of the Eastern Ventura Basin, California

The 2015 Fillmore swarm occurred about 6 km west of the city of Fillmore in Ventura, California, and was located beneath the eastern part of the actively subsiding Ventura basin at depths from 11.8 to 13.8 km, similar to two previous swarms in the area. Template‐matching event detection showed that it started on 5 July 2015 at 2:21 UTC with an M ∼1.0 earthquake. The swarm exhibited unusual episodic spatial and temporal migrations and unusual diversity in the nodal planes of the focal mechanisms as compared to the simple hypocenter‐defined plane. It was also noteworthy because it consisted of >1400 events of M ≥ 0.0, with M 2.8 being the largest event. We suggest that fluids released by metamorphic dehydration processes, migration of fluids along a detachment zone, and cascading asperity failures caused this prolific earthquake swarm, but other mechanisms (such as simple mainshock–aftershock stress triggering or a regional aseismic creep event) are less likely. Dilatant strengthening may be a mechanism that causes the temporal decay of the swarm as pore‐pressure drop increased the effective normal stress, and counteracted the instability driving the swarm

Gene response profiles for Daphnia pulex exposed to the environmental stressor cadmium reveals novel crustacean metallothioneins

<p>Abstract</p> <p>Background</p> <p>Genomic research tools such as microarrays are proving to be important resources to study the complex regulation of genes that respond to environmental perturbations. A first generation cDNA microarray was developed for the environmental indicator species <it>Daphnia pulex</it>, to identify genes whose regulation is modulated following exposure to the metal stressor cadmium. Our experiments revealed interesting changes in gene transcription that suggest their biological roles and their potentially toxicological features in responding to this important environmental contaminant.</p> <p>Results</p> <p>Our microarray identified genes reported in the literature to be regulated in response to cadmium exposure, suggested functional attributes for genes that share no sequence similarity to proteins in the public databases, and pointed to genes that are likely members of expanded gene families in the <it>Daphnia </it>genome. Genes identified on the microarray also were associated with cadmium induced phenotypes and population-level outcomes that we experimentally determined. A subset of genes regulated in response to cadmium exposure was independently validated using quantitative-realtime (Q-RT)-PCR. These microarray studies led to the discovery of three genes coding for the metal detoxication protein metallothionein (MT). The gene structures and predicted translated sequences of <it>D. pulex </it>MTs clearly place them in this gene family. Yet, they share little homology with previously characterized MTs.</p> <p>Conclusion</p> <p>The genomic information obtained from this study represents an important first step in characterizing microarray patterns that may be diagnostic to specific environmental contaminants and give insights into their toxicological mechanisms, while also providing a practical tool for evolutionary, ecological, and toxicological functional gene discovery studies. Advances in <it>Daphnia </it>genomics will enable the further development of this species as a model organism for the environmental sciences.</p

Genetic Inactivation of Chlamydia trachomatis Inclusion Membrane Protein CT228 Alters MYPT1 Recruitment, Extrusion Production, and Longevity of Infection

Chlamydia trachomatis is an obligate intracellular pathogen with global health and economic impact. Upon infection, C. trachomatis resides within a protective niche, the inclusion, wherein it replicates and usurps host cell machinery and resources. The inclusion membrane is the key host-pathogen interface that governs specific protein-protein interactions to manipulate host signaling pathways. At the conclusion of the infection cycle, C. trachomatis exits the host cell via lysis or extrusion. Extrusion depends on the phosphorylation state of myosin light chain 2 (MLC2); the extent of phosphorylation is determined by the ongoing opposing activities of myosin phosphatase (MYPT1) and myosin kinase (MLCK). Previously, it was shown that MYPT1 is recruited to the inclusion and interacts with CT228 for regulation of host cell egress. In this study, we generated a targeted chromosomal mutation of CT228 (L2-ΔCT228) using the TargeTron system and demonstrate a loss of MYPT1 recruitment and increase in extrusion production in vitro. Mutation of CT228 did not affect chlamydial growth in cell culture or recruitment of MLC2. Moreover, we document a delay in clearance of L2-ΔCT228 during murine intravaginal infection as well as a reduction in systemic humoral response, relative to L2-wild type. Taken together, the data suggest that loss of MYPT1 recruitment (as a result of CT228 disruption) regulates the degree of host cell exit via extrusion and affects the longevity of infection in vivo

Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis.

The TAR DNA-binding protein 43 (TDP-43) has been identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin inclusions (FTLD-U), defining a novel class of neurodegenerative conditions: the TDP-43 proteinopathies. The first pathogenic mutations in the gene encoding TDP-43 (TARDBP) were recently reported in familial and sporadic ALS patients, supporting a direct role for TDP-43 in neurodegeneration. In this study, we report the identification and functional analyses of two novel and one known mutation in TARDBP that we identified as a result of extensive mutation analyses in a cohort of 296 patients with variable neurodegenerative diseases associated with TDP-43 histopathology. Three different heterozygous missense mutations in exon 6 of TARDBP (p.M337V, p.N345K, and p.I383V) were identified in the analysis of 92 familial ALS patients (3.3%), while no mutations were detected in 24 patients with sporadic ALS or 180 patients with other TDP-43-positive neurodegenerative diseases. The presence of p.M337V, p.N345K, and p.I383V was excluded in 825 controls and 652 additional sporadic ALS patients. All three mutations affect highly conserved amino acid residues in the C-terminal part of TDP-43 known to be involved in protein-protein interactions. Biochemical analysis of TDP-43 in ALS patient cell lines revealed a substantial increase in caspase cleaved fragments, including the approximately 25 kDa fragment, compared to control cell lines. Our findings support TARDBP mutations as a cause of ALS. Based on the specific C-terminal location of the mutations and the accumulation of a smaller C-terminal fragment, we speculate that TARDBP mutations may cause a toxic gain of function through novel protein interactions or intracellular accumulation of TDP-43 fragments leading to apoptosis

The novel mTOR inhibitor RAD001 (Everolimus) induces antiproliferative effects in human pancreatic neuroendocrine tumor cells

Background/Aim: Tumors exhibiting constitutively activated PI(3) K/Akt/mTOR signaling are hypersensitive to mTOR inhibitors such as RAD001 (everolimus) which is presently being investigated in clinical phase II trials in various tumor entities, including neuroendocrine tumors (NETs). However, no preclinical data about the effects of RAD001 on NET cells have been published. In this study, we aimed to evaluate the effects of RAD001 on BON cells, a human pancreatic NET cell line that exhibits constitutively activated PI(3) K/Akt/mTOR signaling. Methods: BON cells were treated with different concentrations of RAD001 to analyze its effect on cell growth using proliferation assays. Apoptosis was examined by Western blot analysis of caspase-3/PARP cleavage and by FACS analysis of DNA fragmentation. Results: RAD001 potently inhibited BON cell growth in a dose-dependent manner which was dependent on the serum concentration in the medium. RAD001-induced growth inhibition involved G0/G1-phase arrest as well as induction of apoptosis. Conclusion: In summary, our data demonstrate antiproliferative and apoptotic effects of RAD001 in NET cells in vitro supporting its clinical use in current phase II trials in NET patients. Copyright (c) 2007 S. Karger AG, Basel