The history, systematics, and nomenclature of Thalattosuchia (Archosauria: Crocodylomorpha)

The use of more than one nomenclatural code is becoming increasingly common in some biological sub-disciplines. To minimize nomenclatural instability, we have decided to establish a higher level systematization for Thalattosuchia under both the International Code of Phylogenetic Nomenclature (‘PhyloCode’) and the International Code of Zoological Nomenclature (‘Zoological Code’). We undertook a series of phylogenetic analyses with an expanded dataset to examine the origins of Thalattosuchia within Crocodylomorpha, and determined the clade’s diagnostic characters. Based on these analyses, we provide updated diagnoses for Thalattosuchia and its subclades under both the PhyloCode and Zoological Code. We also introduce two new nomina that are regulated under the PhyloCode (Neothalattosuchia and Euthalattosuchia), and the nomen Dakosaurina, which is registered under both nomenclatural codes. Moreover, we introduce PhyloCode-compliant phylogenetic definitions for Thalattosuchia and its subclades. As we cannot reliably discriminate between the positional hypotheses for Thalattosuchia within Crocodylomorpha, the clades’ origins are as much of a mystery today as they were over a century ago. However, we hope that using the same diagnostic characters to define the same clades, with the same nomina, under both nomenclatural codes will be an example to others to follow

GSK3β inhibition blocks melanoma cell/host interactions by downregulating N-cadherin expression and decreasing FAK phosphorylation.

This study addresses the role of glycogen synthase kinase (GSK)-3β signaling in the tumorigenic behavior of melanoma. Immunohistochemical staining revealed GSK3β to be focally expressed in the invasive portions of 12 and 33% of primary and metastatic melanomas, respectively. GSK3 inhibitors and small interfering RNA (siRNA) knockdown of GSK3β were found to inhibit the motile behavior of melanoma cells in scratch wound, three-dimensional collagen-implanted spheroid, and modified Boyden chamber assays. Functionally, inhibition of GSK3β signaling was found to suppress N-cadherin expression at the messenger RNA and protein levels, and was associated with decreased expression of the transcription factor Slug. Pharmacological and genetic ablation of GSK3β signaling inhibited the adhesion of melanoma cells to both endothelial cells and fibroblasts and prevented transendothelial migration, an effect rescued by the forced overexpression of N-cadherin. A further role for GSK3β signaling in invasion was suggested by the ability of GSK3β inhibitors and siRNA knockdown to block phosphorylation of focal adhesion kinase (FAK) and increase the size of focal adhesions. In summary, we have, to our knowledge, demonstrated a previously unreported role for GSK3β in modulating the motile and invasive behavior of melanoma cells through N-cadherin and FAK. These studies suggest the potential therapeutic utility of inhibiting GSK3β in defined subsets of melanoma

SFRS7-Mediated Splicing of Tau Exon 10 Is Directly Regulated by STOX1A in Glial Cells

Background: In this study, we performed a genome-wide search for effector genes bound by STOX1A, a winged helix transcription factor recently demonstrated to be involved in late onset Alzheimer’s disease and affecting the amyloid processing pathway. Methodology/Principal Findings: Our results show that out of 218 genes bound by STOX1A as identified by chromatinimmunoprecipitation followed by sequencing (ChIP-Seq), the serine/arginine-rich splicing factor 7 (SFRS7) was found to be induced, both at the mRNA and protein levels, by STOX1A after stable transfection in glial cells. The increase in SFRS7 was followed by an increase in the 4R/3R ratios of the microtubule-associated protein tau (MAPT) by differential exon 10 splicing. Secondly, STOX1A also induced expression of total tau both at the mRNA and protein levels. Upregulation of total tau expression (SFRS7-independent) and tau exon 10 splicing (SFRS7-dependent), as shown in this study to be both affected by STOX1A, is known to have implications in neurodegeneration

LSST: from Science Drivers to Reference Design and Anticipated Data Products

(Abridged) We describe here the most ambitious survey currently planned in the optical, the Large Synoptic Survey Telescope (LSST). A vast array of science will be enabled by a single wide-deep-fast sky survey, and LSST will have unique survey capability in the faint time domain. The LSST design is driven by four main science themes: probing dark energy and dark matter, taking an inventory of the Solar System, exploring the transient optical sky, and mapping the Milky Way. LSST will be a wide-field ground-based system sited at Cerro Pach\'{o}n in northern Chile. The telescope will have an 8.4 m (6.5 m effective) primary mirror, a 9.6 deg$^2$ field of view, and a 3.2 Gigapixel camera. The standard observing sequence will consist of pairs of 15-second exposures in a given field, with two such visits in each pointing in a given night. With these repeats, the LSST system is capable of imaging about 10,000 square degrees of sky in a single filter in three nights. The typical 5$\sigma$ point-source depth in a single visit in $r$ will be $\sim 24.5$ (AB). The project is in the construction phase and will begin regular survey operations by 2022. The survey area will be contained within 30,000 deg$^2$ with $\delta<+34.5^\circ$, and will be imaged multiple times in six bands, $ugrizy$, covering the wavelength range 320--1050 nm. About 90\% of the observing time will be devoted to a deep-wide-fast survey mode which will uniformly observe a 18,000 deg$^2$ region about 800 times (summed over all six bands) during the anticipated 10 years of operations, and yield a coadded map to $r\sim27.5$. The remaining 10\% of the observing time will be allocated to projects such as a Very Deep and Fast time domain survey. The goal is to make LSST data products, including a relational database of about 32 trillion observations of 40 billion objects, available to the public and scientists around the world.Comment: 57 pages, 32 color figures, version with high-resolution figures available from https://www.lsst.org/overvie

Maternal smoking during pregnancy and subcutaneous fat mass in early childhood. The Generation R Study

Maternal smoking during pregnancy increases the risk of obesity in the offspring. Not much is known about the associations with other measures of body composition. We assessed the associations of maternal smoking during pregnancy with the development of subcutaneous fat mass measured as peripheral and central skinfold thickness measurements in early childhood, in a population-based prospective cohort study from early fetal life onward in the city of Rotterdam, The Netherlands. The study was performed in 907 mothers and their children at the ages of 1.5, 6 and 24 months. As compared to non-smoking mothers, mothers who continued smoking during pregnancy were more likely to have a younger age and a lower educational level. Their children had a lower birth weight, higher risk of small size for gestational age and were breastfed for a shorter duration (P-values <0.01). We did not observe differences in peripheral, central and total subcutaneous fat mass between the offspring of non-smoking mothers, mothers who smoked in first trimester only and mothers who continued smoking during pregnancy (P > 0.05). Also, the reported number of cigarettes smoked by mothers in both first and third trimester of pregnancy were not associated with peripheral, central and total subcutaneous fat mass in the offspring at the ages of 1.5, 6 and 24 months. Our findings suggest that fetal exposure to cigarette smoke during pregnancy does not influence subcutaneous fat mass in early childhood. Follow-up studies are needed in children at older ages and to identify associations of maternal smoking during pregnancy with other measures of body composition

Staphylococcus aureus infection dynamics

Staphylococcus aureus is a human commensal that can also cause systemic infections. This transition requires evasion of the immune response and the ability to exploit different niches within the host. However, the disease mechanisms and the dominant immune mediators against infection are poorly understood. Previously it has been shown that the infecting S. aureus population goes through a population bottleneck, from which very few bacteria escape to establish the abscesses that are characteristic of many infections. Here we examine the host factors underlying the population bottleneck and subsequent clonal expansion in S. aureus infection models, to identify underpinning principles of infection. The bottleneck is a common feature between models and is independent of S. aureus strain. Interestingly, the high doses of S. aureus required for the widely used "survival" model results in a reduced population bottleneck, suggesting that host defences have been simply overloaded. This brings into question the applicability of the survival model. Depletion of immune mediators revealed key breakpoints and the dynamics of systemic infection. Loss of macrophages, including the liver Kupffer cells, led to increased sensitivity to infection as expected but also loss of the population bottleneck and the spread to other organs still occurred. Conversely, neutrophil depletion led to greater susceptibility to disease but with a concomitant maintenance of the bottleneck and lack of systemic spread. We also used a novel microscopy approach to examine abscess architecture and distribution within organs. From these observations we developed a conceptual model for S. aureus disease from initial infection to mature abscess. This work highlights the need to understand the complexities of the infectious process to be able to assign functions for host and bacterial components, and why S. aureus disease requires a seemingly high infectious dose and how interventions such as a vaccine may be more rationally developed

Diversity and carbon storage across the tropical forest biome

Tropical forests are global centres of biodiversity and carbon storage. Many tropical countries aspire to protect forest to fulfil biodiversity and climate mitigation policy targets, but the conservation strategies needed to achieve these two functions depend critically on the tropical forest tree diversity-carbon storage relationship. Assessing this relationship is challenging due to the scarcity of inventories where carbon stocks in aboveground biomass and species identifications have been simultaneously and robustly quantified. Here, we compile a unique pan-tropical dataset of 360 plots located in structurally intact old-growth closed-canopy forest, surveyed using standardised methods, allowing a multi-scale evaluation of diversity-carbon relationships in tropical forests. Diversity-carbon relationships among all plots at 1 ha scale across the tropics are absent, and within continents are either weak (Asia) or absent (Amazonia, Africa). A weak positive relationship is detectable within 1 ha plots, indicating that diversity effects in tropical forests may be scale dependent. The absence of clear diversity-carbon relationships at scales relevant to conservation planning means that carbon-centred conservation strategies will inevitably miss many high diversity ecosystems. As tropical forests can have any combination of tree diversity and carbon stocks both require explicit consideration when optimising policies to manage tropical carbon and biodiversity.Additional co-authors: Kofi Affum-Baffoe, Shin-ichiro Aiba, Everton Cristo de Almeida, Edmar Almeida de Oliveira, Patricia Alvarez-Loayza, Esteban Álvarez Dávila, Ana Andrade, Luiz E. O. C. Aragão, Peter Ashton, Gerardo A. Aymard C., Timothy R. Baker, Michael Balinga, Lindsay F. Banin, Christopher Baraloto, Jean-Francois Bastin, Nicholas Berry, Jan Bogaert, Damien Bonal, Frans Bongers, Roel Brienen, José Luís C. Camargo, Carlos Cerón, Victor Chama Moscoso, Eric Chezeaux, Connie J. Clark, Álvaro Cogollo Pacheco, James A. Comiskey, Fernando Cornejo Valverde, Eurídice N. Honorio Coronado, Greta Dargie, Stuart J. Davies, Charles De Canniere, Marie Noel Djuikouo K., Jean-Louis Doucet, Terry L. Erwin, Javier Silva Espejo, Corneille E. N. Ewango, Sophie Fauset, Ted R. Feldpausch, Rafael Herrera, Martin Gilpin, Emanuel Gloor, Jefferson S. Hall, David J. Harris, Terese B. Hart, Kuswata Kartawinata, Lip Khoon Kho, Kanehiro Kitayama, Susan G. W. Laurance, William F. Laurance, Miguel E. Leal, Thomas Lovejoy, Jon C. Lovett, Faustin Mpanya Lukasu, Jean-Remy Makana, Yadvinder Malhi, Leandro Maracahipes, Beatriz S. Marimon, Ben Hur Marimon Junior, Andrew R. Marshall, Paulo S. Morandi, John Tshibamba Mukendi, Jaques Mukinzi, Reuben Nilus, Percy Núñez Vargas, Nadir C. Pallqui Camacho, Guido Pardo, Marielos Peña-Claros, Pascal Pétronelli, Georgia C. Pickavance, Axel Dalberg Poulsen, John R. Poulsen, Richard B. Primack, Hari Priyadi, Carlos A. Quesada, Jan Reitsma, Maxime Réjou-Méchain, Zorayda Restrepo, Ervan Rutishauser, Kamariah Abu Salim, Rafael P. Salomão, Ismayadi Samsoedin, Douglas Sheil, Rodrigo Sierra, Marcos Silveira, J. W. Ferry Slik, Lisa Steel, Hermann Taedoumg, Sylvester Tan, John W. Terborgh, Sean C. Thomas, Marisol Toledo, Peter M. Umunay, Luis Valenzuela Gamarra, Ima Célia Guimarães Vieira, Vincent A. Vos, Ophelia Wang, Simon Willcock & Lise Zemagh

Phylogenetic diversity of Amazonian tree communities

This is the peer reviewed version of the following article: Honorio Coronado, E. N., Dexter, K. G., Pennington, R. T., Chave, J., Lewis, S. L., Alexiades, M. N., Alvarez, E., Alves de Oliveira, A., Amaral, I. L., Araujo-Murakami, A., Arets, E. J. M. M., Aymard, G. A., Baraloto, C., Bonal, D., Brienen, R., Cerón, C., Cornejo Valverde, F., Di Fiore, A., Farfan-Rios, W., Feldpausch, T. R., Higuchi, N., Huamantupa-Chuquimaco, I., Laurance, S. G., Laurance, W. F., López-Gonzalez, G., Marimon, B. S., Marimon-Junior, B. H., Monteagudo Mendoza, A., Neill, D., Palacios Cuenca, W., Peñuela Mora, M. C., Pitman, N. C. A., Prieto, A., Quesada, C. A., Ramirez Angulo, H., Rudas, A., Ruschel, A. R., Salinas Revilla, N., Salomão, R. P., Segalin de Andrade, A., Silman, M. R., Spironello, W., ter Steege, H., Terborgh, J., Toledo, M., Valenzuela Gamarra, L., Vieira, I. C. G., Vilanova Torre, E., Vos, V., Phillips, O. L. (2015), Phylogenetic diversity of Amazonian tree communities. Diversity and Distributions, 21: 1295–1307. doi: 10.1111/ddi.12357, which has been published in final form at 10.1111/ddi.12357Aim: To examine variation in the phylogenetic diversity (PD) of tree communities across geographical and environmental gradients in Amazonia. Location: Two hundred and eighty-three c. 1 ha forest inventory plots from across Amazonia. Methods: We evaluated PD as the total phylogenetic branch length across species in each plot (PDss), the mean pairwise phylogenetic distance between species (MPD), the mean nearest taxon distance (MNTD) and their equivalents standardized for species richness (ses.PDss, ses.MPD, ses.MNTD). We compared PD of tree communities growing (1) on substrates of varying geological age; and (2) in environments with varying ecophysiological barriers to growth and survival. Results: PDss is strongly positively correlated with species richness (SR), whereas MNTD has a negative correlation. Communities on geologically young- and intermediate-aged substrates (western and central Amazonia respectively) have the highest SR, and therefore the highest PDss and the lowest MNTD. We find that the youngest and oldest substrates (the latter on the Brazilian and Guiana Shields) have the highest ses.PDss and ses.MNTD. MPD and ses.MPD are strongly correlated with how evenly taxa are distributed among the three principal angiosperm clades and are both highest in western Amazonia. Meanwhile, seasonally dry tropical forest (SDTF) and forests on white sands have low PD, as evaluated by any metric. Main conclusions: High ses.PDss and ses.MNTD reflect greater lineage diversity in communities. We suggest that high ses.PDss and ses.MNTD in western Amazonia results from its favourable, easy-to-colonize environment, whereas high values in the Brazilian and Guianan Shields may be due to accumulation of lineages over a longer period of time. White-sand forests and SDTF are dominated by close relatives from fewer lineages, perhaps reflecting ecophysiological barriers that are difficult to surmount evolutionarily. Because MPD and ses.MPD do not reflect lineage diversity per se, we suggest that PDss, ses.PDss and ses.MNTD may be the most useful diversity metrics for setting large-scale conservation priorities.FINCyT - PhD studentshipSchool of Geography of the University of LeedsRoyal Botanic Garden EdinburghNatural Environment Research Council (NERC)Gordon and Betty Moore FoundationEuropean Union's Seventh Framework ProgrammeERCCNPq/PELDNSF - Fellowshi

Control of Metabolic Homeostasis by Stress Signaling Is Mediated by the Lipocalin NLaz

Metabolic homeostasis in metazoans is regulated by endocrine control of insulin/IGF signaling (IIS) activity. Stress and inflammatory signaling pathways—such as Jun-N-terminal Kinase (JNK) signaling—repress IIS, curtailing anabolic processes to promote stress tolerance and extend lifespan. While this interaction constitutes an adaptive response that allows managing energy resources under stress conditions, excessive JNK activity in adipose tissue of vertebrates has been found to cause insulin resistance, promoting type II diabetes. Thus, the interaction between JNK and IIS has to be tightly regulated to ensure proper metabolic adaptation to environmental challenges. Here, we identify a new regulatory mechanism by which JNK influences metabolism systemically. We show that JNK signaling is required for metabolic homeostasis in flies and that this function is mediated by the Drosophila Lipocalin family member Neural Lazarillo (NLaz), a homologue of vertebrate Apolipoprotein D (ApoD) and Retinol Binding Protein 4 (RBP4). Lipocalins are emerging as central regulators of peripheral insulin sensitivity and have been implicated in metabolic diseases. NLaz is transcriptionally regulated by JNK signaling and is required for JNK-mediated stress and starvation tolerance. Loss of NLaz function reduces stress resistance and lifespan, while its over-expression represses growth, promotes stress tolerance and extends lifespan—phenotypes that are consistent with reduced IIS activity. Accordingly, we find that NLaz represses IIS activity in larvae and adult flies. Our results show that JNK-NLaz signaling antagonizes IIS and is critical for metabolic adaptation of the organism to environmental challenges. The JNK pathway and Lipocalins are structurally and functionally conserved, suggesting that similar interactions represent an evolutionarily conserved system for the control of metabolic homeostasis