Convergent, Parallel and Correlated Evolution of Trophic Morphologies in the Subfamily Schizothoracinae from the Qinghai-Tibetan Plateau

Schizothoracine fishes distributed in the water system of the Qinghai-Tibetan plateau (QTP) and adjacent areas are characterized by being highly adaptive to the cold and hypoxic environment of the plateau, as well as by a high degree of diversity in trophic morphology due to resource polymorphisms. Although convergent and parallel evolution are prevalent in the organisms of the QTP, it remains unknown whether similar evolutionary patterns have occurred in the schizothoracine fishes. Here, we constructed for the first time a tentative molecular phylogeny of the schizothoracine fishes based on the complete sequences of the cytochrome b gene. We employed this molecular phylogenetic framework to examine the evolution of trophic morphologies. We used Pagel's maximum likelihood method to estimate the evolutionary associations of trophic morphologies and food resource use. Our results showed that the molecular and published morphological phylogenies of Schizothoracinae are partially incongruent with respect to some intergeneric relationships. The phylogenetic results revealed that four character states of five trophic morphologies and of food resource use evolved at least twice during the diversification of the subfamily. State transitions are the result of evolutionary patterns including either convergence or parallelism or both. Furthermore, our analyses indicate that some characters of trophic morphologies in the Schizothoracinae have undergone correlated evolution, which are somewhat correlated with different food resource uses. Collectively, our results reveal new examples of convergent and parallel evolution in the organisms of the QTP. The adaptation to different trophic niches through the modification of trophic morphologies and feeding behaviour as found in the schizothoracine fishes may account for the formation and maintenance of the high degree of diversity and radiations in fish communities endemic to QTP

A case of behavioural diversification in male floral function – the evolution of thigmonastic pollen presentation

The authors gratefully acknowledge funding provided by an Else-Neumann-Stipendium (http://www.fu-berlin.de/sites/promovieren/drs/nachwuchs/nachwuchs/nafoeg.html), Deutscher Akademischer Austausch Dienst (DAAD) and botconsult GmbH at different stages of data acquisition. We thank Tobias Grass, Joana Bergmann and Franziska Weber (Freie Universität Berlin) for help with data collection in the field and in the greenhouse. Nicole Schmandt, Federico Luebert, Juliana Chacón and Dietmar Quant (Universität Bonn) provided help in the molecular laboratory and the edition of the molecular dataset. We furthermore thank Markus Ackermann (Koblenz) for providing photographs, Philipp Klein (Berlin) for editing the video and Katy Jones (Berlin) for helpful comments on an earlier version of the manuscript. Rafael Acuña has been supported by the ALECOSTA scholarship program. Coverage of the article processing charge by the German Research Foundation via the Open Access Publication Fund of the Freie Universität Berlin is gratefully acknowledged.Peer reviewedPublisher PD

Effects of circadian disruption on physiology and pathology: from bench to clinic (and back)

Nested within the hypothalamus, the suprachiasmatic nuclei (SCN) represent a central biological clock that regulates daily and circadian (i.e., close to 24 h) rhythms in mammals. Besides the SCN, a number of peripheral oscillators throughout the body control local rhythms and are usually kept in pace by the central clock. In order to represent an adaptive value, circadian rhythms must be entrained by environmental signals or zeitgebers, the main one being the daily light?dark (LD) cycle. The SCN adopt a stable phase relationship with the LD cycle that, when challenged, results in abrupt or chronic changes in overt rhythms and, in turn, in physiological, behavioral, and metabolic variables. Changes in entrainment, both acute and chronic, may have severe consequences in human performance and pathological outcome. Indeed, animal models of desynchronization have become a useful tool to understand such changes and to evaluate potential treatments in human subjects. Here we review a number of alterations in circadian entrainment, including jet lag, social jet lag (i.e., desynchronization between body rhythms and normal time schedules), shift work, and exposure to nocturnal light, both in human subjects and in laboratory animals. Finally, we focus on the health consequences related to circadian/entrainment disorders and propose a number of approaches for the management of circadian desynchronization.Fil: Chiesa, Juan José. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Duhart, José Manuel. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Casiraghi, Leandro Pablo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Paladino, Natalia. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bussi, Ivana Leda. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Golombek, Diego Andrés. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Contrasting views on the role of mesenchymal stromal/stem cells in tumour growth : a systematic review of experimental design

The effect of mesenchymal stromal/stem cells (MSCs) on tumour growth remains controversial. Experimental evidence supports both an inhibitory and a stimulatory effect. We have assessed factors responsible for the contrasting effects of MSCs on tumour growth by doing a meta-analysis of existing literature between 2000 and May 2017. We assessed 183 original research articles comprising 338 experiments. We considered (a) in vivo and in vitro experiments, (b) whether in vivo studies were syngeneic or xenogeneic, and (c) if animals were immune competent or deficient. Furthermore, the sources and types of cancer cells and MSCs were considered together with modes of cancer induction and MSC administration. 56% of all 338 experiments reported that MSCs promote tumour growth. 78% and 79% of all experiments sourced human MSCs and cancer cells, respectively. MSCs were used in their naïve and engineered form in 86% and 14% of experiments, respectively, the latter to produce factors that could alter either their activity or that of the tumour. 53% of all experiments were conducted in vitro with 60% exposing cancer cells to MSCs via coculture. Of all in vivo experiments, 79% were xenogeneic and 63% were conducted in immune-competent animals. Tumour growth was inhibited in 80% of experiments that used umbilical cord-derived MSCs, whereas tumour growth was promoted in 64% and 57% of experiments that used bone marrow- and adipose tissue-derived MSCs, respectively. This contrasting effect of MSCs on tumour growth observed under different experimental conditions may reflect differences in experimental design. This analysis calls for careful consideration of experimental design given the large number of MSC clinical trials currently underway.The South African Medical Research Council in terms of the SAMRC’s Flagship Award Project SAMRC-RFA-UFSP-01-2013/STEM CELLS, the SAMRC Extramural Stem Cell Research and Therapy Unit, the National Research Foundation of South Africa (grant no. 86942), the National Health Laboratory Services Research Trust (grant no. 94453), the University of Pretoria Research Development Programme (A0Z778), the University of Pretoria Vice Chancellor’s Postdoctoral Fellowship and the Institute for Cellular and Molecular Medicine of the University of Pretoria.http://www.springer.comseries/5584hj2019ImmunologyOral Pathology and Oral Biolog

Stratospheric aerosol evolution after Pinatubo simulated with a coupled size-resolved aerosol–chemistry–climate model, SOCOL-AERv1.0

We evaluate how the coupled aerosol–chemistry– climate model SOCOL-AERv1.0 represents the influence of the 1991 eruption of Mt. Pinatubo on stratospheric aerosol properties and atmospheric state. The aerosol module is coupled to the radiative and chemical modules and includes comprehensive sulfur chemistry and microphysics, in which the particle size distribution is represented by 40 size bins with radii spanning from 0.39 nm to 3.2 µm. SOCOL-AER simulations are compared with satellite and in situ measurements of aerosol parameters, temperature reanalyses, and ozone observations. In addition to the reference model configuration, we performed series of sensitivity experiments looking at different processes affecting the aerosol layer. An accurate sedimentation scheme is found to be essential to prevent particles from diffusing too rapidly to high and low altitudes. The aerosol radiative feedback and the use of a nudged quasibiennial oscillation help to keep aerosol in the tropics and significantly affect the evolution of the stratospheric aerosol burden, which improves the agreement with observed aerosol mass distributions. The inclusion of van der Waals forces in the particle coagulation scheme suggests improvements in particle effective radius, although other parameters (such as aerosol longevity) deteriorate. Modification of the Pinatubo sulfur emission rate also improves some aerosol parameters, while it worsens others compared to observations. Observations themselves are highly uncertain and render it difficult to conclusively judge the necessity of further model reconfiguration. The model revealed problems in reproducing aerosol sizes above 25 km and also in capturing certain features of the ozone response. Besides this, our results show that SOCOL-AER is capable of predicting the most important global-scale atmospheric effects following volcanic eruptions, which is also a prerequisite for an improved understanding of solar geoengineering effects from sulfur injections to the stratospher

Deciphering the Acylation Pattern of Yersinia enterocolitica Lipid A

<div><p>Pathogenic bacteria may modify their surface to evade the host innate immune response. <em>Yersinia enterocolitica</em> modulates its lipopolysaccharide (LPS) lipid A structure, and the key regulatory signal is temperature. At 21°C, lipid A is hexa-acylated and may be modified with aminoarabinose or palmitate. At 37°C, <em>Y. enterocolitica</em> expresses a tetra-acylated lipid A consistent with the 3′-O-deacylation of the molecule. In this work, by combining genetic and mass spectrometric analysis, we establish that <em>Y. enterocolitica</em> encodes a lipid A deacylase, LpxR, responsible for the lipid A structure observed at 37°C. Western blot analyses indicate that LpxR exhibits latency at 21°C, deacylation of lipid A is not observed despite the expression of LpxR in the membrane. Aminoarabinose-modified lipid A is involved in the latency. 3-D modelling, docking and site-directed mutagenesis experiments showed that LpxR D31 reduces the active site cavity volume so that aminoarabinose containing Kdo₂-lipid A cannot be accommodated and, therefore, not deacylated. Our data revealed that the expression of <em>lpxR</em> is negatively controlled by RovA and PhoPQ which are necessary for the lipid A modification with aminoarabinose. Next, we investigated the role of lipid A structural plasticity conferred by LpxR on the expression/function of <em>Y. enterocolitica</em> virulence factors. We present evidence that motility and invasion of eukaryotic cells were reduced in the <em>lpxR</em> mutant grown at 21°C. Mechanistically, our data revealed that the expressions of <em>flhDC</em> and <em>rovA</em>, regulators controlling the flagellar regulon and invasin respectively, were down-regulated in the mutant. In contrast, the levels of the virulence plasmid (pYV)-encoded virulence factors Yops and YadA were not affected in the <em>lpxR</em> mutant. Finally, we establish that the low inflammatory response associated to <em>Y. enterocolitica</em> infections is the sum of the anti-inflammatory action exerted by pYV-encoded YopP and the reduced activation of the LPS receptor by a LpxR-dependent deacylated LPS.</p> </div