bluuebunny/crossref_metadata_2025_split huggingface dataset:
Asexual genome evolution in the apomictic Ranunculus auricomus complex: examining the effects of hybridization and mutation accumulation
Authors: Pellino Marco , Hojsgaard Diego , Schmutzer Thomas , Scholz Uwe , Hörandl Elvira , Vogel Heiko , Sharbel Timothy F. 
Published: October 2013

AbstractAsexual lineages are thought to be prone to extinction because of deleterious mutation accumulation (Muller's ratchet). Here, we analyse genomic effects of hybridity, polyploidy and allelic divergence in apomictic plants, and identify loci under divergent selection among sexual/apomictic lineages. RNAseq was used to sequence the flower‐specific transcriptomes of five genotypes of the Ranunculus auricomus complex, representing three sexual and two apomictic reproductive biotypes. The five sequence libraries were pooled and de novo assembly performed, and the resultant assembly was used as a backbone for a subsequent alignment of each separate library. High‐quality single‐nucleotide (SNP) and insertion–deletion (indel) polymorphisms were mined from each library. Annotated genes for which open reading frames (ORF) could be determined were analysed for signatures of divergent versus stabilizing selection. A comparison between all genotypes supports the hypothesis of Pleistocene hybrid origin of both apomictic genotypes from R. carpaticola and R. cassubicifolius, with subsequent allelic divergence of apomictic lineages (Meselson effect). Pairwise comparisons of nonsynonymous (dN) to synonymous (dS) substitution rate ratios between apomictic and sexual genotypes for 1231 genes demonstrated similar distributions for all comparisons, although 324 genes demonstrated outlier (i.e. elevated) dN/dS ratios. Gene ontology analyses of these outliers revealed significant enrichment of genes associated with reproduction including meiosis and gametogenesis, following predictions of divergent selection between sexual and apomictic reproduction, although no significant signal of genome‐wide mutation accumulation could be identified. The results suggest that gene function should be considered in order to understand effects of mutation accumulation in asexual lineages.
Genetic assignment of recruits reveals short‐ and long‐distance larval dispersal in Pocillopora damicornis on the Great Barrier Reef
Authors: Torda G. , Lundgren P. , Willis B. L. , van Oppen M. J. H. 
Published: October 2013

AbstractUnderstanding connectivity of coral populations among and within reefs over ecologically significant timescales is essential for developing evidence‐based management strategies, including the design of marineprotected areas. Here, we present the first assessment of contemporary connectivity among populations of two Molecular Operational Taxonomic Units (MOTUs) of the brooding coral Pocillopora damicornis. We used individual‐based genetic assignment methods to identify the proportions of philopatric and migrant larval recruits, settling over 12 months at sites around Lizard Island (northern Great Barrier Reef [GBR]) and over 24 months at sites around the Palms Islands (central GBR). Overall, we found spatially and temporally variable rates of self‐recruitment and dispersal, demonstrating the importance of variation in local physical characteristics in driving dispersal processes. Recruitment patterns and inferred dispersal distances differed between the two P. damicornis MOTUs, with type α recruits exhibiting predominantly philopatric recruitment, while the majority of type β recruits were either migrants from identified putative source populations or assumed migrants based on genetic exclusion from all known populations. While P. damicornis invests much energy into brooding clonal larvae, we found that only 15% and 7% of type α and type β recruits, respectively, were clones of sampled adult colonies or other recruits, challenging the hypothesis that reproduction is predominantly asexual in this species on the GBR. We explain high rates of self‐recruitment and low rates of clonality in these MOTUs by suggesting that locally retained larvae originate predominantly from spawned gametes, while brooded larvae are mainly vagabonds.
Nitrogen deposition alters plant–fungal relationships: linking belowground dynamics to aboveground vegetation change
Authors: Dean Sarah L. , Farrer Emily C. , Taylor D. Lee , Porras‐Alfaro Andrea , Suding Katharine N. , Sinsabaugh Robert L. 
Published: October 2013

AbstractNitrogen (N) deposition rates are increasing globally due to anthropogenic activities. Plant community responses to N are often attributed to altered competitive interactions between plants, but may also be a result of microbial responses to N, particularly root‐associated fungi (RAF), which are known to affect plant fitness. In response to N, Deschampsia cespitosa, a codominant plant in the alpine tundra at Niwot Ridge (CO), increases in abundance, while Geum rossii, its principal competitor, declines. Importantly, G. rossii declines with N even in the absence of its competitor. We examined whether contrasting host responses to N are associated with altered plant–fungal symbioses, and whether the effects of N are distinct from effects of altered plant competition on RAF, using 454 pyrosequencing. Host RAF communities were distinct (only 9.4% of OTUs overlapped). N increased RAF diversity in G. rossii, but decreased it in D. cespitosa. D. cespitosa RAF communities were more responsive to N than G. rossii RAF communities, perhaps indicating a flexible microbial community aids host adaptation to nutrient enrichment. Effects of removing D. cespitosa were distinct from effects of N on G. rossii RAF, and D. cespitosa presence reversed RAF diversity response to N. The most dominant G. rossii RAF order, Helotiales, was the most affected by N, declining from 83% to 60% of sequences, perhaps indicating a loss of mutualists under N enrichment. These results highlight the potential importance of belowground microbial dynamics in plant responses to N deposition.
Genetic signatures of natural selection in response to air pollution in red spruce (Picea rubens, Pinaceae)
Authors: Bashalkhanov Stanislav , Eckert Andrew J. , Rajora Om P. 
Published: October 2013

AbstractOne of the most important drivers of local adaptation for forest trees is climate. Coupled to these patterns, however, are human‐induced disturbances through habitat modification and pollution. The confounded effects of climate and disturbance have rarely been investigated with regard to selective pressure on forest trees. Here, we have developed and used a population genetic approach to search for signals of selection within a set of 36 candidate genes chosen for their putative effects on adaptation to climate and human‐induced air pollution within five populations of red spruce (Picea rubens Sarg.), distributed across its natural range and air pollution gradient in eastern North America. Specifically, we used FST outlier and environmental correlation analyses to highlight a set of seven single nucleotide polymorphisms (SNPs) that were overly correlated with climate and levels of sulphate pollution after correcting for the confounding effects of population history. Use of three age cohorts within each population allowed the effects of climate and pollution to be separated temporally, as climate‐related SNPs (n = 7) showed the strongest signals in the oldest cohort, while pollution‐related SNPs (n = 3) showed the strongest signals in the youngest cohorts. These results highlight the usefulness of population genetic scans for the identification of putatively nonneutral evolution within genomes of nonmodel forest tree species, but also highlight the need for the development and application of robust methodologies to deal with the inherent multivariate nature of the genetic and ecological data used in these types of analyses.
Tracing horizontal Wolbachia movements among bees (Anthophila): a combined approach using multilocus sequence typing data and host phylogeny
Authors: Gerth Michael , Röthe Juliane , Bleidorn Christoph 
Published: October 2013

AbstractThe endosymbiotic bacterium Wolbachia enhances its spread via vertical transmission by generating reproductive effects in its hosts, most notably cytoplasmic incompatibility (CI). Additionally, frequent interspecific horizontal transfer is evident from a lack of phylogenetic congruence between Wolbachia and its hosts. The mechanisms of this lateral transfer are largely unclear. To identify potential pathways of Wolbachia movements, we performed multilocus sequence typing of Wolbachia strains from bees (Anthophila). Using a host phylogeny and ecological data, we tested various models of horizontal endosymbiont transmission. In general, Wolbachia strains seem to be randomly distributed among bee hosts. Kleptoparasite‐host associations among bees as well as other ecological links could not be supported as sole basis for the spread of Wolbachia. However, cophylogenetic analyses and divergence time estimations suggest that Wolbachia may persist within a host lineage over considerable timescales and that strictly vertical transmission and subsequent random loss of infections across lineages may have had a greater impact on Wolbachia strain distribution than previously estimated. Although general conclusions about Wolbachia movements among arthropod hosts cannot be made, we present a framework by which precise assumptions about shared evolutionary histories of Wolbachia and a host taxon can be modelled and tested.
Comparison of population genetic patterns in two widespread freshwater mussels with contrasting life histories in western North America
Authors: Mock K. E. , Brim Box J. C. , Chong J. P. , Furnish J. , Howard J. K. 
Published: October 2013

AbstractWe investigate population genetic structuring in Margaritifera falcata, a freshwater mussel native to western North America, across the majority of its geographical range. We find shallow rangewide genetic structure, strong population‐level structuring and very low population diversity in this species, using both mitochondrial sequence and nuclear microsatellite data. We contrast these patterns with previous findings in another freshwater mussel species group (Anodonta californiensis/A. nuttalliana) occupying the same continental region and many of the same watersheds. We conclude that differences are likely caused by contrasting life history attributes between genera, particularly host fish requirements and hermaphroditism. Further, we demonstrate the occurrence of a ‘hotspot’ for genetic diversity in both groups of mussels, occurring in the vicinity of the lower Columbia River drainage. We suggest that stream hierarchy may be responsible for this pattern and may produce similar patterns in other widespread freshwater species.
Myosin Phosphatase Isoforms as Determinants of Smooth Muscle Contractile Function and Calcium Sensitivity of Force Production
Authors: Dippold Rachael P. , Fisher Steven A. 
Published: October 2013

AbstractThe dephosphorylation of myosin by the MP causes smooth muscle relaxation. MP is also a key target of signals that regulate vascular tone and thus blood flow and pressure. Here, we review studies from the past two decades that support the hypothesis that the regulated expression of MP subunits is a critical determinant of smooth muscle responses to constrictor and dilator signals. In particular, the highly regulated splicing of the regulatory subunit Mypt1 Exon 24 is proposed to tune sensitivity to NO/cGMP‐mediated relaxation. The regulated transcription of the MP inhibitory subunit CPI‐17 is proposed to determine sensitivity to agonist‐mediated constriction. The expression of these subunits is specific in the microcirculation and varies in developmental and disease contexts. To date, the relationship between MP subunit expression and vascular function in these different contexts is correlative; confirmation of the hypothesis will require the generation of genetically engineered mice to test the role of MP subunits and their isoforms in the specificity of vascular smooth muscle responses to constrictor and dilator signals.
Structure–function studies of Escherichia coli RnlA reveal a novel toxin structure involved in bacteriophage resistance
Authors: Wei Yong , Gao Zeng‐Qiang , Otsuka Yuichi , Naka Kenta , Yonesaki Tetsuro , Zhang Heng , Dong Yu‐Hui 
Published: October 2013

SummaryEscherichia coli RnlA–RnlB is a newly identified toxin–antitoxin (TA) system that plays a role in bacteriophage resistance. RnlA functions as a toxin with mRNA endoribonuclease activity and the cognate antitoxin RnlB inhibits RnlA toxicity in E. coli cells. Interestingly, T4 phage encodes the antitoxin Dmd, which acts against RnlA to promote its own propagation, suggesting that RnlA‐Dmd represents a novel TA system. Here, we have determined the crystal structure of RnlA refined to 2.10 Å. RnlA is composed of three independent domains: NTD (N‐terminal domain), NRD (N repeated domain) and DBD (Dmd‐binding domain), which is an organization not previously observed among known toxin structures. Small‐angle X‐ray scattering (SAXS) analysis revealed that RnlA forms a dimer in solution via interactions between the DBDs from both monomers. The in vitro and in vivo functional studies showed that among the three domains, only the DBD is responsible for recognition and inhibition by Dmd and subcellular location of RnlA. In particular, the helix located at the C‐terminus of DBD plays a vital role in binding Dmd. Our comprehensive studies reveal the key region responsible for RnlA toxicity and provide novel insights into its structure–function relationship.
The ADP‐glucose pyrophosphorylase from Streptococcus mutans provides evidence for the regulation of polysaccharide biosynthesis in Firmicutes
Authors: Asención Diez Matías D. , Demonte Ana M. , Guerrero Sergio A. , Ballicora Miguel A. , Iglesias Alberto A. 
Published: October 2013

SummaryStreptococcus mutans is the leading cause of dental caries worldwide. The bacterium accumulates a glycogen‐like internal polysaccharide, which mainly contributes to its carionegic capacity. S. mutans has two genes (glgC and glgD) respectively encoding putative ADP‐glucose pyrophosphorylases (ADP‐Glc PPase), a key enzyme for glycogen synthesis in most bacteria. Herein, we report the molecular cloning and recombinant expression of both genes (separately or together) followed by the characterization of the respective enzymes. When expressed individually GlgC had ADP‐Glc PPase activity, whereas GlgD was inactive. Interestingly, the coexpressed GlgC/GlgD protein was one order of magnitude more active than GlgC alone. Kinetic characterization of GlgC and GlgC/GlgD pointed out remarkable differences between them. Fructose‐1,6‐bis‐phosphate activated GlgC by twofold, but had no effect on GlgC/GlgD. Conversely, phospho‐enol‐pyruvate and inorganic salts inhibited GlgC/GlgD without affecting GlgC. However, in the presence of fructose‐1,6‐bis‐phosphate GlgC acquired a GlgC/GlgD‐like behaviour, becoming sensitive to the stated inhibitors. Results indicate that S. mutans ADP‐Glc PPase is an allosteric regulatory enzyme exhibiting sensitivity to modulation by key intermediates of carbohydrates metabolism in the cell. The particular regulatory properties of the S. mutans enzyme agree with phylogenetic analysis, where GlgC and GlgD proteins found in other Firmicutes arrange in distinctive clusters.
Knowledge Spillovers, Search, and Creation in China's Emerging Market
Authors: Li Haiyang , Zhang Yan (Anthea) , Lyles Marjorie 
Published: October 2013

AbstractPrior research and the articles included in this special issue demonstrate that in emerging markets in general and in China in particular, knowledge spillovers exist between foreign firms and domestic firms. As domestic markets become more sophisticated, and competition between domestic firms and foreign firms becomes stronger, knowledge is flowing to and being sourced in many different directions: from overseas head offices to foreign firms then on to domestic firms; from domestic firms to domestic firms; and from domestic firms to foreign firms, and back to the multinational corporations' head offices in the form of reverse spillovers and reverse innovation. We propose that knowledge spillovers, search, and creation in an emerging market are a dynamic and reciprocal process with knowledge flowing between and among foreign and domestic firms. This represents a fertile field for future research and we have identified a number of areas ripe for study.
External Knowledge Search Strategies in China's Technology Ventures: The Role of Managerial Interpretations and Ties
Authors: Liu Jingjiang , Chen Lu , Kittilaksanawong Wiboon 
Published: October 2013

AbstractDrawing on the threat-rigidity hypothesis, we examine how managerial opportunity and threat interpretations of external environments affect a technology venture's choice of external knowledge search strategies in an emerging market. Results from a sample of 141 technology ventures in China reveal that opportunity interpretation directly and positively influences both the breadth and depth of external search, whereas threat interpretation directly and negatively influences only external search depth. Furthermore, managerial ties strengthen the positive relationship between opportunity interpretation and external search breadth but weaken the positive relationship on external search depth. Managerial ties weaken the negative relationship between threat interpretation and external search breadth but strengthen the negative relationship on external search depth. Implications for both research and practice are offered.
Loss of FUBP1 expression in gliomas predicts FUBP1 mutation and is associated with oligodendroglial differentiation, IDH1 mutation and 1p/19q loss of heterozygosity
Authors: Baumgarten P. , Harter P. N. , Tönjes M. , Capper D. , Blank A.‐E. , Sahm F. , von Deimling A. , Kolluru V. , Schwamb B. , Rabenhorst U. , Starzetz T. , Kögel D. , Rieker R. J. , Plate K. H. , Ohgaki H. , Radlwimmer B. , Zörnig M. , Mittelbronn M. 
Published: October 2013

AimsThe Far Upstream Element [FUSE] Binding Protein 1 (FUBP1) regulates target genes, such as the cell cycle regulators MYC and p21. FUBP1 is up‐regulated in many tumours and acts as an oncoprotein by stimulating proliferation and inhibiting apoptosis. Recently, FUBP1 mutations were identified in approximately 15% of oligodendrogliomas. To date, all reported FUBP1 mutations have been predicted to inactivate FUBP1, which suggests that in contrast to most other tumours FUBP1 may act as a tumour suppressor in oligodendrogliomas.MethodsAs no data are currently available concerning FUBP1 protein levels in gliomas, we examined the FUBP1 expression profiles of human glial tumours by immunohistochemistry and immunofluorescence. We analysed FUBP1 expression related to morphological differentiation, IDH1 and FUBP1 mutation status, 1p/19q loss of heterozygosity (LOH) as well as proliferation rate.ResultsOur findings demonstrate that FUBP1 expression levels are increased in all glioma subtypes as compared with normal central nervous system (CNS) control tissue and are associated with increased proliferation. In contrast, FUBP1 immunonegativity predicted FUBP1 mutation with a sensitivity of 100% and a specificity of 90% in our cohort and was associated with oligodendroglial differentiation, IDH1 mutation and 1p/19q loss of heterozygosity (LOH). Using this approach, we detected a to‐date undescribed FUBP1 mutation in an oligodendroglioma.ConclusionIn summary, our data indicate an association between of FUBP1 expression and proliferation in gliomas. Furthermore, our findings present FUBP1 immunohistochemical analysis as a helpful additional tool for neuropathological glioma diagnostics predicting FUBP1 mutation.
Possible involvement of cathepsin B/D and caspase‐3 in deferoxamine‐related neuroprotection of early brain injury after subarachnoid haemorrhage in rats
Authors: Yu Z‐Q. , Jia Y. , Chen G. 
Published: October 2013

AimsDeferoxamine (DFX) has recently been shown to have a neuroprotective effect in animal models of subarachnoid haemorrhage (SAH). However, the precise mechanisms underlying these effects remain unclear. Our previous studies found that iron overload in lysosomes leads to lysosomal membrane damage and rupture, and then induces cell apoptosis in the oxidative stress conditions in vitro. We therefore analysed the time‐course of the two of major lysosomal cathepsins (cathepsin B/D) and caspase‐3 expression in brain and evaluated how DFX might affect these proteins and the parameters concerning early brain injury (EBI) after SAH.MethodsWe investigated the time‐course of cathepsin B/D and caspase‐3 expression in the cortex after SAH in rats. Furthermore, we assessed the effect of DFX on regulation of cathepsin B/D and caspase‐3 and EBI following SAH. All SAH animals were subjected to a single injection of autologous blood into the prechiasmatic cistern. Protein concentrations were measured using Western blot analysis and immunohistochemistry. The extent of brain oedema was measured using the wet/dry method. Blood–brain barrier (BBB) permeability was assessed using IgG extravasation. Cortical apoptosis was examined using terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling (TUNEL).ResultsCathepsin B/D and caspase‐3 were up‐regulated in the cortices of affected rats after SAH. Levels of both peaked at 48‐h post‐SAH. After intraperitoneal DFX administration, the elevated expression of cathepsin B/D and caspase‐3 was down‐regulated in the cortex 48 h after blood injection. In the DFX‐treated group, early brain damage events, such as brain oedema, BBB impairment, cortical apoptosis, and alterations in clinical behaviour were significantly ameliorated relative to vehicle‐treated SAH rats.ConclusionsThese results suggest that the lysosomal membrane may be damaged after SAH, which leads to the release of proteases (cathepsin B/D) and activates the apoptotic pathway. Iron overload may be one key mechanism underlying SAH‐induced oxidative stress and DFX may protect the lysosomal membrane, inhibit the release of cathepsin B/D, and ameliorate EBI by suppressing iron overload in the acute phase of SAH.
Patterns of microglial cell activation in frontotemporal lobar degeneration
Authors: Lant Suzannah B. , Robinson Andrew C. , Thompson Jennifer C. , Rollinson Sara , Pickering‐Brown Stuart , Snowden Julie S. , Davidson Yvonne S. , Gerhard Alexander , Mann David M. A. 
Published: October 2013

AimsPathological heterogeneity within patients with frontotemporal lobar degeneration (FTLD) in general precludes the accurate assignment of diagnostic subtype in life. The aim of this study was to assess the extent of microglial cell activation in FTLD in order to determine whether it might be possible to employ this as a diagnostic marker in vivo using PET ligand [11C](R)‐PK11195 in order to differentiate cases of FTLD according to histological subtype.MethodsThe distribution and extent of microglial cell activation was assessed semi‐quantitatively in cortical grey and subcortical white matter of CD68 immunostained sections of frontal and temporal cortex from 78 pathologically confirmed cases of FTLD, 13 of Alzheimer's disease (AD) and 13 controls.ResultsSignificantly higher levels of microglial cell activation than controls occurred in all four regions in FTLD, and in three of the four regions in AD. Microglial activation was greater in frontal subcortical white matter in FTLD than AD, whereas it was higher in temporal cortical grey matter in AD than FTLD. Microglial cell activation was significantly higher in temporal subcortical white matter in FTLD‐MAPT than in other genetic (GRN, C9ORF72) or non‐genetic forms of FTLD.ConclusionsThe present study suggests that high levels of microglial cell involvement in temporal lobe (subcortical white matter) might serve as a marker of inherited FTLD associated with intronic mutations in MAPT, with a relatively intense signal in this region in PET studies using [11C](R)‐PK11195 as microglial cell marker could indicate the presence of MAPT mutation in vivo.