bluuebunny/crossref_metadata_2025_split huggingface dataset:
The coral immune response facilitates protection against microbes during tissue regeneration
Authors: van de Water Jeroen A. J. M. , Ainsworth Tracy D. , Leggat William , Bourne David G. , Willis Bette L. , van Oppen Madeleine J. H. 
Published: June 2015

AbstractIncreasing physical damage on coral reefs from predation, storms and anthropogenic disturbances highlights the need to understand the impact of injury on the coral immune system. In this study, we examined the regulation of the coral immune response over 10 days following physical trauma artificially inflicted on in situ colonies of the coral Acropora aspera, simultaneously with bacterial colonization of the lesions. Corals responded to injury by increasing the expression of immune system‐related genes involved in the Toll‐like and NOD‐like receptor signalling pathways and the lectin–complement system in three phases (<2, 4 and 10 days post‐injury). Phenoloxidase activity was also significantly upregulated in two phases (<3 and 10 days post‐injury), as were levels of non‐fluorescent chromoprotein. In addition, green fluorescent protein expression was upregulated in response to injury from 4 days post‐injury, while cyan fluorescent protein expression was reduced. No shifts in the composition of coral‐associated bacterial communities were evident following injury based on 16S rRNA gene amplicon pyrosequencing. Bacteria‐specific fluorescence in situ hybridization also showed no evidence of bacterial colonization of the wound or regenerating tissues. Coral tissues showed near‐complete regeneration of lesions within 10 days. This study demonstrates that corals exhibit immune responses that support rapid recovery following physical injury, maintain coral microbial homeostasis and prevent bacterial infestation that may compromise coral fitness.
Fine‐scale refuges can buffer demographic and genetic processes against short‐term climatic variation and disturbance: a 22‐year case study of an arboreal marsupial
Authors: Banks Sam C. , Lorin Thibault , Shaw Robyn E. , McBurney Lachlan , Blair David , Blyton Michaela D.J. , Smith Annabel L. , Pierson Jennifer C. , Lindenmayer David B. 
Published: June 2015

AbstractEcological disturbance and climate are key drivers of temporal dynamics in the demography and genetic diversity of natural populations. Microscale refuges are known to buffer species’ persistence against environmental change, but the effects of such refuges on demographic and genetic patterns in response to short‐term environmental variation are poorly understood. We quantified demographic and genetic responses of mountain brushtail possums (Trichosurus cunninghami) to rainfall variability (1992–2013) and to a major wildfire. We hypothesized that there would be underlying differences in demographic and genetic processes between an unburnt mesic refuge and a topographically exposed zone that was burnt in 2009. Fire caused a 2‐year decrease in survival in the burnt zone, but the population grew after the fire due to immigration, leading to increased expected heterozygosity. We documented a fire‐related behavioural shift, where the rate of movement by individuals in the unburnt refuge to the burnt zone decreased after fire. Irrespective of the fire, there were long‐term differences in demographic and genetic parameters between the mesic/unburnt refuge and the nonmesic/burnt zone. Survival was high and unaffected by rainfall in the refuge, but lower and rainfall‐dependent in the nonmesic zone. Net movement of individuals was directional, from the mesic refuge to the nonmesic zone, suggesting fine‐scale source–sink dynamics. There were higher expected heterozygosity (HE) and temporal genetic stability in the refuge, but lower HE and marked temporal genetic structure in the exposed habitat, consistent with reduced generational overlap caused by elevated mortality and immigration. Thus, fine‐scale refuges can mediate the short‐term demographic and genetic effects of climate and ecological disturbance.
Palaeo‐islands as refugia and sources of genetic diversity within volcanic archipelagos: the case of the widespread endemic Canarina canariensis (Campanulaceae)
Authors: Mairal M. , Sanmartín I. , Aldasoro J. J. , Culshaw V. , Manolopoulou I. , Alarcón M. 
Published: June 2015

AbstractGeographical isolation by oceanic barriers and climatic stability has been postulated as some of the main factors driving diversification within volcanic archipelagos. However, few studies have focused on the effect that catastrophic volcanic events have had on patterns of within‐island differentiation in geological time. This study employed data from the chloroplast (cpDNA haplotypes) and the nuclear (AFLPs) genomes to examine the patterns of genetic variation in Canarina canariensis, an iconic plant species associated with the endemic laurel forest of the Canary Islands. We found a strong geographical population structure, with a first divergence around 0.8 Ma that has Tenerife as its central axis and divides Canarian populations into eastern and western clades. Genetic diversity was greatest in the geologically stable ‘palaeo‐islands’ of Anaga, Teno and Roque del Conde; these areas were also inferred as the ancestral location of migrant alleles towards other disturbed areas within Tenerife or the nearby islands using a Bayesian approach to phylogeographical clustering. Oceanic barriers, in contrast, appear to have played a lesser role in structuring genetic variation, with intra‐island levels of genetic diversity larger than those between‐islands. We argue that volcanic eruptions and landslides after the merging of the palaeo‐islands 3.5 Ma played key roles in generating genetic boundaries within Tenerife, with the palaeo‐islands acting as refugia against extinction, and as cradles and sources of genetic diversity to other areas within the archipelago.
Real Exchange Rate and Economic Growth: New Empirical Evidence
Authors: Missio Fabrício J. , Jayme Frederico G. , Britto Gustavo , Luis Oreiro José 
Published: June 2015

ABSTRACTThe article empirically analyses the relationship between real exchange rate (RER) and growth rate of output. We first estimate the effect of the index of RER undervaluation on the rate of output growth in two samples of countries from 1978 to 2007. Our contribution is the use of a different dataset that increases the number of countries in the sample, as well as the number of available control variables. In doing so, the article adds to the literature by applying a method that allows for the control of income levels (quantile regressions). So, we present new findings on a non‐linear relationship the RER‐growth nexus. We conclude that maintaining a competitive level of RER has positive effects on growth rate.
Quantitative Imaging In Vivo of Functioning Lymphatic Vessels Around Human Melanoma and Benign Nevi
Authors: Akhras Victoria , Ramakrishnan Rathi , Stanton Anthony W.B. , Levick John R. , Cook Martin G. , Chong Heung , Mortimer Peter S. 
Published: June 2015

AbstractObjectivesThe density of functioning human lymphatics in vivo and of immunohistochemically defined lymphatics was quantified around melanomas, benign nevi, and matched normal skin, to assess the current lymphangiogenesis paradigm. We investigated whether histological and functioning density increased around melanomas compared with benign nevi or matched skin; whether functioning and histological density increased similarly; and whether larger increases occurred around metastatic melanomas.MethodsFunctioning density was quantified in vivo as the total amount of human dermal microlymphatics taking up fluorescent marker injected at the lesion margin. After tissue excision, perilesion histological density was quantified using podoplanin marker D2‐40.ResultsHistological density was raised similarly around metastasising and non‐metastasising melanomas compared with normal skin (+71%, p < 0.0001, n = 32); but was also raised significantly around benign nevi (+17%, p = 0.03, n = 20). In contrast, functioning lymphatic density was substantially reduced around the margins of melanomas (both metastasising and non‐metastasising) compared with benign nevi (by 65%, p = 0.02) or normal skin (by 53%, p = 0.0014).ConclusionsRaised perilesion histological lymphatic density is not unique to melanoma but occurs also around benign nevi. The findings indicated that the number of functioning lateral lymphatics around human melanomas in vivo but not benign nevi is reduced, despite histologically increased numbers of lymphatics.
RNA degradosomes in bacteria and chloroplasts: classification, distribution and evolution of RNase E homologs
Authors: Aït‐Bara Soraya , Carpousis Agamemnon J. 
Published: June 2015

SummaryRibonuclease E (RNase E) of Escherichia coli, which is the founding member of a widespread family of proteins in bacteria and chloroplasts, is a fascinating enzyme that still has not revealed all its secrets. RNase E is an essential single‐strand specific endoribonuclease that is involved in the processing and degradation of nearly every transcript in E. coli. A striking enzymatic property is a preference for substrates with a 5′ monophosphate end although recent work explains how RNase E can overcome the protection afforded by the 5′ triphosphate end of a primary transcript. Other features of E. coli RNase E include its interaction with enzymes involved in RNA degradation to form the multienzyme RNA degradosome and its localization to the inner cytoplasmic membrane. The N‐terminal catalytic core of the RNase E protomer associates to form a tetrameric holoenzyme. Each RNase E protomer has a large C‐terminal intrinsically disordered (ID) noncatalytic region that contains sites for interactions with protein components of the RNA degradosome as well as RNA and phospholipid bilayers. In this review, RNase E homologs have been classified into five types based on their primary structure. A recent analysis has shown that type I RNase E in the γ‐proteobacteria forms an orthologous group of proteins that has been inherited vertically. The RNase E catalytic core and a large ID noncatalytic region containing an RNA binding motif and a membrane targeting sequence are universally conserved features of these orthologs. Although the ID noncatalytic region has low composition and sequence complexity, it is possible to map microdomains, which are short linear motifs that are sites of interaction with protein and other ligands. Throughout bacteria, the composition of the multienzyme RNA degradosome varies with species, but interactions with exoribonucleases (PNPase, RNase R), glycolytic enzymes (enolase, aconitase) and RNA helicases (DEAD‐box proteins, Rho) are common. Plasticity in RNA degradosome composition is due to rapid evolution of RNase E microdomains. Characterization of the RNase E‐PNPase interaction in α‐proteobacteria, γ‐proteobacteria and cyanobacteria suggests that it arose independently several times during evolution, thus conferring an advantage in control and coordination of RNA processing and degradation.
Srr2, a multifaceted adhesin expressed by ST‐17 hypervirulent Group B Streptococcus involved in binding to both fibrinogen and plasminogen
Authors: Six Anne , Bellais Samuel , Bouaboud Abdelouhab , Fouet Agnès , Gabriel Christelle , Tazi Asmaa , Dramsi Shaynoor , Trieu‐Cuot Patrick , Poyart Claire 
Published: June 2015

SummaryThe Group B Streptococcus (GBS) ‘hypervirulent’ ST‐17 clone is strongly associated with invasive neonatal meningitis. Comparative genome analyses revealed that the serine‐rich repeat (Srr) glycoprotein Srr2 is a cell wall‐anchored protein specific for ST‐17 strains, the non‐ST‐17 isolates expressing Srr1. Here, we unravel the binding capacity of GBS Srr proteins to relevant components of the host fibrinolysis pathway. We demonstrate that: (i) Srr2 binds plasminogen and plasmin whereas Srr1 does not; (ii) the ability of ST‐17 strains to bind fibrinogen reflects a high level surface display of Srr2 combined with a higher affinity of Srr2 than Srr1 to bind this ligand; and (iii) Srr2 binding to host plasma proteins results in the formation of bacterial aggregates that are efficiently endocytosed by phagocytes. Importantly, we show that Srr2 increased bacterial survival to phagocytic killing and bacterial persistence in a murine model of meningitis. We conclude that Srr2 is a multifaceted adhesin used by the ST‐17 clone to hijack ligands of the host coagulation system, thereby contributing to bacterial dissemination and invasiveness, and ultimately to meningitis.
Bacillus subtilis SalA is a phosphorylation‐dependent transcription regulator that represses scoC and activates the production of the exoprotease AprE
Authors: Derouiche Abderahmane , Shi Lei , Bidnenko Vladimir , Ventroux Magali , Pigonneau Nathalie , Franz‐Wachtel Mirita , Kalantari Aida , Nessler Sylvie , Noirot‐Gros Marie‐Françoise , Mijakovic Ivan 
Published: June 2015

SummaryBacillus subtilis Mrp family protein SalA has been shown to indirectly promote the production of the exoprotease AprE by inhibiting the expression of scoC, which codes for a repressor of aprE. The exact mechanism by which SalA influences scoC expression has not been clarified previously. We demonstrate that SalA possesses a DNA‐binding domain (residues 1–60), which binds to the promoter region of scoC. The binding of SalA to its target DNA depends on the presence of ATP and is stimulated by phosphorylation of SalA at tyrosine 327. The B. subtilis protein‐tyrosine kinase PtkA interacts specifically with the C‐terminal domain of SalA in vivo and in vitro and is responsible for activating its DNA binding via phosphorylation of tyrosine 327. In vivo, a mutant mimicking phosphorylation of SalA (SalA Y327E) exhibited a strong repression of scoC and consequently overproduction of AprE. By contrast, the non‐phosphorylatable SalA Y327F and the ΔptkA exhibited the opposite effect, stronger expression of scoC and lower production of the exoprotease. Interestingly, both SalA and PtkA contain the same ATP‐binding Walker domain and have thus presumably arisen from the common ancestral protein. Their regulatory interplay seems to be conserved in other bacteria.
Regulation of Plasmodium falciparum Origin Recognition Complex subunit 1 (PfORC1) function through phosphorylation mediated by CDK‐like kinase PK5
Authors: Deshmukh Abhijit S. , Agarwal Meetu , Mehra Parul , Gupta Ashish , Gupta Nidhi , Doerig Christian D. , Dhar Suman Kumar 
Published: June 2015

SummaryPlasmodium falciparum Origin Recognition Complex subunit 1 (PfORC1) has been implicated in DNA replication and var gene regulation. While the C‐terminus is involved in DNA replication, the specific role of N‐terminus has been suggested in var gene regulation in a Sir2‐dependent manner. PfORC1 is localized at the nuclear periphery, where the clustering of chromosomal ends at the early stage of parasite development may be crucial for the regulation of subtelomeric var gene expression. Upon disassembly of telomeric clusters at later stages of parasite development, ORC1 is distributed in the nucleus and parasite cytoplasm where it may be required for its other cellular functions including DNA replication. The level of ORC1 decreases dramatically at the late schizont stage. The mechanisms that mediate regulation of PfORC1 function are largely unknown. Here we show, by the use of recombinant proteins and of transgenic parasites expressing wild type or mutant forms of ORC1, that phosphorylation of the PfORC1‐N terminal domain by the cyclin‐dependent kinase (CDK) PfPK5 abolishes DNA‐binding activity and leads to changes in subcellular localization and proteasome‐mediated degradation of the protein in schizonts. These results reveal that PfORC1 phosphorylation by a CDK is central to the regulation of important biological functions like DNA replication and var gene silencing.
The durably resistant rice cultivar Digu activates defence gene expression before the full maturation of Magnaporthe oryzae appressorium
Authors: Li Weitao , Liu Ya , Wang Jing , He Min , Zhou Xiaogang , Yang Chao , Yuan Can , Wang Jichun , Chern Mawsheng , Yin Junjie , Chen Weilan , Ma Bingtian , Wang Yuping , Qin Peng , Li Shigui , Ronald Pamela , Chen Xuewei 
Published: June 2015

SummaryRice blast caused by the fungal pathogen Magnaporthe oryzae is one of the most destructive diseases worldwide. Although the rice–M. oryzae interaction has been studied extensively, the early molecular events that occur in rice before full maturation of the appressorium during M. oryzae invasion are unknown. Here, we report a comparative transcriptomics analysis of the durably resistant rice variety Digu and the susceptible rice variety Lijiangxintuanheigu (LTH) in response to infection by M. oryzae (5, 10 and 20 h post‐inoculation, prior to full development of the appressorium). We found that the transcriptional responses differed significantly between these two rice varieties. Gene ontology and pathway analyses revealed that many biological processes, including extracellular recognition and biosynthesis of antioxidants, terpenes and hormones, were specifically activated in Digu shortly after infection. Forty‐eight genes encoding receptor kinases (RKs) were significantly differentially regulated by M. oryzae infection in Digu. One of these genes, LOC_Os08g10300, encoding a leucine‐rich repeat RK from the LRR VIII‐2 subfamily, conferred enhanced resistance to M. oryzae when overexpressed in rice. Our study reveals that a multitude of molecular events occur in the durably resistant rice Digu before the full maturation of the appressorium after M. oryzae infection and that membrane‐associated RKs play important roles in the early response.
Borrelia burgdorferi sensu lato and co‐infections with Anaplasma phagocytophilum and Rickettsia spp. in Ixodes ricinus in Hamburg, Germany
Authors: MAY K. , JORDAN D. , FINGERLE V. , STRUBE C. 
Published: June 2015

AbstractTo obtain initial data on Borrelia burgdorferi sensu lato (Spirochaetales: Spirochaetaceae) in Ixodes ricinus (Ixodida: Ixodidae) ticks in Hamburg, Germany, 1400 questing ticks were collected by flagging at 10 different public recreation areas in 2011 and analysed using probe‐based quantitative real‐time polymerase chain reaction. The overall rate of infection with B. burgdorferi s.l. was 34.1%; 30.0% of adults were infected (36.7% of females and 26.0% of males), as were 34.5% of nymphs. Significant differences in tick infection rates were observed between the spring and summer/autumn months, as well as among sampling locations. Borrelia genospecies identification by reverse line blotting was successful in 43.6% of positive tick samples. The most frequent genospecies was Borrelia garinii/Borrelia bavariensis, followed by Borrelia afzelii, Borrelia valaisiana, B. burgdorferi sensu stricto, Borrelia spielmanii, Borrelia bissettii and Borrelia lusitaniae. Based on previously published data, co‐infection of Borrelia and Rickettsiales spp. was determined in 25.8% of ticks. Overall, 22.9% of ticks were co‐infected with Rickettsia spp. (Rickettsiales: Rickettsiaceae), 1.7% with Anaplasma phagocytophilum (Rickettsiales: Anaplasmataceae), and 1.2% with both pathogens. Study results show a high prevalence of Borrelia‐positive ticks in recreation areas in the northern German city of Hamburg and the potential health risk to humans in these areas should not be underestimated.
Neuronal DNA damage response‐associated dysregulation of signalling pathways and cholesterol metabolism at the earliest stages of Alzheimer‐type pathology
Authors: Simpson Julie E. , Ince Paul G. , Minett Thais , Matthews Fiona E. , Heath Paul R. , Shaw Pamela J. , Goodall Emily , Garwood Claire J. , Ratcliffe Laura E. , Brayne Carol , Rattray Magnus , Wharton Stephen B. ,   the MRC Cognitive Function and Ageing Neuropathology Study Group
Published: June 2015

AimsOxidative damage and an associated DNA damage response (DDR) are evident in mild cognitive impairment and early Alzheimer's disease, suggesting that neuronal dysfunction resulting from oxidative DNA damage may account for some of the cognitive impairment not fully explained by Alzheimer‐type pathology.MethodsFrontal cortex (Braak stage 0–II) was obtained from the Medical Research Council's Cognitive Function and Ageing Study cohort. Neurones were isolated from eight cases (four high and four low DDR) by laser capture microdissection and changes in the transcriptome identified by microarray analysis.ResultsTwo thousand three hundred seventy‐eight genes were significantly differentially expressed (1690 up‐regulated, 688 down‐regulated, P < 0.001) in cases with a high neuronal DDR. Functional grouping identified dysregulation of cholesterol biosynthesis, insulin and Wnt signalling, and up‐regulation of glycogen synthase kinase 3β. Candidate genes were validated by quantitative real‐time polymerase chain reaction. Cerebrospinal fluid levels of 24(S)‐hydroxycholesterol associated with neuronal DDR across all Braak stages (rs = 0.30, P = 0.03).ConclusionsA persistent neuronal DDR may result in increased cholesterol biosynthesis, impaired insulin and Wnt signalling, and increased GSK3β, thereby contributing to neuronal dysfunction independent of Alzheimer‐type pathology in the ageing brain.
Polyglutamine aggregation inHuntington's disease and spinocerebellar ataxia type 3: similar mechanisms in aggregate formation
Authors: Seidel K. , Siswanto S. , Fredrich M. , Bouzrou M. , Brunt E. R. , van Leeuwen F. W. , Kampinga H. H. , Korf H. ‐W. , Rüb U. , den Dunnen W. F. A. 
Published: June 2015

AimsPolyglutamine (polyQ) diseases are characterized by the expansion of a polymorphic glutamine sequence in disease‐specific proteins and exhibit aggregation of these proteins. This is combated by the cellular protein quality control (PQC) system, consisting of chaperone‐mediated refolding as well as proteasomal and lysosomal degradation pathways. Our recent study in thepolyQdisease spinocerebellar ataxia type 3 (SCA3) suggested a distinct pattern of protein aggregation andPQCdysregulation.MethodsTo corroborate these findings we have investigated immunohistochemically stained 5 μm sections from different brain areas ofHuntington's disease (HD) andSCA3patients.ResultsIrrespective of disease and brain region, we observed peri‐ and intranuclearpolyQprotein aggregates. A subset of neurones with intranuclear inclusions bodies exhibited signs of proteasomal dysfunction, up‐regulation ofHSPA1Aand re‐distribution ofDNAJB1. The extent of the observed effects varied depending on brain area and disease protein.ConclusionsOur results suggest a common sequence, in which formation of cytoplasmic and nuclear inclusions precede proteasomal impairment and induction of the cellular stress response. Clearly, impairment of thePQCis not the primary cause for inclusion formation, but rather a consequence that might contribute to neuronal dysfunction and death. Notably, the inclusion pathology is not directly correlated to the severity of the degeneration in different areas, implying that different populations of neurones respond topolyQaggregation with varying efficacy and that protein aggregation outside the neuronal perikaryon (e.g. axonal aggregates) or other effects ofpolyQaggregation, which are more difficult to visualize, may contribute to neurodegeneration.