bluuebunny/crossref_metadata_2025_split huggingface dataset:
Invasion success and genetic diversity of introduced populations of guppiesPoecilia reticulatain Australia
Authors: LINDHOLM ANNA K. , BREDEN FELIX , ALEXANDER HEATHER J. , CHAN WOON‐KHIONG , THAKURTA SUMITA G. , BROOKS ROBERT 
Published: August 2005

AbstractHigh genetic diversity is thought to characterize successful invasive species, as the potential to adapt to new environments is enhanced and inbreeding is reduced. In the last century, guppies,Poecilia reticulata,repeatedly invaded streams in Australia and elsewhere. Quantitative genetic studies of one Australian guppy population have demonstrated high additive genetic variation for autosomal and Y‐linked morphological traits. The combination of colonization success, high heritability of morphological traits, and the possibility of multiple introductions to Australia raised the prediction that neutral genetic diversity is high in introduced populations of guppies. In this study we examine genetic diversity at nine microsatellite and one mitochondrial locus for seven Australian populations. We used mtDNA haplotypes from the natural range of guppies and from domesticated varieties to identify source populations. There were a minimum of two introductions, but there was no haplotype diversity within Australian populations, suggesting a founder effect. This was supported by microsatellite markers, as allelic diversity and heterozygosity were severely reduced compared to one wild source population, and evidence of recent bottlenecks was found. Between Australian populations little differentiation of microsatellite allele frequencies was detected, suggesting that population admixture has occurred historically, perhaps due to male‐biased gene flow followed by bottlenecks. Thus success of invasion of Australia and high additive genetic variance in Australian guppies are not associated with high levels of diversity at molecular loci. This finding is consistent with the release of additive genetic variation by dominance and epistasis following inbreeding, and with disruptive and negative frequency‐dependent selection on fitness traits.
Genetic structure of the whitefly Bemisia tabaci in the Asia–Pacific region revealed using microsatellite markers
Authors: DE BARRO P. J. 
Published: August 2005

Abstract Bemisia tabaci (Hemiptera: Aleyrodidae) is a haplo‐diploid species of sap‐feeding insect belonging to the group of insects commonly known as whiteflies. From earlier analyses of mitochondrial and ribosomal markers it has been concluded that in the Asia–Pacific region there were three major indigenous races as well as a large collection of genotypes with no clear association with any race. This new study uses 15 microsatellite loci and demonstrates that the indigenous Asia–Pacific genotypes can be split into six genetic populations with little or no gene flow between them. These bare only superficial similarity to the mitochondrial and ribosomal defined races. Moreover, four of the six can be further split into two subpopulations that again show little evidence gene flow between them. While the patterns reflect a strong geographical structure, physical barriers alone cannot explain all the observed structure. Differential host‐plant utilization explained some of the substructure, but could not explain the overall structure. The roles of mating interference and Wolbachia in developing the genetic structure are considered. The lack of gene flow between genetic populations and some subpopulations further suggests that the barriers were either sufficiently impermeable to immigration or that reproductive isolation and competitive interactions were sufficiently strong to prevent gene flow. If the latter is the case, it suggests that there may be as many as 10 morphologically indistinguishable species indigenous to the Asia–Pacific region.
Species status and phylogeography of two closely related Coptolabrus species (Coleoptera: Carabidae) in South Korea inferred from mitochondrial and nuclear gene sequences
Authors: ZHANG A. B. , KUBOTA K. , TAKAMI Y. , KIM J. L. , KIM J. K. , SOTA T. 
Published: August 2005

AbstractWe investigated the species status and intraspecific phylogeography in South Korea of two ground beetle species, Coptolabrus jankowskii and Coptolabrus smaragdinus (Coleoptera: Carabidae), using statistical parsimony networks and nested clade analyses based on sequences from the mitochondrial cytochrome oxidase subunit I (COI) and nuclear phosphoenolpyruvate carboxykinase (PepCK) and wingless (Wg) genes. Although traditional parsimony tree construction generally failed to resolve interspecific relationships and construct biologically meaningful genealogies, analysis using statistical parsimony networks yielded statistically significant inter‐ and intraspecific genealogical structures. We found that although these two species represent a notable case of trans‐species polymorphisms in both mitochondrial and nuclear gene sequences, their status as separate species was evidenced by the nonrandom association between species and nested clades at various nesting levels. The exceptional occurrence of shared identical or very similar COI sequences was considered to be the result of introgressive hybridization. In addition, range expansion and fragmentation events across the Korean Peninsula and adjacent islands were inferred from nested clade phylogeographical analyses. The COI gene revealed the geographical divergence of major eastern and western clades and historical biogeographical events within each major clade, whereas the nuclear PepCK gene, which did not reveal corresponding east–west clades, indicated past fragmentation and range expansion across wide areas that may have been the result of older biogeographical events. Thus, phylogeographical inferences drawn from analyses of mitochondrial and nuclear genes can reveal different and potentially complementary information about phylogeographical processes.
A genome‐wide screen identifies a Bordetella type III secretion effector and candidate effectors in other species
Authors: Panina Ekaterina M. , Mattoo Seema , Griffith Natasha , Kozak Natalia A. , Yuk Ming H. , Miller Jeff F. 
Published: August 2005

Summary Bordetella bronchiseptica utilizes a type III secretion system (TTSS) for induction of non‐apoptotic cytotoxicity in host cells and modulation of host immunity. The identity of Bordetella TTSS effectors, however, has remained elusive. Here we report a genome‐wide screen for TTSS effectors based on shared biophysical and functional characteristics of class I chaperones and their frequent colocalization with TTSS effectors. When applied to B. bronchiseptica, the screen identified the first TTSS chaperone‐effector locus, btcA‐bteA, and we experimentally confirmed its function. Expression of bteA is co‐ordinated with expression of TTSS apparatus genes, BteA is secreted through the TTSS of B. bronchiseptica, it is required for cytotoxicity towards mammalian cells, and it is highly conserved in the human‐adapted subspecies B. pertussis and B. parapertussis. Transfection of bteA into epithlieal cells results in rapid cell death, indicating that BteA alone is sufficient to induce potent cytotoxicity. Finally, an in vitro interaction between BteA and BtcA was demonstrated. The search for TTSS chaperones and effectors was then expanded to other bacterial genomes, including mammalian and insect pathogens, where we identified a large number of novel candidate chaperones and effectors. Although the majority of putative effectors are proteins of unknown function, several have similarities to eukaryotic protein domains or previously identified effectors from other species.
Chromosomal DNA transfer in Mycobacterium smegmatis is mechanistically different from classical Hfr chromosomal DNA transfer
Authors: Wang Jun , Karnati Pavan K. , Takacs Carter M. , Kowalski Joseph C. , Derbyshire Keith M. 
Published: August 2005

SummaryClassical conjugal DNA transfer of chromosomal DNA in bacteria requires the presence of a cis‐acting site, oriT, in the chromosome. Acquisition of an oriT occurs if a conjugative plasmid integrates into the chromosome to form an Hfr donor strain, which can transfer extensive regions of chromosomal DNA. Because oriT sequences are unique, and because transfer occurs in a 5′ to 3′ direction, the frequency with which a particular gene is inherited by the recipient depends on the gene's location: those closest to the 3′ side of oriT are transferred most efficiently. In addition, as the entire chromosome must be transferred to regenerate oriT, Hfr transconjugants never become donors. Here we describe novel aspects of a chromosomal DNA transfer system in Mycobacterium smegmatis. We demonstrate that there are multiple transfer initiations from a donor chromosome and, as a result, the inheritance of any gene is location‐independent. Transfer is not contiguous; instead, multiple non‐linked segments of DNA can be inherited in a recipient. However, we show that, with appropriate selection, segments of DNA at least 266 kb in length can be transferred. In further contrast to Hfr transfer, transconjugants can become donors, suggesting that the recipient chromosome contains multiple cis‐acting sequences required for transfer, but lacks the trans‐acting transfer functions. We exploit these observations to map a donor‐determining locus in the M. smegmatis chromosome using genetic linkage analysis. Together, these studies further underline the unique nature of the M. smegmatis chromosomal transfer system.
CsgA is a pathogen‐associated molecular pattern of Salmonella enterica serotype Typhimurium that is recognized by Toll‐like receptor 2
Authors: Tükel Çagla , Raffatellu Manuela , Humphries Andrea D. , Wilson R. Paul , Andrews‐Polymenis Helene L. , Gull Tamara , Figueiredo Josely F. , Wong Michelle H. , Michelsen Kathrin S. , Akçelik Mustafa , Adams L. Garry , Bäumler Andreas J. 
Published: August 2005

SummaryKnowledge about the origin and identity of the microbial products recognized by the innate immune system is important for understanding the pathogenesis of inflammatory diseases. We investigated the potential role of Salmonella enterica serotype Typhimurium fimbriae as pathogen‐associated molecular patterns (PAMPs) that may stimulate innate pathways of inflammation. We screened a panel of 11 mutants, each carrying a deletion of a different fimbrial operon, for their enteropathogenicity using the calf model of human gastroenteritis. One mutant (csgBA) was attenuated in its ability to elicit fluid accumulation and GROα mRNA expression in bovine ligated ileal loops. The mechanism by which thin curled fimbriae encoded by the csg genes contribute to inflammation was further investigated using tissue culture. The S. Typhimurium csgBA mutant induced significantly less IL‐8 production than the wild type in human macrophage‐like cells. Purified thin curled fimbriae induced IL‐8 expression in human embryonic kidney (HEK293) cells transfected with Toll‐like receptor (TLR) 2/CD14 but not in cells transfected with TLR5, TLR4/MD2/CD14 or TLR11. Fusion proteins between the major fimbrial subunit of thin curled fimbriae (CsgA) and glutathione‐S‐transferase (GST) elicited IL‐8 production in HEK293 cells transfected with TLR2/CD14. Proteinase K treatment abrogated IL‐8 production elicited in these cells by GST–CsgA, but not by synthetic lipoprotein. GST–CsgA elicited more IL‐6 production than GST in bone marrow‐derived macrophages from TLR2+/+ mice, while there was no difference in IL‐6 secretion between GST–CsgA and GST in macrophages from TLR2–/– mice. These data suggested that CsgA is a PAMP that is recognized by TLR2.
Dual regulatory pathways integrating the RcsC–RcsD–RcsB signalling system control enterohaemorrhagic Escherichia coli pathogenicity
Authors: Tobe Toru , Ando Hiroki , Ishikawa Hiroko , Abe Hiroyuki , Tashiro Kosuke , Hayashi Tetsuya , Kuhara Satoru , Sugimoto Nakaba 
Published: August 2005

SummaryBacterial pathogenesis is strictly regulated in response to changes in environmental conditions. A His–Asp phosphorelay system consisting of a sensor kinase and response regulator is used by Gram‐positive and Gram‐negative bacteria to control gene expression in response to environmental stimuli. We screened His–Asp phosphorelay systems for their effect on virulence expression in enterohaemorrhagic Escherichia coli (EHEC), and found rcsD or rcsB overexpression enhanced locus for enterocyte effacement (LEE) gene transcription and adherence to Caco‐2 cells through transcriptional activation of the ler regulatory gene. An EHEC‐specific regulator GrvA, encoded by ECs1274, was required for ler transcription activation by RcsB. Furthermore, GrvA activated ler transcription in E. coli K12. Stimulation of the RcsDCB regulatory system by RcsF overexpression slightly increased EspB expression in the wild type but not the ECs1274 mutant. However, EspB expression in an rcsB deletion mutant increased compared with wild type, suggesting that RcsB negatively regulates LEE gene expression and that active RcsB protein is present under normal growth conditions. Deletion of pchA, which encodes a positive regulator for ler, abolished the effect of the rcsB deletion, suggesting that pchA mediated the negative RcsB effect. pchA transcript levels decreased when RcsB expression increased. Thus, LEE gene transcription may be regulated by RcsB through two oppositely regulated O157‐specific regulators, PchA and GrvA.
The Helicobacter pylori MutS protein confers protection from oxidative DNA damage
Authors: Wang Ge , Alamuri Praveen , Humayun M. Zafri , Taylor Diane E. , Maier Robert J. 
Published: August 2005

SummaryThe human gastric pathogenic bacterium Helicobacter pylori lacks a MutSLH‐like DNA mismatch repair system. Here, we have investigated the functional roles of a mutS homologue found in H. pylori, and show that it plays an important physiological role in repairing oxidative DNA damage. H. pylori mutS mutants are more sensitive than wild‐type cells to oxidative stress induced by agents such as H2O2, paraquat or oxygen. Exposure of mutS cells to oxidative stress results in a significant (∼10‐fold) elevation of mutagenesis. Strikingly, most mutations in mutS cells under oxidative stress condition are G:C to T:A transversions, a signature of 8‐oxoguanine (8‐oxoG). Purified H. pylori MutS protein binds with a high specific affinity to double‐stranded DNA (dsDNA) containing 8‐oxoG as well as to DNA Holliday junction structures, but only weakly to dsDNA containing a G:A mismatch. Under oxidative stress conditions, mutS cells accumulate higher levels (approximately threefold) of 8‐oxoG DNA lesions than wild‐type cells. Finally, we observe that mutS mutant cells have reduced colonization capacity in comparison to wild‐type cells in a mouse infection model.
Requirement of the dephospho‐form of enzyme IIANtr for derepression of Escherichia coli K‐12 ilvBN expression
Authors: Lee Chang‐Ro , Koo Byoung‐Mo , Cho Seung‐Hyon , Kim Yu‐Jung , Yoon Mi‐Jeong , Peterkofsky Alan , Seok Yeong‐Jae 
Published: August 2005

SummaryWhile the proteins of the phosphoenolpyruvate:carbohydrate phosphotransferase system (carbohydrate PTS) have been shown to regulate numerous targets, little such information is available for the nitrogen‐metabolic phosphotransferase system (nitrogen‐metabolic PTS). To elucidate the physiological role of the nitrogen‐metabolic PTS, we carried out phenotype microarray (PM) analysis with Escherichia coli K‐12 strain MG1655 deleted for the ptsP gene encoding the first enzyme of the nitrogen‐metabolic PTS. Together with the PM data, growth studies revealed that a ptsN (encoding enzyme IIANtr) mutant became extremely sensitive to leucine‐containing peptides (LCPs), while both ptsP (encoding enzyme INtr) and ptsO (encoding NPr) mutants were more resistant than wild type. The toxicity of LCPs was found to be due to leucine and the dephospho‐form of enzyme IIANtr was found to be necessary to neutralize leucine toxicity. Further studies showed that the dephospho‐form of enzyme IIANtr is required for derepression of the ilvBN operon encoding acetohydroxy acid synthase I catalysing the first step common to the biosynthesis of the branched‐chain amino acids.
PchR‐box recognition by the AraC‐type regulator PchR of Pseudomonas aeruginosa requires the siderophore pyochelin as an effector
Authors: Michel Laurent , González Nicolas , Jagdeep Steve , Nguyen‐Ngoc Tu , Reimmann Cornelia 
Published: August 2005

SummaryUnder iron limitation, the opportunistic human pathogen Pseudomonas aeruginosa produces the siderophore pyochelin. When secreted into the extracellular environment, pyochelin complexes ferric ions and delivers them, via the outer membrane receptor FptA, to the bacterial cytoplasm. Extracellular pyochelin also acts as a signalling molecule, inducing the expression of pyochelin biosynthesis and uptake genes by a mechanism involving the AraC‐type regulator PchR. We have identified a 32 bp conserved sequence element (PchR‐box) in promoter regions of pyochelin‐controlled genes and we show that the PchR‐box in the pchR‐pchDCBA intergenic region is essential for the induction of the pyochelin biosynthetic operon pchDCBA and the repression of the divergently transcribed pchR gene. PchR was purified as a fusion with maltose‐binding protein (MBP). Mobility shift assays demonstrated specific binding of MBP‐PchR to the PchR‐box in the presence, but not in the absence of pyochelin and iron. PchR‐box mutations that interfered with pyochelin‐dependent regulation in vivo, also affected pyochelin‐dependent PchR‐box recognition in vitro. We conclude that pyochelin, probably in its iron‐loaded state, is the intracellular effector required for PchR‐mediated regulation. The fact that extracellular pyochelin triggers this regulation suggests that the siderophore can enter the cytoplasm.
Diurnal and seasonal variation in root xylem embolism in neotropical savanna woody species: impact on stomatal control of plant water status
Authors: DOMEC J‐C. , SCHOLZ F. G. , BUCCI S. J. , MEINZER F. C. , GOLDSTEIN G. , VILLALOBOS‐VEGA R. 
Published: August 2005

ABSTRACTVulnerability to water‐stress‐induced embolism and variation in the degree of native embolism were measured in lateral roots of four co‐occurring neotropical savanna tree species. Root embolism varied diurnally and seasonally. Late in the dry season, loss of root xylem conductivity reached 80% in the afternoon when root water potential (Ψroot) was about −2.6 MPa, and recovered to 25–40% loss of conductivity in the morning when Ψroot was about −1.0 MPa. Daily variation in Ψroot decreased, and root xylem vulnerability and capacitance increased with rooting depth. However, all species experienced seasonal minimum Ψroot close to complete hydraulic failure independent of their rooting depth or resistance to embolism. Predawn Ψroot was  lower  than  Ψsoil when  Ψsoil was  relatively  high  (>−0.7 MPa) but became less negative than Ψsoil later in the dry season, consistent with a transition from a disequilibrium between plant and soil Ψ induced by nocturnal transpiration to one induced by hydraulic redistribution of water from deeper soil layers. Shallow longitudinal root incisions external to the xylem prevented reversal of embolism overnight, suggesting that root mechanical integrity was necessary for recovery, consistent with the hypothesis that if embolism is a function of tension, refilling may be a function of internal pressure imbalances. All species shared a common relationship in which maximum daily stomatal conductance declined linearly with increasing afternoon loss of root conductivity over the course of the dry season. Daily embolism and refilling in roots is a common occurrence and thus may be an inherent component of a hydraulic signaling mechanism enabling stomata to maintain the integrity of the hydraulic pipeline in long‐lived structures such as stems.
Secondary metabolites influence Arabidopsis/Botrytis interactions: variation in host production and pathogen sensitivity
Authors: Kliebenstein Daniel J. , Rowe Heather C. , Denby Katherine J. 
Published: August 2005

SummaryNumerous studies have suggested that plant/pathogen interactions are partially mediated via plant secondary metabolite production and corresponding pathogen tolerance. However, there are inconsistent reports on the ability of particular compounds to provide resistance to a pathogen. Most of these studies have focused on individual isolates of a given pathogen, suggesting that pathogens vary in their sensitivity to plant‐produced toxins. We tested variability in virulence among pathogen isolates, and the impact on this by plant production of, and pathogen tolerance to, secondary metabolites. Botrytis cinerea isolates showed differing sensitivity to purified camalexin, and camalexin‐sensitive isolates produced larger lesions on camalexin‐deficient Arabidopsis genotypes than on the wild type. In contrast, the camalexin‐insensitive isolate produced lesions of similar size on wild‐type and camalexin‐deficient Arabidopsis. Additional analysis with Arabidopsis secondary metabolite biosynthetic mutants suggests that Botrytis also has variable sensitivity to phenylpropanoids and glucosinolates. Furthermore, Botrytis infection generates a gradient of secondary metabolite responses emanating from the developing lesion, with the Botrytis isolate used determining the accumulation pattern. Collectively, our results indicate that Arabidopsis/Botrytis interactions are influenced at the metabolic level by variations in toxin production in the host and sensitivity in the pathogen.
AtDEK1 is essential for specification of embryonic epidermal cell fate
Authors: Johnson Kim L. , Degnan Kathryn A. , Ross Walker J. , Ingram Gwyneth C. 
Published: August 2005

SummaryThe specification of epidermal (L1) identity occurs early during plant embryogenesis. Here we show that, in Arabidopsis, AtDEK1 encodes a key component of the embryonic L1 cell‐layer specification pathway. Loss of AtDEK1 function leads to early embryo lethality characterized by a severe loss of cell organization in the embryo proper and abnormal cell divisions within the suspensor. Markers for L1 identity, ACR4 and ATML1, are not expressed in homozygous mutant embryos. In order to clarify the function of AtDEK1 further, an RNAi knockdown approach was used. This allowed embryos to partially complete embryogenesis before losing AtDEK1 activity. Resulting seedlings showed a specific loss of epidermal cell identity within large portions of the cotyledons. In addition, meristem structure and function was systematically either reduced or entirely lost. AtDEK1 expression is not restricted to the L1 epidermal cell layer at any stage in development. This is consistent with AtDEK1 playing an upstream role in the continuous generation or interpretation of positional information required for epidermal specification. Our results not only identify a specific role for AtDEK1 during embryogenesis, but underline the potential key importance of L1 specification at the globular stage for subsequent progression through embryogenesis.