bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relating predation mortality to broad‐scale habitat selection
Authors: McLOUGHLIN PHILIP D. , DUNFORD JESSE S. , BOUTIN STAN 
Published: July 2005

SummaryFew studies have related metrics of fitness to broad‐scale, multivariate patterns of resource selection.Our objective was to relate long‐term predation‐mortality patterns for adult woodland caribou [Rangifer tarandus caribou(Banfield)] from Alberta, Canada (1991–2002), with patterns of multivariate habitat selection.We first compared probabilities of radio‐tracked caribou dying (n = 55) from predation in habitats within the home range, controlling for habitat availability, with that expected from habitat selection probabilities for the same animals during life. We then compared survival rates of caribou (n = 141) possessing dissimilar patterns of habitat selection using a Cox proportional hazards regression model.Patterns in habitat‐specific predation mortality differed significantly from expected given probabilities of habitat selection during life (P < 0·0001). Cox regression indicated that mortality rates of caribou due to predation were affected significantly by and can be predicted from patterns of selection (P = 0·02).Our results strongly suggest that uplands (primarily mixed deciduous and coniferous forest) present caribou with higher than expected levels of predation risk, and that caribou can avoid predation by maximizing selection of peatlands (open, conifer‐dominated bogs and fens).Approaches presented in this study may be useful for ecologists interested in assessing the influence of mortality factors on broad‐scale, multivariate resource selection. Linking metrics of fitness to multivariate resource selection will enable us to ask questions of evolutionary ecology once restricted to only the finest ecological scales.
Metapopulation consequences of site fidelity for colonially breeding mammals and birds
Authors: MATTHIOPOULOS JASON , HARWOOD JOHN , THOMAS LEN 
Published: July 2005

Summary

Many far‐ranging bird and mammal species aggregate in colonies to breed, and most individuals remain faithful to one colony. Here, we use modelling to explore the consequences of this site fidelity for the metapopulation dynamics of such species.
We develop a spatially explicit model of the annual transfer process between colonies. We apply it to different spatial arrangements of 20 identical colonies and thus demonstrate that connectivity alone can, in the short term, give rise to heterogeneity in colony size.
We place the annual transfer model within a state‐structured population model and examine the consequences of local and global density dependence for long‐term dynamics. For each scenario, we investigate the implications of the strength of site fidelity, the cost of migration and the population's intrinsic growth rate.
Our results suggest that, under local density dependence, site fidelity slows down the colonization process and can temporarily trap the entire population in a subset of the available potential colonies. When site fidelity is strong, the metapopulation follows a step‐like trajectory. Population growth occurs only rarely because individuals must overcome their site‐fidelity to found new colonies. Even though this effect is temporary, it renders the entire metapopulation vulnerable to rare catastrophic collapses.
Under global density dependence, site fidelity imposes competition between colonies for the limiting resource. Stochastic events lead to the dominance of certain colonies and the temporary extinction of others. If site fidelity is strong, it can permanently prevent the metapopulation from occupying all available potential colonies.
We conclude that, irrespective of the mechanism of population regulation, colonially breeding species that show strong site fidelity are likely to occupy only a portion of the breeding habitat available to them.
A common mechanism explaining the evolution of female‐limited and both‐sex Batesian mimicry in butterflies
Authors: OHSAKI NAOTA 
Published: July 2005

Summary

Batesian mimicry describes the situation in which a palatable mimic resembles an unpalatable model. In some species of butterflies, both sexes mimic, but in others only females do. Two mechanisms have been proposed to generate female‐limited mimicry: sexual selection via female choice, and sexual selection via male–male competition. Each is not satisfactory because of too many exceptions.
I hypothesized that reductions in physiological life span because of mimicry constituted the costs, while extensions of ecological life span because of mimicry constituted the benefits. Mimicry would result from the balance of a costs/benefits relationship; when balances are favourable, mimicry occurs.
Non‐mimetic females of female‐limited mimicry butterfly Papilio polytes lived longer than its mimetic females in a butterfly farm greenhouse. Therefore, reduction in physiological life span must be a cost of mimicry.
Male‐biased sex ratios were found in 11 of the 14 non‐mimetic and non‐model species netted in the Kakamega tropical rainforest in west Kenya, in other one species almost equivalent, and in remaining two species female‐biased. For each species, the sexes netted less frequently had more beak marks than those netted more frequently. That is, the biased sex ratios could be responsible for the higher predation rates of the opposite sex.
Predators may have selectively attacked females with wider thoraxes, which flew at higher levels and flew more quickly. However, attack rates on males of some species may be high or low regardless of thorax width.
As the benefits accrue largely to females with wider thorax due to female‐biased predation, balances of costs/benefits relationships divide participating species into three theoretical groups: those in which the adaptation is favourable for both sexes; favourable only for females; and unfavourable for both sexes.
In female‐limited mimics of five species, thorax widths varied, whereas thoraxes tended to be wider in both‐sex mimics of four species.
Climate predictability and breeding phenology in red deer: timing and synchrony of rutting and calving in Norway and France
Authors: LOE L. E. , BONENFANT C. , MYSTERUD A. , GAILLARD J.‐M. , LANGVATN R. , KLEIN F. , CALENGE C. , ERGON T. , PETTORELLI N. , STENSETH N. C. 
Published: July 2005

Summary

Timing and synchrony of reproduction are regarded as crucially important factors for fitness in seasonal environments. Natural selection has probably favoured temperate and arctic female herbivores that match reproduction with onset of plant growth in spring. However, breeding synchrony may also be affected by variation in phenotypic quality of females in a population, because females in poor body condition have been found to delay ovulation and subsequent calving.
We compared breeding phenology, i.e. the timing and synchrony of rutting (roaring, sexual aggregation) and calving of red deer (Cervus elaphus L.) in France (latitude: 49°N) and Norway (latitude: 63°N). We hypothesized (H1) that calving and rutting were later at the site with latest onset of plant growth.
We further quantified overall environmental predictability as the sum of annual constancy and seasonality and tested three different (not mutually exclusive) hypotheses about breeding synchrony: (H2a) the population experiencing most seasonal plant phenology should show the highest breeding synchrony; (H2b) overall predictability of plant phenology should determine breeding synchrony; and (H2c) breeding should be more synchronized in the population with lowest female body weight variation within age classes because they ovulate more synchronously.
Calving and rutting, as well as onset of plant phenology, were later in Norway than in France, complying with the first hypothesis. Plant growth in spring was overall more predictable and also more seasonal in Norway than France. Hence we expected higher breeding synchrony in Norway than in France according to H2a and H2b. Variance in female body weight was slightly higher in France than in Norway, which should also cause more synchronized breeding in Norway than in France (H2c). Contrary to all predictions, variance in rutting and calving dates was around two times higher in Norway than in France.
We suggest two alternative explanations of breeding synchrony. A more variable topography in Norway can make optimal birth date more variable on a local scale than in France, thereby maintaining a higher genetic variance for calving date in Norwegian red deer. Further, population age structure may play a role, as ovulation varies according to female age. Clearly, processes of breeding synchrony are far more complex than previously realized.
Interaction of Rv1625c, a mycobacterial class IIIa adenylyl cyclase, with a mammalian congener
Authors: Guo Ying Lan , Kurz Ursula , Schultz Anita , Linder Jürgen U. , Dittrich Dorothea , Keller Christine , Ehlers Stefan , Sander Peter , Schultz Joachim E. 
Published: July 2005

SummaryThe adenylyl cyclase Rv1625c from Mycobacterium tuberculosis codes for a protein with six transmembrane spans and a catalytic domain, i.e. it corresponds to one half of the pseudoheterodimeric mammalian adenylyl cyclases (ACs). Rv1625c is active as a homodimer. We investigated the role of the Rv1625c membrane domain and demonstrate that it efficiently dimerizes the protein resulting in a 7.5‐fold drop in Km for ATP. Next, we generated a duplicated Rv1625c AC dimer by a head‐to‐tail concatenation. This produced an AC with a domain order exactly as the mammalian pseudoheterodimers. It displayed positive cooperativity and a 60% increase of vmax compared with the Rv1625c monomer. Further, we probed the compatibility of mycobacterial and mammalian membrane domains. The second membrane anchor in the Rv1625c concatamer was replaced with membrane domain I or II of rabbit type V AC. The mycobacterial and either mammalian membrane domains are compatible with each other and both recombinant proteins are active. A M. tuberculosis Rv1625c knockout strain was assayed in a mouse infection model. In vitro growth characteristics and in vivo organ infection and mortality were unaltered in the knockout strain indicating that AC Rv1625c alone is not a virulence factor.
Disruption of the developmental programme of Trypanosoma brucei by genetic ablation of TbZFP1, a differentiation‐enriched CCCH protein
Authors: Hendriks Edward F. , Matthews Keith R. 
Published: July 2005

SummaryThe regulation of differentiation is particularly important in microbial eukaryotes that inhabit multiple environments. The parasite Trypanosoma brucei is an extreme example of this, requiring exquisite gene regulation during transmission from mammals to the tsetse fly vector. Unusually, trypanosomes rely almost exclusively on post‐transcriptional mechanisms for regulated gene expression. Hence, RNA binding proteins are potentially of great significance in controlling stage‐regulated processes. We have previously identified TbZFP1 as a trypanosome molecule transiently enriched during differentiation to tsetse midgut procyclic forms. This small protein (101 amino acids) contains the unusual CCCH zinc finger, an RNA binding motif. Here, we show that genetic ablation of TbZFP1 compromises repositioning of the mitochondrial genome, a specific event in the strictly regulated differentiation programme. Despite this, other events that occur both before and after this remain intact. Significantly, this phenotype correlates with the TbZFP1 expression profile during differentiation. This is the first genetic disruption of a developmental regulator in T. brucei. It demonstrates that programmed events in parasite development can be uncoupled at the molecular level. It also further supports the importance of CCCH proteins in key aspects of trypanosome cell function.
Horizontal transfer of Yersinia high‐pathogenicity island by the conjugative RP4 attB target‐presenting shuttle plasmid
Authors: Antonenka Uladzimir , Nölting Christina , Heesemann Jürgen , Rakin Alexander 
Published: July 2005

SummaryThe high‐pathogenicity island (HPI) encodes a highly efficient yersiniabactin system of iron acquisition responsible for mouse lethality in Yersinia. Although the HPI is widely disseminated among Enterobacteriaceae it lacks functions necessary for its replication and transmission. Therefore, the mechanism of its horizontal transfer and circulation is completely obscure. On the other hand, the HPI is a genetically active island in the bacterial cell. It encodes a functional recombinase and is able to transpose to new targets on the chromosome. Here we report on a possible mechanism of the HPI dissemination based on site‐specific recombination of the excised HPI with the attB‐presenting (asn tRNA gene) RP4 promiscuous conjugative shuttle plasmid. The resulting cointegrate can be transferred by conjugation to a new host, where it dissociates, and the released HPI integrates into any unoccupied asn tRNA gene target in the genome. This mechanism has been proven both with the ‘mini’ island carrying only the attP recognition site and genes coding for recombination enzymes and with the complete HPI labelled with an antibiotic resistance marker. After acquisition of the mobilized complete form of the HPI, the ability of the HPI‐cured Yersinia enterocolitica WA‐TH– strain to produce yersiniabactin has been restored. Such ‘trapping’ of pathogenicity islands and subsequent shuffling to new hosts by a conjugative replicon carrying a suitable attB site could be applied to other functional integrative elements and explain wide dissemination of PAIs.
Polyphosphate kinase regulates error‐prone replication by DNA polymerase IV in Escherichia coli
Authors: Stumpf Jeffrey D. , Foster Patricia L. 
Published: July 2005

SummaryThe ppk gene encodes polyphosphate kinase (Ppk), an enzyme that catalyses the polymerization of inorganic phosphate into long chains of polyphosphate (polyP). An insertion mutation in ppk causes a decrease in adaptive mutation in Escherichia coli strain FC40. Adaptive mutation in FC40 mostly results from error‐prone DNA polymerase IV (Pol IV), encoded by dinB; most of the antimutagenic phenotype of the ppk mutant disappears in a dinB mutant strain. In addition, the ppk mutant causes a decrease in growth‐dependent mutations produced by overexpressing Pol IV. However, the amount of Pol IV protein is unchanged in the ppk mutant strain, indicating that the activity or fidelity of Pol IV is altered. Adaptive mutation is inhibited both by the absence of Ppk, which results in low amounts of polyP, and by overproduction of Ppk, which results in high amounts of polyP, suggesting that an optimal level of polyP is necessary. Taken together, these results suggest a novel mechanism involving polyP that directly or indirectly regulates DNA polymerase activity or fidelity.
BrgE is a regulator of Myxococcus xanthus development
Authors: Pham Vinh D. , Shebelut Conrad W. , Zumstein Erin J. , Singer Mitchell 
Published: July 2005

SummaryWe report here the identification and characterization of a member of the Myxococcus xanthus SdeK signal transduction pathway, BrgE. This protein was identified as an SdeK‐interacting component using a yeast two‐hybrid screen, and we further confirmed this interaction by the glutathione S‐transferase (GST) pulldown assay. Additional yeast two‐hybrid analyses revealed that BrgE preferentially interacts with the putative amino‐terminal sensor domain of SdeK, but not with the carboxy‐terminal kinase domain. A brgE insertion strain was shown to be blocked in development between aggregation and mound formation, and decreased by 50‐fold in viable spore production compared with the parental wild type. These phenotypes are similar to those of sdeK mutants. The brgE mutation also altered expression of a sample of Tn5 lac developmental markers that are also SdeK regulated. Finally, we demonstrated that a brgE sdeK double mutant has a more severe sporulation defect than either of the two single mutants, suggesting that BrgE and SdeK act synergistically to regulate wild‐type levels of sporulation. In sum, these data suggest that BrgE operates as an auxiliary factor to stimulate the SdeK signal transduction pathway by directly binding to the amino‐terminal sensor domain of SdeK.
Large increases in attractant concentration disrupt the polar localization of bacterial chemoreceptors
Authors: Lamanna Allison C. , Ordal George W. , Kiessling Laura L. 
Published: July 2005

SummaryIn bacterial chemotaxis, the chemoreceptors [methyl‐accepting chemotaxis proteins (MCPs)] transduce chemotactic signals through the two‐component histidine kinase CheA. At low but not high attractant concentrations, chemotactic signals must be amplified. The MCPs are organized into a polar lattice, and this organization has been proposed to be critical for signal amplification. Although evidence in support of this model has emerged, an understanding of how signals are amplified and modulated is lacking. We probed the role of MCP localization under conditions wherein signal amplification must be inhibited. We tested whether a large increase in attractant concentration (a change that should alter receptor occupancy from c. 0% to > 95%) would elicit changes in the chemoreceptor localization. We treated Escherichia coli or Bacillus subtilis with a high level of attractant, exposed cells to the cross‐linking agent paraformaldehyde and visualized chemoreceptor location with an anti‐MCP antibody. A marked increase in the percentage of cells displaying a diffuse staining pattern was obtained. In contrast, no increase in diffuse MCP staining is observed when cells are treated with a repellent or a low concentration of attractant. For B. subtilis mutants that do not undergo chemotaxis, the addition of a high concentration of attractant has no effect on MCP localization. Our data suggest that interactions between chemoreceptors are decreased when signal amplification is unnecessary.
Ability of IncP‐9 plasmid pM3 to replicate in Escherichia coli is dependent on both rep and par functions
Authors: Sevastsyanovich Yanina R. , Titok Marina A. , Krasowiak Renata , Bingle Lewis E. H. , Thomas Christopher M. 
Published: July 2005

SummaryIncP‐9 plasmids are common in Pseudomonas species and can be transferred to other Gram‐negative eubacteria but tend not to be stably maintained outside their natural host genus. A 1.3 kb ori V‐rep fragment from IncP‐9 plasmid pM3 was sufficient for autonomous replication in Pseudomonas putida but not in Escherichia coli. Replication of ori V‐rep in E. coli was restored when additional rep was provided in trans, suggesting that the replication defect resulted from insufficient rep expression from its natural promoter. A promoter deficiency in E. coli was confirmed by reporter gene assays, transcriptional start point mapping and mutation of the promoter recognition elements. Dissection of the pM3 mini‐replicon, pMT2, showed that this replication deficiency in E. coli is suppressed by additional determinants from its par operon: ParB, which can be supplied in trans, and its target, the par operon promoter, required in cis to ori V‐rep. We propose that ParB binding to its target either changes plasmid DNA and thus promoter conformation or by spreading or looping contacts RNAP at the rep promoter so that rep expression is sufficient to activate ori V.
Zap1 activation domain 1 and its role in controlling gene expression in response to cellular zinc status
Authors: Herbig Andrew , Bird Amanda J. , Swierczek Sabina , McCall Keith , Mooney Michelle , Wu Chang‐Yi , Winge Dennis R. , Eide David J. 
Published: July 2005

SummaryThe Zap1 transcription factor is a central player in zinc homeostasis in yeast. This protein regulates the expression of genes involved in zinc accumulation and storage. For most of its target genes, Zap1 activates expression in zinc‐limited cells and this function is inhibited in replete cells. Zap1 has two activation domains, AD1 and AD2, which are independently regulated by zinc status. In this study, we characterized AD1 and its regulation by zinc. AD1 was mapped using deletions to residues 332–402 of Zap1. The region required for the zinc responsiveness of this activation domain, designated ‘ZRDAD1, was mapped to residues 182–502. Thus, AD1 is embedded within its larger zinc‐responsive domain. Using a combination of in silico analysis, random mutagenesis and site‐directed mutagenesis, we identified key residues within ZRDAD1 required for its regulation by zinc. Most of these residues are cysteines and histidines that could potentially serve as Zn(II) ligands. These results suggest that ZRDAD1 senses zinc by direct Zn(II) binding. Consistent with this hypothesis, purified ZRDAD1 bound multiple Zn(II) ions. Finally, our results indicate that, in the context of the full‐length Zap1 protein, AD1 and AD2 are both critical to the full control of gene expression in response to zinc.
Function of the thioredoxin proteins in Cryptococcus neoformans during stress or virulence and regulation by putative transcriptional modulators
Authors: Missall Tricia A. , Lodge Jennifer K. 
Published: July 2005

SummaryThe thioredoxin system, consisting of thioredoxin, thioredoxin reductase and NADPH, is known to protect cells against oxidative stress. This disulphide reducing system is present in Cryptococcus neoformans and consists of two small, dithiol thioredoxin proteins and one thioredoxin reductase. In this study, we describe the thioredoxin proteins, Trx1 and Trx2, and present their importance not only to stress resistance, but also to the virulence of C. neoformans. Using real‐time polymerase chain reaction, we show the induction of both thioredoxin genes during oxidative and nitrosative stress. We describe through deletion studies that the trx1Δ mutant has a severe growth defect and is sensitive to multiple stresses, while the trx2Δ mutant is only sensitive to nitric oxide stress. Using gene replacement studies, we demonstrate that the thioredoxin protein products are partially redundant in function, but there is differential gene regulation which is especially important to nitrosative stress resistance. We have also identified two putative transcription factors, Atf1 and Yap4, which appear to differentially regulate the thioredoxin system under different conditions. Atf1 is necessary for oxidative stress induction, and Yap4 is necessary for nitrosative stress induction of the thioredoxin genes in C. neoformans. While these two putative transcription factors each appear to be dispensable for survival in macrophages and virulence in mice, we show the more highly expressed thioredoxin, TRX1, is necessary for survival of C. neoformans in the oxidative environment of macrophages and important for virulence of this fungal pathogen.