bluuebunny/crossref_metadata_2025_split huggingface dataset:
Who are the missing parents? Grandparentage analysis identifies multiple sources of gene flow into a wild population
Authors: CHRISTIE MARK R. , MARINE MELANIE L. , BLOUIN MICHAEL S. 
Published: January 2011

AbstractIn order to increase the size of declining salmonid populations, supplementation programmes intentionally release fish raised in hatcheries into the wild. Because hatchery‐born fish often have lower fitness than wild‐born fish, estimating rates of gene flow from hatcheries into wild populations is essential for predicting the fitness cost to wild populations. Steelhead trout (Oncorhynchus mykiss) have both freshwater resident and anadromous (ocean‐going) life history forms, known as rainbow trout and steelhead, respectively. Juvenile hatchery steelhead that ‘residualize’ (become residents rather than go to sea as intended) provide a previously unmeasured route for gene flow from hatchery into wild populations. We apply a combination of parentage and grandparentage methods to a three‐generation pedigree of steelhead from the Hood River, Oregon, to identify the missing parents of anadromous fish. For fish with only one anadromous parent, 83% were identified as having a resident father while 17% were identified as having a resident mother. Additionally, we documented that resident hatchery males produced more offspring with wild anadromous females than with hatchery anadromous females. One explanation is the high fitness cost associated with matings between two hatchery fish. After accounting for all of the possible matings involving steelhead, we find that only 1% of steelhead genes come from residualized hatchery fish, while 20% of steelhead genes come from wild residents. A further 23% of anadromous steelhead genes come from matings between two resident parents. If these matings mirror the proportion of matings between residualized hatchery fish and anadromous partners, then closer to 40% of all steelhead genes come from wild trout each generation. These results suggest that wild resident fish contribute substantially to endangered steelhead ‘populations’ and highlight the need for conservation and management efforts to fully account for interconnected Oncorhynchus mykiss life histories.
and D do not replace FST
Authors: WHITLOCK MICHAEL C. 
Published: January 2011

AbstractThe genetic differentiation among populations is affected by mutation as well as by migration, drift and selection. For loci with high mutation rates, such as microsatellites, the amount of mutation can influence the values of indices of differentiation such as GST and FST. For many purposes, this effect is undesirable, and as a result, new indices such as and D have been proposed to measure population differentiation. This paper shows that these new indices are not effective measures of the causes or consequences of population structure. Both and D depend heavily on mutation rate, but both are insensitive to any population genetic process when the mutation rate is high relative to the migration rate. Furthermore, D is specific to the locus being measured, and so little can be inferred about the population demography from D. However, at equilibrium, D may provide an index of whether a particular marker is more strongly affected by mutation than by migration. I argue that FST is a more important summary of the effects of population structure than D and that RST or other measures that explicitly account for the mutation process are much better than GST, , or D for highly mutable markers. Markers with lower mutation rates will often be easier to interpret.
Proteins encoded by the mre gene cluster in Streptomyces coelicolor A3(2) cooperate in spore wall synthesis
Authors: Kleinschnitz Eva‐Maria , Heichlinger Andrea , Schirner Kathrin , Winkler Juliane , Latus Annette , Maldener Iris , Wohlleben Wolfgang , Muth Günther 
Published: January 2011

SummaryIt is still an open question how an intracellular cytoskeleton directs the synthesis of the peptidoglycan exoskeleton. In contrast to MreB of rod‐shaped bacteria, which is essential for lateral cell wall synthesis, MreB of Streptomyces coelicolor has a role in sporulation. To study the function of the S. coelicolor mre gene cluster consisting of mreB, mreC, mreD, pbp2 and sfr, we generated non‐polar replacement mutants. The individual mutants were viable and growth of substrate mycelium was not affected. However, all mutants produced enlarged spores, which frequently germinated prematurely and were sensitive to heat, high osmolarity and cell wall damaging agents. Protein–protein interaction assays by bacterial two‐hybrid analyses indicated that the S. coelicolor Mre proteins form a spore wall synthesizing complex, which closely resembles the lateral wall synthesizing complex of rod‐shaped bacteria. Screening of a genomic library identified several novel putative components of this complex. One of them (sco2097) was deleted. The Δsco2097 mutant formed sensitive spores with an aberrant morphology, demonstrating that SCO2097 is a new player in cell morphogenesis of Streptomyces. Our results suggest that all Mre proteins cooperate with the newly identified proteins in the synthesis of the thickened spore wall required to resist detrimental environmental conditions.
The outer membrane protein LptO is essential for the O‐deacylation of LPS and the co‐ordinated secretion and attachment of A‐LPS and CTD proteins in Porphyromonas gingivalis
Authors: Chen Yu‐Yen , Peng Benjamin , Yang Qiaohui , Glew Michelle D. , Veith Paul D. , Cross Keith J. , Goldie Kenneth N. , Chen Dina , O'Brien‐Simpson Neil , Dashper Stuart G , Reynolds Eric C. 
Published: January 2011

Summary Protein substrates of a novel secretion system of Porphyromonas gingivalis contain a conserved C‐terminal domain (CTD) essential for secretion and attachment to the cell surface. Inactivation of lptO (PG0027) or porT produced mutants that lacked surface protease activity and an electron‐dense surface layer. Both mutants showed co‐accumulation of A‐LPS and unmodified CTD proteins in the periplasm. Lipid profiling by mass spectrometry showed the presence of both tetra‐ and penta‐acylated forms of mono‐phosphorylated lipid A in the wild‐type and porT mutant, while only the penta‐acylated forms of mono‐phosphorylated lipid A were found in the lptO mutant, indicating a specific role of LptO in the O‐deacylation of mono‐phosphorylated lipid A. Increased levels of non‐phosphorylated lipid A and the presence of novel phospholipids in the lptO mutant were also observed that may compensate for the missing mono‐phosphorylated tetra‐acylated lipid A in the outer membrane (OM). Molecular modelling predicted LptO to adopt a β‐barrel structure characteristic of an OM protein, supported by the enrichment of LptO in OM vesicles. The results suggest that LPS deacylation by LptO is linked to the co‐ordinated secretion of A‐LPS and CTD proteins by a novel secretion and attachment system to form a structured surface layer.
tRNA accumulation and suppression of the bldA phenotype during development in Streptomyces coelicolor
Authors: Pettersson B. M. Fredrik , Kirsebom Leif A. 
Published: January 2011

SummaryStreptomyces coelicolor undergoes distinct morphological changes as it grows on solid media where spores differentiate into vegetative and aerial mycelium that is followed by the production of spores. Deletion of bldA, encoding the rare tRNALeuUAA, blocks development at the stage of vegetative mycelium formation. From previous data it appears that tRNALeuUAA accumulates relatively late during growth while two other tRNAs do not. Here, we studied the expression of 17 different tRNAs including bldA tRNA, and the RNA subunit of the tRNA processing endoribonuclease RNase P. Our results showed that all selected tRNAs and RNase P RNA increased with time during development. However, accumulation of bldA tRNA and another rare tRNALeu isoacceptor started at an earlier stage compared with the other tRNAs. We also introduced the bldA tRNA anticodon (UAA) into other tRNAs and introduced these into a bldA deletion strain. In particular, one such mutant tRNA derived from the tRNALeuCAA isoacceptor suppressed the bldA phenotype. Thus, the bldA tRNA scaffold is not critical for function as a regulator of S. coelicolor cell differentiation. Further substitution experiments, in which the 5′‐ and 3′‐flanking regions of the suppressor tRNA were changed, indicated that these regions were important for the suppression.
Magnesium depletion triggers production of an immune modulating diterpenoid in Mycobacterium tuberculosis
Authors: Mann Francis M. , VanderVen Brian C. , Peters Reuben J. 
Published: January 2011

SummaryMycobacterium tuberculosis (Mtb) is the causative agent of the human disease Tuberculosis, and remains a worldwide health threat responsible for ∼ 1.7 million deaths annually. During infection, Mtb prevents acidification of the engulfing phagosome, thus blocking endocytic progression and eventually leading to stable residence. The diterpenoid metabolite isotuberculosinol (isoTb) exhibits biological activity indicative of a role in this early arrest of phagosome maturation. Presumably, isoTb production should be induced by phagosomal entry. However, the relevant enzymatic genes are not transcriptionally upregulated during engulfment. Previous examination of the initial biosynthetic enzyme (Rv3377c/MtHPS) involved in isoTb biosynthesis revealed striking inhibition by its Mg2+ cofactor, leading to the hypothesis that the depletion of Mg2+ observed upon phagosomal engulfment may act to trigger isoTb biosynthesis. While Mtb is typically grown in relatively high levels of Mg2+ (0.43 mM), shifting Mtb to media with phagosomal levels (0.1 mM) led to a significant (∼ 10‐fold) increase in accumulation of the MtHPS product, halimadienyl diphosphate, as well as easily detectable amounts of the derived bioactive isoTb. These results demonstrate isoTb production by Mtb specifically under conditions that mimic phagosomal cation concentrations, and further support a role for isoTb in the Mtb infection process.
Downregulation of katG expression is associated with isoniazid resistance in Mycobacterium tuberculosis
Authors: Ando Hiroki , Kitao Tomoe , Miyoshi‐Akiyama Tohru , Kato Seiya , Mori Toru , Kirikae Teruo 
Published: January 2011

SummaryIsoniazid (INH) is a key agent in the treatment of tuberculosis. In Mycobacterium tuberculosis, INH is converted to its active form by KatG, a catalase‐peroxidase, and attacks InhA, which is essential for the synthesis of mycolic acids. We sequenced furA–katG and fabG1–inhA in 108 INH‐resistant (INHr) and 51 INH‐susceptible (INHs) isolates, and found three mutations in the furA–katG intergenic region (Intg‐7a, Inta‐10c and Intg‐12a) in four of 108 INHr isolates (4%), and the furAc41t mutation with an amino acid substitution in 18 INHr isolates (17%). These mutations were not found in any of 51 INHs isolates tested. We reconstructed these mutations in isogenic strains to determine whether they conferred INH resistance. We found that the Intg‐7a, Inta‐10c and Intg‐12a single mutations in the furA–katG intergenic region decreased katG expression and conferred INH resistance. In contrast, the furAc41t mutation was not sufficient to confer INH resistance. These results suggested that downregulation of katG is a mechanism of INH resistance in M. tuberculosis and that mutations in the furA–katG intergenic region play a role in this resistance mechanism.
The morphogene AmiC2 is pivotal for multicellular development in the cyanobacterium Nostoc punctiforme
Authors: Lehner Josef , Zhang Yao , Berendt Susanne , Rasse Tobias M. , Forchhammer Karl , Maldener Iris 
Published: January 2011

SummaryFilamentous cyanobacteria of the order Nostocales are primordial multicellular organisms, a property widely considered unique to eukaryotes. Their filaments are composed of hundreds of mutually dependent vegetative cells and regularly spaced N2‐fixing heterocysts, exchanging metabolites and signalling molecules. Furthermore, they may differentiate specialized spore‐like cells and motile filaments. However, the structural basis for cellular communication within the filament remained elusive. Here we present that mutation of a single gene, encoding cell wall amidase AmiC2, completely changes the morphology and abrogates cell differentiation and intercellular communication. Ultrastructural analysis revealed for the first time a contiguous peptidoglycan sacculus with individual cells connected by a single‐layered septal cross‐wall. The mutant forms irregular clusters of twisted cells connected by aberrant septa. Rapid intercellular molecule exchange takes place in wild‐type filaments, but is completely abolished in the mutant, and this blockage obstructs any cell differentiation, indicating a fundamental importance of intercellular communication for cell differentiation in Nostoc. AmiC2–GFP localizes in the cell wall with a focus in the cross walls of dividing cells, implying that AmiC2 processes the newly synthesized septum into a functional cell–cell communication structure during cell division. AmiC2 thus can be considered as a novel morphogene required for cell–cell communication, cellular development and multicellularity.
Assembly and stability of flagellar motor in Escherichia coli
Authors: Li Hui , Sourjik Victor 
Published: January 2011

SummaryBacterial flagellar motor is a highly ordered and complex supramolecular structure that powers rotation of flagella and serves as a type III export apparatus for flagellar assembly. Motor biogenesis represents a formidable example of self‐assembly, but little is known about early steps of the motor structure formation. Here we used a combination of fluorescence microscopy techniques to dissect the order of the motor assembly in Escherichia coli cells, to map in vivo the underlying protein interactions and to investigate dynamics of protein exchange in the assembled motor structure. Our data suggest that motor self‐assembly is initiated by oligomerization of the membrane export apparatus protein FlhA, which is followed by the recruitment of the MS ring component FliF and by the ordered association of other motor proteins. The assembly process combines the hierarchy with cooperativity, whereby the association of each subsequent motor structure stabilizes the growing assembly. Our results provide a novel and so far the most complete view of the early steps in flagellar motor assembly and improve understanding of the motor structure and regulation.
A multifaceted genomics approach allows the isolation of the rice Pia‐blast resistance gene consisting of two adjacent NBS‐LRR protein genes
Authors: Okuyama Yudai , Kanzaki Hiroyuki , Abe Akira , Yoshida Kentaro , Tamiru Muluneh , Saitoh Hiromasa , Fujibe Takahiro , Matsumura Hideo , Shenton Matt , Galam Dominique Clark , Undan Jerwin , Ito Akiko , Sone Teruo , Terauchi Ryohei 
Published: January 2011

SummaryThe Oryza sativa (rice) resistance gene Pia confers resistance to the blast fungus Magnaporthe oryzae carrying the AVR‐Pia avirulence gene. To clone Pia, we employed a multifaceted genomics approach. First, we selected 12 R‐gene analog (RGA) genes encoding nucleotide binding site‐leucine rich repeats (NBS‐LRRs) proteins from a region on chromosome 11 that shows linkage to Pia. By using seven rice accessions, we examined the association between Pia phenotypes and DNA polymorphisms in the 10 genes, which revealed three genes (Os11gRGA3–Os11gRGA5) exhibiting a perfect association with the Pia phenotypes. We also screened ethyl methane sulfonate (EMS)‐treated mutant lines of the rice cultivar ‘Sasanishiki’ harboring Pia, and isolated two mutants that lost the Pia phenotype. DNA sequencing of Os11gRGA3–Os11gRGA5 from the two mutant lines identified independent mutations of major effects in Os11gRGA4. The wild‐type ‘Sasanishiki’ allele of Os11gRGA4 (SasRGA4) complemented Pia function in both mutants, suggesting that SasRGA4 is necessary for Pia function. However, when the rice cultivar ‘Himenomochi’ lacking Pia was transfected with SasRGA4, the Pia phenotype was not recovered. An additional complementation study revealed that the two NBS‐LRR‐type R genes, SasRGA4 and SasRGA5, that are located next to each other and oriented in the opposite direction are necessary for Pia function. A population genetics analysis of SasRGA4 and SasRGA5 suggests that the two genes are under long‐term balancing selection.
Arabidopsis homologues of the histone chaperone ASF1 are crucial for chromatin replication and cell proliferation in plant development
Authors: Zhu Yan , Weng Minjie , Yang Yue , Zhang Chi , Li Ziyu , Shen Wen‐Hui , Dong Aiwu 
Published: January 2011

SummaryAnti‐silencing function1 (ASF1) is an evolutionarily conserved histone chaperone. Studies in yeast and animals indicate that ASF1 proteins play important roles in various chromatin‐based processes, including gene transcription, DNA replication and repair. While two genes encoding ASF1 homologues, AtASF1A and AtASF1B, are found in the Arabidopsis genome, their function has not been studied. Here we report that both AtASF1A and AtASF1B proteins bind histone H3, and are localized in the cytoplasm and the nucleus. Loss‐of‐function of either AtASF1A or AtASF1B did not show obvious defects, whereas simultaneous knockdown of both genes in the double mutant Atasf1ab drastically inhibited plant growth and caused abnormal vegetative and reproductive organ development. The Atasf1ab mutant plants exhibit cell number reduction, S‐phase delay/arrest, and reduced polyploidy levels. Selective up‐regulation of expression of a subset of genes, including those involved in S‐phase checkpoints and the CYCB1;1 gene at the G2‐to‐M transition, was observed in Atasf1ab. Furthermore, the Atasf1ab‐triggered replication fork stalling constitutively activates the DNA damage checkpoint and repair genes, including ATM, ATR, PARP1 and PARP2 as well as several genes of the homologous recombination (HR) pathway but not genes of the non‐homologous end joining (NHEJ) pathway. In spite of the activation of repair genes, an increased level of DNA damage was detected in Atasf1ab, suggesting that defects in the mutant largely exceed the available capacity of the repair machinery. Taken together, our study establishes crucial roles for the AtASF1A and AtASF1B genes in chromatin replication, maintenance of genome integrity and cell proliferation during plant development.
Extramammary Paget’s disease of the unilateral axilla: a review of seven cases in a 20‐year experience
Authors: Chiu Cheng‐Sheng , Yang Chih‐Hsun , Chen Chien‐Hsun 
Published: January 2011

AbstractBackground  Extramammary Paget’s disease (EMPD) is an uncommon malignancy that occurs on apocrine‐rich skin. EMPD of the axillary region is extremely rare and is not well documented.Objectives  The aim of the study is to review our experience with axillary EMPD with regard to initial examination, treatment, and long‐term outcome.Methods  A retrospective study of inpatient files with the diagnosis of axillary EMPD was made. The data were collected regarding patient demographics, symptoms, surgical treatments, and time to recurrence. Follow‐up information was obtained as well.Results  Seven patients with a median age of 67.6 years were diagnosed with axillary EMPD during a 20‐year period from 1989 to 2008. The male‐female ratio was 1 : 1.3. All patients had a unilateral axillary occurrence, with three in the left and four in the right side. Patients typically presented with a chronic erythematous to brownish plaque with or without pruritus. All patients were treated with wide excision with margins up to 2–3 cm. There were no recurrences after surgery during the follow‐up period.Conclusions  Extramammary Paget’s disease of the axillary region is a rare finding even in a large medical center. The disease process is generally a prolonged one without remarkable symptoms. The prognosis of axillary EMPD is relatively good, and long‐term follow‐up is recommended.
Control of the myiasis‐producing fly, Lucilia sericata, with Egyptian essential oils
Authors: Khater Hanem F. , Hanafy Abeer , Abdel‐Mageed Abla D. , Ramadan Mohamed Y. , El‐Madawy Reham S. 
Published: January 2011

AbstractBackground  Myiasis caused by Lucilia sericata (Diptera: Calliphoridae) is widely distributed throughout the world and affects both humans and animals. In addition, L. sericata larvae and adults may play a role in spreading causal agents of mycobacterial infections. Therefore, it is important to establish new and safe alternative methods of controlling this blowfly.Methods  The insecticidal effectiveness of four commercially available essential oils [lettuce (Lactuca sativa), chamomile (Matricaria chamomilla), anise (Pimpinella anisum), rosemary (Rosmarinus officinalis)] against third larval instars of L. sericata was evaluated. The effects of sublethal concentrations of these oils on pupation rates, adult emergences, sex ratios, and morphological anomalies were also determined.Results  The oils were highly toxic to L. sericata larvae, with median lethal concentrations (LC50) of 0.57%, 0.85%, 2.74%, and 6.77% for lettuce, chamomile, anise, and rosemary oils, respectively. Pupation rates were markedly decreased after treatment with 8% lettuce oil, and adult emergence was suppressed by 2% lettuce and chamomile oils. Morphological abnormalities were recorded after treatment with all tested oils, and lettuce was the major cause of deformation. There was a predominance of males over females (4 : 1) after treatment with lower concentrations of chamomile and rosemary; such a skew toward males would lead to a population decline.Conclusions  The four tested oils are inexpensive and may represent new botanical insecticides for controlling blowflies.
Relevance of autoimmune thyroiditis in children and adolescents with vitiligo
Authors: Uncu Sibel , Yaylı Savaş , Bahadır Sevgi , Ökten Ayşenur , Alpay Köksal 
Published: January 2011

AbstractBackground  Vitiligo is the most common pigmentation‐related disorder worldwide. An autoimmune etiology is widely considered, and genetic factors may play an important role in its pathogenesis. The purpose of this study was to assess the incidence of thyroid dysfunctions and autoimmune thyroiditis in children with vitiligo and to identify related factors.Methods  Fifty children with vitiligo and 50 control children were enrolled. Data on age, onset, duration, disease activity, presence of thyroid disorder, other autoimmune diseases, halo nevi, poliosis, and mucosal vitiligo were determined. Serum free triiodothyronine, free thyroxine, total T3, total T4, thyroid‐stimulating hormone, and antibodies to thyroperoxidase and thyroglobulin were measured. Thyroid gland efficiency was evaluated.Results  The mean age at onset of vitiligo was 7.26 ± 4.43 years. The duration of vitiligo was 2.26 ± 2.95 years. Vulgaris‐type vitiligo was the most common form in our patients (56%), and 42% reported at least one family member with thyroid disorder, autoimmune disease, or both. Overt hypothyroidism or hyperthyroidism were not detected. We found a significant association between autoimmune thyroiditis and both sex and disease duration (P = 0.046 and P = 0.07, respectively), but no association between autoimmune thyroiditis and age, age at onset of vitiligo, halo nevi, poliosis, mucosal involvement, disease activity, or family history of vitiligo, autoimmunity, or thyroid disorders.Conclusions  Children with vitiligo show an increased incidence of autoimmune thyroiditis. Children with vitiligo, especially girls and subjects with generalized/vulgaris‐type vitiligo, should be screened annually for thyroid function and antithyroid antibodies to assist in the early diagnosis and therapy of autoimmune thyroiditis.