bluuebunny/crossref_metadata_2025_split huggingface dataset:
FrzZ, a dual CheY‐like response regulator, functions as an output for the Frz chemosensory pathway of Myxococcus xanthus
Authors: Inclán Yuki F. , Vlamakis Hera C. , Zusman David R. 
Published: June 2007

Summary Myxococcus xanthus utilizes two distinct motility systems for movement (gliding) on solid surfaces: adventurous motility (A‐motility) and social motility (S‐motility). Both systems are regulated by the Frz signal transduction pathway, which controls cell reversals required for directed motility and fruiting body formation. The Frz chemosensory system, unlike the Escherichia coli chemotaxis system, contains proteins with multiple response regulator domains: FrzE, a CheA–CheY hybrid protein, and FrzZ, a CheY–CheY hybrid protein. Previously, the CheY domain of FrzE was hypothesized to act as the response regulator output of the Frz system. In this study, using a genetic suppressor screen, we identified FrzZ and showed FrzZ is epistatic to FrzE, demonstrating that FrzZ is the principal output component of the pathway. We constructed M. xanthus point mutations in the phosphoaccepting aspartate residues of FrzZ and demonstrated the respective roles of these residues in group and single cell motility. We also performed in vitro assays and showed rapid phosphotransfer between the CheA domain of FrzE and each of the CheY domains of FrzZ. These experiments showed that FrzZ plays a direct role as an output of the Frz chemosensory pathway and that both CheY domains of FrzZ are functional.
Genomic analysis of protein–DNA interactions in bacteria: insights into transcription and chromosome organization
Authors: Wade Joseph T. , Struhl Kevin , Busby Stephen J. W. , Grainger David C. 
Published: June 2007

SummaryChromatin immunoprecipitation (ChIP) is a powerful method to measure protein–DNA interactions in vivo, and it can be applied on a genomic scale with microarray technology (ChIP‐chip). ChIP‐chip has been used extensively to map DNA–protein interactions across eukaryotic chromosomes. Here we review recent applications of ChIP‐chip to the study of bacteria, which provide important and unexpected insights into transcription and chromosome organization.
The (1,3)β‐d‐glucan synthase subunit Bgs1p is responsible for the fission yeast primary septum formation
Authors: Cortés Juan Carlos G. , Konomi Mami , Martins Ivone M. , Muñoz Javier , Moreno M. Belén , Osumi Masako , Durán Angel , Ribas Juan Carlos 
Published: June 2007

SummaryCytokinesis is a crucial event in the cell cycle of all living cells. In fungal cells, it requires co‐ordinated contraction of an actomyosin ring and synthesis of both plasmatic membrane and a septum structure that will constitute the new cell wall end. Schizosaccharomyces pombe contains four essential putative (1,3)β‐d‐glucan synthase catalytic subunits, Bgs1p to Bgs4p. Here we examined the function of Bgs1p in septation by studying the lethal phenotypes of bgs1+ shut‐off and bgs1Δ cells and demonstrated that Bgs1p is responsible and essential for linear (1,3)β‐d‐glucan and primary septum formation. bgs1+ shut‐off generates a more than 300‐fold Bgs1p reduction, but the septa still present large amounts of disorganized linear (1,3)β‐d‐glucan and partial primary septa. Conversely, both structures are absent in bgs1Δ cells, where there is no Bgs1p. The septum analysis of bgs1+‐repressed cells indicates that linear (1,3)β‐d‐glucan is necessary but not sufficient for primary septum formation. Linear (1,3)β‐d‐glucan is the polysaccharide that specifically interacts with the fluorochrome Calcofluor white in fission yeast. We also show that in the absence of Bgs1p abnormal septa are formed, but the cells cannot separate and eventually die.
Effective killing of the human pathogen Candida albicans by a specific inhibitor of non‐essential mitotic kinesin Kip1p
Authors: Chua Penelope R. , Roof David M. , Lee Yan , Sakowicz Roman , Clarke David , Pierce Dan , Stephens Thoryn , Hamilton Matthew , Morgan Brad , Morgans David , Nakai Takashi , Tomasi Adam , Maxon Mary E. 
Published: June 2007

SummaryKinesins from the bipolar (Kinesin‐5) family are conserved in eukaryotic organisms and play critical roles during the earliest stages of mitosis to mediate spindle pole body separation and formation of a bipolar mitotic spindle. To date, genes encoding bipolar kinesins have been reported to be essential in all organisms studied. We report the characterization of CaKip1p, the sole member of this family in the human pathogenic yeast Candida albicans. C. albicans Kip1p appears to localize to the mitotic spindle and loss of CaKip1p function interferes with normal progression through mitosis. Inducible excision of CaKIP1 revealed phenotypes unique to C. albicans, including viable homozygous Cakip1 mutants and an aberrant spindle morphology in which multiple spindle poles accumulate in close proximity to each other. Expression of the C. albicans Kip1 motor domain in Escherichia coli produced a protein with microtubule‐stimulated ATPase activity that was inhibited by an aminobenzothiazole (ABT) compound in an ATP‐competitive fashion. This inhibition results in ‘rigor‐like’, tight association with microtubules in vitro. Upon treatment of C. albicans cells with the ABT compound, cells were killed, and terminal phenotype analysis revealed an aberrant spindle morphology similar to that induced by loss of the CaKIP1 gene. The ABT compound discovered is the first example of a fungal spindle inhibitor targeted to a mitotic kinesin. Our results also show that the non‐essential nature and implementation of the bipolar motor in C. albicans differs from that seen in other organisms, and suggest that inhibitors of a non‐essential mitotic kinesin may offer promise as cidal agents for antifungal drug discovery.
RecA‐mediated excision repair: a novel mechanism for repairing DNA lesions at sites of arrested DNA synthesis
Authors: Bichara Marc , Pinet Isabelle , Lambert Iain B. , Fuchs Robert P. P. 
Published: June 2007

SummaryIn Escherichia coli, bulky DNA lesions are repaired primarily by nucleotide excision repair (NER). Unrepaired lesions encountered by DNA polymerase at the replication fork create a blockage which may be relieved through RecF‐dependent recombination. We have designed an assay to monitor the different mechanisms through which a DNA polymerase blocked by a single AAF lesion may be rescued by homologous double‐stranded DNA sequences. Monomodified single‐stranded plasmids exhibit low survival in non‐SOS induced E. coli cells; we show here that the presence of a homologous sequence enhances the survival of the damaged plasmid more than 10‐fold in a RecA‐dependent way. Remarkably, in an NER proficient strain, 80% of the surviving colonies result from the UvrA‐dependent repair of the AAF lesion in a mechanism absolutely requiring RecA and RecF activity, while the remaining 20% of the surviving colonies result from homologous recombination mechanisms. These results uncover a novel mechanism – RecA‐mediated excision repair – in which RecA‐dependent pairing of the mono‐modified single‐stranded template with a complementary sequence allows its repair by the UvrABC excinuclease.
The analysis of recurrence risk as an epidemiological tool
Authors: Wilcox Allen J. 
Published: June 2007

SummaryRecurrence risk provides information on the heterogeneity of risk in the population, and thus is useful for aetiological studies. While recurrence risk is observable in many areas of epidemiology, it is particularly accessible in the study of perinatal events. High recurrence rates of pregnancy problems suggest genetic causes, but can also reflect the presence of persistent environmental causes. Specific patterns of recurrence risk can provide further clues about the relative importance of genetic vs. environmental factors, for example through comparisons of recurring pregnancy problems in women who change their male partner and women who keep the same partner. Interpretation of recurrence risk is subject to confusion from bias and confounding, and some examples are discussed. In addition to providing information on causality, recurrence risk offers a means for more efficient design of aetiological studies.
Intergenerational exchange and perinatal risks: a note on interpretation of generational recurrence risks
Authors: Lie Rolv T. 
Published: June 2007

SummaryPopulation‐based data that cover reproductive health outcomes across two complete generations have recently become available in the Nordic countries. Such data enable estimation of recurrence risks from one generation to the next of different conditions such as birth defects or pre‐eclampsia. Risks related to a singleton pregnancy involve the contribution of three individuals: the mother, the father and the fetus. A paternal contribution is mainly through the father’s contribution of half of the alleles of the fetus. A maternal contribution may occur in three fundamentally different ways. First, the mother provides half of the genomic alleles to the fetus, with contribution of paternal alleles completing the whole genome. Second, the mother provides the fetal environment and possible susceptibility to complications during pregnancy which she may have inherited from her mother. Finally, she provides the fetal mitochondria. Because of these different contributions, recurrence from mother to offspring is fundamentally different from recurrence from father to offspring. How recurrence risks reflect and shape the underlying contributions to overall perinatal risk is illustrated through a review of published data from Norway on gestational age, pre‐eclampsia and birth defects.
Partner change, birth interval and risk of pre‐eclampsia: a paradoxical triangle
Authors: Zhang Jun 
Published: June 2007

SummaryImmunology has been hypothesised to play a critical role in the development of pre‐eclampsia. A number of epidemiological studies have shown that multiparous women who changed partner had an increased risk of pre‐eclampsia in the following pregnancy compared with multiparous women with the same partner. However, partner change is often associated with a long birth interval. Two recent papers using data from the same birth registry reported that, after controlling for birth interval, partner change was associated with a reduced risk of pre‐eclampsia. Based on a causal diagram, the author argues conceptually that birth interval is not a confounder but more likely to be a collider. Controlling for or stratifying birth interval in the association between partner change and risk of pre‐eclampsia could be inappropriate and may have produced a spurious association.
Partner change and perinatal outcomes: a systematic review
Authors: Zhang Jun , Patel Geeta 
Published: June 2007

SummaryEpidemiological studies suggest that partner change may affect perinatal outcomes in subsequent pregnancies. We conducted a systematic review on the association between paternity change and perinatal outcomes. We searched the literature in MEDLINE using keywords ‘paternity’, ‘partner’, ‘pre‐eclampsia’, ‘preterm birth’, ‘low birth weight’, and ‘birth defects’ from 1966 to 2005. We identified 19 studies that examined the association between partner change and specific perinatal outcomes: 12 on pre‐eclampsia or hypertension in pregnancy, three on birth defects, three on preterm birth, and two on low birthweight.Partner change was consistently associated with an increased risk of pre‐eclampsia or hypertension in pregnancy in 11 of 12 studies (the unadjusted relative risk [RR] ranging from 1.2 to 8.3). However, after controlling for birth interval as a confounder in multivariate analysis, two studies using the same birth registry data showed a modestly reduced risk in relation to partner change (RR = 0.84 and 0.73, respectively), while two studies found a slightly increased risk (both RR = 1.3). Retrospective cohort studies presented inconsistent findings on the association between partner change and risk of preterm birth and low birthweight. Finally, three population‐based cohort studies demonstrated that partner change significantly reduced the recurrence of the same or similar birth defects in subsequent births (RRs ranging from 0.1 to 0.76). We conclude that partner change reduces the risk of recurrent same birth defects. However, epidemiological evidence on the effect of partner change on pre‐eclampsia, preterm birth and low birthweight is inconclusive. Whether birth interval should be controlled for in the association between partner change and pre‐eclampsia warrants caution.
Measuring the accuracy and completeness of linking certificates for deliveries to the same woman
Authors: Adams Melissa M. , Kirby Russell S. 
Published: June 2007

SummaryNo standards exist for reporting the accuracy and completeness of pregnancy histories created by linking the birth and fetal death certificates for all the deliveries occurring to one woman. To link certificates, analysts use deterministic and/or probabilistic approaches. Errors in linkage occur randomly and non‐randomly. Any type of error can cause incorrect estimation of the magnitude of relationships. Methods for assessing linkage correctness are proposed. Analysts can detect errors in linkage by comparing the linkage results with the pregnancy history reported by the mother. The analyst interviews a random sample of women, ascertaining the dates and outcomes (stillbirth or live birth) for their births and, if the linkage used certificates from one state, the state where they occurred. For each woman, he/she then assesses the accuracy and completeness of this linkage by comparing it with her reported pregnancy history. An alternative approach is to chronologically sequence each woman's births. The parity for the most recent birth shows the number of babies born to the same woman and should equal the number of births that the analyst linked. In the absence of maternally reported pregnancy histories, an analyst can use data on the certificates to assess linkage correctness. Although this will show whether the correct number of births have been linked, it provides no information concerning the accuracy of linkages. It may be, however, the most universally applicable way of reporting the completeness of the linkage of deliveries.
Stage‐specific immune responses in human Necator americanus infection
Authors: GEIGER S. M. , CALDAS I. R. , MC GLONE B. E. , CAMPI‐AZEVEDO A. C. , DE OLIVEIRA L. M. , BROOKER S. , DIEMERT D. , CORRÊA‐OLIVEIRA R. , BETHONY J. M. 
Published: June 2007

Summary We describe how hookworms interact with their human hosts by comparing lymphocyte phenotyping, proliferative responses, and cytokine and chemokine secretion patterns in adults who are either mono‐infected with Necator americanus or egg‐negative controls resident in an area of high transmission in Brazil. Cellular immune responses against crude hookworm antigen extracts from different developmental stages were evaluated simultaneously. Principal component analysis (PCA) was used to reduce the standardized immune responses. Random effects multivariate regression was then used to investigate whether principal components (PC) differ between the two groups once potential confounders and effect modifiers have been accounted for. Although hookworm patients had reduced percentages of T and B cells, they had higher levels of activated CD4+ T and CD19+ B cells. This state of ‘immune activation’ coincided with lower proliferative responses, especially to third‐stage larval antigen. Cytokine levels in mono‐infected adults were also lower and characterized by a mixed Th1/Th2‐type profile. Excretory/secretory antigen from adult worms was a potent modulator of the immune response, resulting in diminished TNF‐α and IL‐10 secretion in peripheral blood mononuclear cells (PBMC) from hookworm infected patients. We propose that the longevity of hookworms in their human hosts results from a stage‐specific, down‐modulation of the immune response.
The role of the secretory immune response in the infection by Entamoeba histolytica
Authors: Carrero J. C. , Cervantes‐Rebolledo C. , Aguilar‐Díaz H. , Díaz‐Gallardo M. Y. , Laclette J. P. , Morales‐Montor J. 
Published: June 2007

Summary Intestinal infection with the protozoan parasite Entamoeba histolytica elicits a local immune response with rising of specific secretory IgA (sIgA) antibodies detectable in several compartments associated to mucosa. Anti‐amoebic sIgA antibodies have been reported in faeces, saliva, bile and breast milk from dysenteric patients and research trying to elucidate their role in protection has recently intensified. IgA antibodies inhibit the in vitro adherence of E. histolytica trophozoites to epithelial cell monolayers by recognizing several membrane antigens, including the galactose‐binding lectin (Gal‐lectin), main surface molecule involved in adherence, and the serine and cystein‐rich proteins, all of them potential vaccine candidates. In fact, the presence of sIgA anti‐Gal lectin in faeces of patients recovered from amoebic liver abscess (ALA) was associated with immunity to E. dispar. Moreover, the combined nasal and intraperitoneal vaccination of C3H/HeJ mice with native and recombinant Gal‐lectin protected mice against an intracecal challenge with virulent E. histolytica trophozoites, protection that seemed to be associated with the induction of specific intestinal sIgA antibodies. Therefore, the stimulation of intestinal secretory response by mucosal delivery of amoebic antigens has been positioned as a promising strategy for inducing protection against human amoebiasis.
Toxoplasma gondii infection induces apoptosis in noninfected macrophages: role of nitric oxide and other soluble factors
Authors: NISHIKAWA Y. , KAWASE O. , VIELEMEYER O. , SUZUKI H. , JOINER K. A. , XUAN X. , NAGASAWA H. 
Published: June 2007

SUMMARY Apoptosis has been found to help in the defence against pathogens. Infection with the obligate intracellular parasite Toxoplasma gondii is known to trigger host‐cell apoptosis. When using a T. gondii‐infected macrophage cell line, J774A.1, treatment with IFN‐γ significantly enhanced apoptosis in noninfected bystander cells while parasitized cells became relatively resistant. Infection and IFN‐γ treatment activated the expression of inducible nitric oxide synthase (iNOS), and the production of nitric oxide (NO) and treatment of cells with an iNOS inhibitor, NG‐monomethlyl‐l‐arginine acetate (l‐NMMA) reduced the apoptosis frequency. However, the reversal was only partial suggesting that not only NO, but also other, as of yet, unknown factors are induced. Finally, we studied the effect in vivo by infecting mice with either a virulent or an avirulent strain. Challenge with the virulent strain lead to a higher parasite burden, induced host‐cell apoptosis in peritoneal cells, and produced higher levels of IFN‐γ and NO. Moreover, treatment of mice with a NO synthase inhibitor, aminoguanidine, partially inhibited the host‐cell apoptosis induced by the parasite infection. Altogether, our findings indicate that apoptosis in bystander host cells is due to the secretion of NO and other soluble factors released by parasite‐infected cells.
Description and applications of a rapid and sensitive non‐radioactive microplate‐based assay for maximum and initial activity of D‐ribulose‐1,5‐bisphosphate carboxylase/oxygenase
Authors: SULPICE RONAN , TSCHOEP HENDRIK , VON KORFF MARIA , BÜSSIS DIRK , USADEL BJÖRN , HÖHNE MELANIE , WITUCKA‐WALL HANNA , ALTMANN THOMAS , STITT MARK , GIBON YVES 
Published: June 2007

ABSTRACTD‐ribulose‐1,5‐bisphosphate carboxylase/oxygenase (Rubisco) catalyses the first step in photosynthetic carbon assimilation and represents the largest sink for nitrogen in plants. Improvement of its kinetic properties or the efficiency with which it is used in planta would benefit photosynthesis, nitrogen and water use efficiency, and yield. This paper presents a new non‐radioactive microplate‐based assay, which determines the product [3‐phosphoglycerate (3‐PGA)] in an enzymic cycle between glycerol‐3‐phosphate dehydrogenase and glycerol‐3‐phosphate oxidase. High sensitivity permits use of highly diluted extracts, and a short reaction time to avoid problems due to fall‐off. Throughput was several hundreds of samples per person per day. Sensitivity and convenience compared favourably with radioisotopic assays, which were previously used to assay Rubisco. Its use is illustrated in three applications. (1) Maximal and initial activities and the Km for ribulose‐1,5‐bisphosphate were determined in raw extracts of leaves from several species. Similar values were obtained from those in the literature. (2) Diurnal changes were compared in rosettes of wild‐type (WT) Arabidopsis and the starchless pgm mutant. Despite these dramatic differences in carbon metabolism, Rubisco activity and activation were similar in both genotypes. (3) A preliminary association mapping study was performed with 118 Arabidopsis accessions, using 183 markers that probably cover ∼3–8% of the total genome. At a P‐value < 0.005, two, two and no quantitative trait loci (QTL) were found for Rubisco maximal activity, initial activity and activation state, respectively. Inspection of the genomic regions that span these markers revealed these QTL involved genes not previously implicated in the regulation of Rubisco expression or activity.
The temperature response of C3and C4photosynthesis
Authors: SAGE ROWAN F. , KUBIEN DAVID S. 
Published: June 2007

ABSTRACTWe review the current understanding of the temperature responses of C3and C4photosynthesis across thermal ranges that do not harm the photosynthetic apparatus. In C3species, photosynthesis is classically considered to be limited by the capacities of ribulose 1·5‐bisphosphate carboxylase/oxygenase (Rubisco), ribulose bisphosphate (RuBP) regeneration orPiregeneration. Using both theoretical and empirical evidence, we describe the temperature response of instantaneous net CO2assimilation rate (A) in terms of these limitations, and evaluate possible limitations onAat elevated temperatures arising from heat‐induced lability of Rubisco activase. In C3plants, Rubisco capacity is the predominant limitation onAacross a wide range of temperatures at low CO2(<300 µbar), while at elevated CO2, the limitation shifts toPiregeneration capacity at suboptimal temperatures, and either electron transport capacity or Rubisco activase capacity at supraoptimal temperatures. In C4plants, Rubisco capacity limitsAbelow 20 °C in chilling‐tolerant species, but the control overAat elevated temperature remains uncertain. Acclimation of C3photosynthesis to suboptimal growth temperature is commonly associated with a disproportional enhancement of thePiregeneration capacity. Above the thermal optimum, acclimation ofAto increasing growth temperature is associated with increased electron transport capacity and/or greater heat stability of Rubisco activase. In many C4species from warm habitats, acclimation to cooler growth conditions increases levels of Rubisco and C4cycle enzymes which then enhanceAbelow the thermal optimum. By contrast, few C4species adapted to cooler habitats increase Rubisco content during acclimation to reduced growth temperature; as a result,Achanges little at suboptimal temperatures. Global change is likely to cause a widespread shift in patterns of photosynthetic limitation in higher plants. Limitations in electron transport and Rubisco activase capacity should be more common in the warmer, high CO2conditions expected by the end of the century.