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At least 73 records · Page 4Linked to original sources
PubMed2006

LrhA regulates rpoS translation in response to the Rcs phosphorelay system in Escherichia coli.

Regulation of the Escherichia coli stationary-phase sigma factor RpoS is complex and occurs at multiple levels in response to different environmental stresses. One protein that reduces RpoS levels is the transcription factor LrhA, a global regulator of flagellar synthesis. Here we clarify the mechanism of this repression and provide insight into the signaling pathways that feed into this regulation. We show that LrhA represses RpoS at the level of translation in a manner that is dependent on the small RNA (sRNA) chaperone Hfq. Although LrhA also represses the transcription of the sRNA RprA, its regulation of RpoS mainly occurs independently of RprA. To better understand the physiological signals affecting this pathway, a transposon mutagenesis screen was carried out to find factors affecting LrhA activity levels. The RcsCDB phosphorelay system, a cell envelope stress-sensing pathway, was found to repress lrhA synthesis. In addition, mutations in the gene encoding the DNA motor protein FtsK induce lrhA synthesis, which may explain why such strains fail to accumulate RpoS in stationary phase.

Bacterial Proteins↗
PubMed2005

Specific recognition and cleavage of the plus-strand primer by reverse transcriptase.

Reverse transcriptases (RTs) of retroviruses and long terminal repeat (LTR)-retrotransposons possess DNA polymerase and RNase H activities. During reverse transcription these activities are necessary for the programmed sequence of events that include template switching and primer processing. Integrase then inserts the completed cDNA into the genome of the host cell. The RT of the LTR-retrotransposon Tf1 was subjected to random mutagenesis, and the resulting transposons were screened with genetic assays to test which mutations reduced reverse transcription and which inhibited integration. We identified a cluster of mutations in the RNase H domain of RT that were surprising because they blocked integration without reducing cDNA levels. The results of immunoblots demonstrated that these mutations did not reduce levels of RT or integrase. DNA blots showed that the mutations did not lower the amounts of full-length cDNA. The sequences of the 3' ends of the cDNA revealed that mutations within the cluster in RNase H specifically reduced the removal of the polypurine tract (PPT) primer from the ends of the cDNA. These results indicate that primer removal is not a necessary component of reverse transcription. The residues mutated in Tf1 RNase H are conserved in human immunodeficiency virus type 1 and make direct contact with DNA opposite the PPT. Thus, our results identify a conserved element in RT that contacts the PPT and is specifically required for PPT removal.

DNA, Viral↗
PubMed2025

Identification of OxyR as an activator of type 1 fimbriae (fim) in Salmonella enterica serovar Typhi.

Salmonella enterica serovar Typhi (S. Typhi) encodes 14 fimbrial gene clusters, including the mannose-binding type 1 fimbriae known as Fim. Type 1 fimbriae have been implicated in biofilm formation and adhesion to host cells in Salmonella. However, their regulation in S. Typhi remains largely unknown. To identify genes affecting the regulation of fim in S. Typhi, we employed both a targeted and a genome-wide transposon-based screening approach. Overall, we identified 18 potential regulators of fim expression: 10 activators and 8 repressors. Two genes involved in the electron transport chain, yqiC and ndh, which encode the type II NADH dehydrogenase NDH-2, were identified. Both YqiC and NDH-2 contribute to the production of reactive oxygen species, prompting an investigation into the roles of oxidative stress response regulators OxyR and SoxR. We found that only OxyR regulates fim expression, which was specific to S. Typhi. OxyR acts by directly binding to the fimA promoter region. This study paves the way for future development of anti-adhesion strategies through the identification of 14 novel regulators for the most prominent fimbriae of S. Typhi.IMPORTANCEAdhesion mediated by fimbriae is one of the critical steps in the infection process. Therefore, it is essential to better understand the regulation of type 1 fimbriae (fim) in the human-specific pathogen Salmonella enterica serovar Typhi, the etiologic agent of typhoid fever. In this study, we identified 18 distinct mutants with altered regulation of fim. Furthermore, we confirmed that the DNA-binding protein OxyR directly regulates fim expression. Importantly, we also demonstrated regulatory differences in fim expression between S. Typhi and S. Typhimurium, as six of the genes identified altering fim expression in S. Typhi either did not affect fim expression in S. Typhimurium or had the contrary effect. This highlights fundamental differences between these serovars and emphasizes the need to investigate and compare aspects of gene regulation in S. Typhi.

Salmonella typhi↗
PubMed1985

[Effect of dioxidine, antineoplastic agents and other mutagens on the precise excision of Tn1 and Tn10 transposons in E. coli K12].

Induction of precise excision of transposons Tn1 and Tn10 from the genes met::Tn1 and cys::Tn10 by chemical agents, having mutagenic and DNA damaging activities, has been studied. The drugs dioxydin, NMU, photrin, phopurine, thiophosphamid, rongeron as well as sodium azide, 2-NP, DDDTDP are shown to differ in their ability to stimulate the precise excision of transposons of different classes and in the efficiency of stimulated process. Results of the present paper are in proof of the possible using of experimental model, based on registering the precise excision of transposons, for screening the mutagenic and cancerogenic activities of chemical agents from the environment.

Antineoplastic Agents↗
PubMed1992

Cloning of a locus involved in Streptococcus mutans intracellular polysaccharide accumulation and virulence testing of an intracellular polysaccharide-deficient mutant.

The streptococcal transposon Tn916 (Tcr) was used to isolate mutants of Streptococcus mutans altered in glycogen accumulation to investigate whether glycogenlike intracellular polysaccharides (IPS) play an important role in S. mutans-induced caries formation. S. mutans UA130 (serotype c) was transformed with the Escherichia coli plasmid pAM620 (Tn916), and the resultant transposon libraries were screened for glycogen content by iodine staining. A transposon mutant, designated SMS201, demonstrated a glycogen-deficient phenotype on glucose-enriched medium. Quantitative electron microscopy confirmed that IPS concentrations were significantly reduced in SMS201 relative to the wild-type progenitor strain, UA130. Importantly, reversion to wild type correlated at all times with loss of the transposon. Transposon excisants were used to facilitate cloning of the streptococcal gene(s) involved in glycogen biosynthesis and storage. A 2.1-kb chromosomal determinant (glgR) which encodes a putative regulator of S. mutans glycogen accumulation was isolated. A stable deletion mutation (delta glgR) was subsequently generated in E. coli and introduced into S. mutans by allelic exchange. The resultant glycogen synthesis-deficient mutant, SMS203, demonstrated a significantly reduced cariogenic potential (P less than 0.01) on the buccal, sulcal, and proximal surfaces of teeth in germfree rats, relative to animals challenged with the glycogen synthesis-proficient progenitor strain, UA130. These observations confirm previous reports (J. M. Tanzer, M. L. Freedman, F. N. Woodiel, R. L. Eifert, and L. A. Rinehimer, p. 597-616, in H. M. Stiles, W. J. Loesche, and T. L. O'Brien, ed., Proceedings in Microbiology. Aspects of Dental Caries. Special Supplement to Microbiology Abstracts, vol. 3, 1976) which implicate IPS as significant contributors to the S. mutans cariogenic process.

Animals↗
PubMed2002

Promoter-trapping in Saccharomyces cerevisiae by radiation-assisted fragment insertion.

Non-homologous insertion (NHI) of DNA fragments into genomic DNA is a method widely used in insertional mutagenesis screens. In the yeast Saccharomyces cerevisiae, the efficiency of NHI is very low. Here we report that its efficiency can be increased by gamma-irradiation of recipient cells at the time of transformation. Radiation-assisted NHI depends on YKU70, but its efficiency is not improved by inactivation of RAD5 or RAD52. In a pilot study, we generated 102 transformant clones expressing a lacZ reporter gene under standard conditions (30 degrees C, rich medium). The site of insertion was determined in a subset of eight clones in which lacZ expression was altered by UV-irradiation. A comparison with published data revealed that three of the eight genes identified in our screen have not been targeted by large-scale transposon-based insertion screens. This suggests that radiation-assisted NHI offers a more homogeneous coverage of the genome than methods relying on transposons or retroviral elements.

Fungal Proteins↗
PubMed1996

Identification, cloning, and expression of the Escherichia coli pyrazinamidase and nicotinamidase gene, pncA.

Pyrazinamide (PZA) is one of the three most important drugs for treatment of Mycobacterium tuberculosis infections. The antibacterial activity of PZA requires a bacterial enzyme, pyrazinamidase (PZAase), which hydrolyzes PZA to form pyrazinoic acid and ammonia. Most PZA-resistant clinical M. tuberculosis isolates lack PZAase activity. With the goal of eventually identifying and characterizing the M.tuberculosis PZAase gene, we began with the more tractable organism, Escherichia coli, which also has PZAase activity. We screened a transposon-generated E. coli insertion mutant library, using a qualitative PZAase assay. Two PZAase-negative mutants out of 4,000 colonies screened were identified. In each mutant, the transposon interrupted the same 639-bp open reading frame (ORF), ORF1. The expression of ORF1 on a multicopy plasmid complemented a PZAase-negative mutant, leading to PZAase activity levels approximately 10-fold greater than those of the wild type. PZA has a structure similar to that of nicotinamide, a pyridine nucleotide cycle intermediate, so we tested our strains for nicotinamidase activity (EC 3.5.1.19) (genetic locus pncA). The construct with multiple plasmid copies of ORF1 had an approximately 10-fold increase in levels of nicotinamidase activity. This overexpressing strain could utilize nicotinamide as a sole nitrogen source, through wild-type E. coli cannot. We conclude that a single E. coli enzyme accounts for both PZAase and nicotinamidase activities and that ORF1 is the E.coli PZAase and nicotinamidase gene, pncA.

Amidohydrolases↗
PubMed1997

Mutagenesis of Burkholderia pseudomallei with Tn5-OT182: isolation of motility mutants and molecular characterization of the flagellin structural gene.

Burkholderia pseudomallei is a human and animal pathogen in tropical regions, especially Southeast Asia and northern Australia. Currently little is known about the genetics and molecular biology of this organism. In this report, we describe the mutagenesis of B. pseudomallei with the transposon Tn5-OT182. B. pseudomallei 1026b transposon mutants were obtained at a frequency of 4.6 x 10(-4) per initial donor cell, and the transposon inserted randomly into the chromosome. We used Tn5-OT182 to identify the flagellin structural gene, fliC. We screened 3,500 transposon mutants and identified 28 motility mutants. Tn5-OT182 integrated into 19 unique genetic loci encoding proteins with homology to Escherichia coli and Salmonella typhimurium flagellar and chemotaxis proteins. Two mutants, MM35 and MM36, contained Tn5-OT182 integrations in fliC. We cloned and sequenced fliC and used it to complement MM35 and MM36 in trans. The fliC transcriptional start site and a sigmaF-like promoter were identified by primer extension analysis. We observed a significant difference in the expression of two distinct fliC-lacZ transcriptional fusions during bacterial growth, suggesting the presence of a latent intragenic transcriptional terminator in fliC. There was no significant difference in the virulence of 1026b compared to that of MM36 in diabetic rats or Syrian hamsters, suggesting that flagella and/or motility are probably not virulence determinants in these animal models of B. pseudomallei infection. A phylogenetic analysis based on the flagellins from a variety of bacterial species supported the recent transfer of B. pseudomallei from the genus Pseudomonas to Burkholderia.

Amino Acid Sequence↗
PubMed2025

The Mycobacterium tuberculosis Transposon Sequencing Database (MtbTnDB): A Large-Scale Guide to Genetic Conditional Essentiality.

Characterizing genetic essentiality across various conditions is fundamental for understanding gene function. Transposon sequencing (TnSeq) is a powerful technique to generate genome-wide essentiality profiles in bacteria and has been extensively applied to Mycobacterium tuberculosis (Mtb). Dozens of TnSeq screens have yielded valuable insights into the biology of Mtb in vitro, inside macrophages, and in model host organisms. Despite their value, these Mtb TnSeq profiles have not been standardized or collated into a single, easily searchable database. This results in significant challenges when attempting to query and compare these resources, limiting our ability to obtain a comprehensive and consistent understanding of genetic conditional essentiality in Mtb. We address this problem by building a central repository of publicly available Mtb TnSeq screens, the Mtb transposon sequencing database (MtbTnDB). The MtbTnDB is a living resource that encompasses to date ≈150 standardized TnSeq screens, enabling open access to data, visualizations, and functional predictions through an interactive web app (www.mtbtndb.app). We conduct several statistical analyses on the complete database, such as demonstrating that (i) genes in the same genomic neighborhood have similar TnSeq profiles, and (ii) clusters of genes with similar TnSeq profiles are enriched for genes from similar functional categories. We further analyze the performance of machine learning models trained on TnSeq profiles to predict the functional annotation of orphan genes in Mtb. By facilitating the comparison of TnSeq screens across conditions, the MtbTnDB will accelerate the exploration of conditional genetic essentiality, provide insights into the functional organization of Mtb genes, and help predict gene function in this important human pathogen.

DNA Transposable Elements↗
PubMed2002

Identification of motility and autoagglutination Campylobacter jejuni mutants by random transposon mutagenesis.

Campylobacter jejuni has been identified as the leading cause of acute bacterial diarrhea in the United States, yet compared with other enteric pathogens, considerably less is understood concerning the virulence factors of this human pathogen. A random in vivo transposon mutagenesis system was recently developed for the purpose of creating a library of C. jejuni transformants. A total of 1,065 C. jejuni transposon mutants were screened for their ability to swarm on motility agar plates and autoagglutinate in liquid cultures; 28 mutants were subsequently identified. The transposon insertion sites were obtained by using random-primed PCR, and the putative genes responsible for these phenotypes were identified. Of these mutants, all 28 were found to have diminished motility (0 to 86% that of the control). Seventeen motility mutants had insertions in genes with strong homology to functionally known motility and chemotaxis genes; however, 11 insertions were in genes of unknown function. Twenty motility mutants were unable to autoagglutinate, suggesting that the expression of flagella is correlated with autoagglutination (AAG). However, four mutants expressed wild-type levels of surface FlaA, as indicated by Western blot analysis, yet were unable to autoagglutinate (Cj1318, Cj1333, Cj1340c, and Cj1062). These results suggest that FlaA is necessary but not sufficient to mediate the AAG phenotype. Furthermore, two of the four AAG mutants (Cj1333 and Cj1062) were unable to invade INT-407 intestinal epithelial cells, as determined by a gentamicin treatment assay. These data identify novel genes important for motility, chemotaxis, and AAG and demonstrate their potential role in virulence.

Agglutination↗
PubMed1993

Evidence of mobilization of hobo transposons in a P-element mutagenesis screen.

In Drosophila melanogaster, mutations in Su(var) and En(var) loci either suppress or enhance position effect variegation, respectively. Towards the cloning of these genes we have induced, recovered, and characterized a series of Su(var) mutations located on the third chromosome. These mutations were recovered from a P-element mutagenesis scheme in which the third chromosome P[ry+ delta 2-3](99B) element would provide transposase in trans to mobilize a single nonautonomous P transposon, P[pUCHSNeo](9C), located on the X chromosome. Although this cross scheme induces mobilization of the X-chromosome P transposons and its subsequent reinsertion onto the autosomes, none of the Su(var) mutations recovered could be associated with P-transposon insertions. Further investigation of these mutations by in situ hybridization showed that another mobile element that can be mobilized in hybrids, hobo, was associated with these mutations. We conclude that the mobilization and reinsertion of the hobo elements, through an inadvertent hybrid HE dysgenic cross, is most likely responsible for the Su(var) mutations recovered from this P-element mutagenesis. The association of hobo element with this Su(var) locus will facilitate its cloning and offers the possibility of hobo transposon tagging other Su(var) loci.

Animals↗
PubMed2005

Mycobacterial mutants with defective control of phagosomal acidification.

The pathogenesis of mycobacterial infection is associated with an ability to interfere with maturation of the phagosomal compartment after ingestion by macrophages. Identification of the mycobacterial components that contribute to this phenomenon will allow rational design of novel approaches to the treatment and prevention of tuberculosis. Microarray-based screening of a transposon library was used to identify mutations that influence the fate of Mycobacterium bovis bacille Calmette-Guérin (BCG) following uptake by macrophages. A screen based on bacterial survival during a 3-d infection highlighted genes previously implicated in growth of Mycobacterium tuberculosis in macrophages and in mice, together with a number of other virulence genes including a locus encoding virulence-associated membrane proteins and a series of transporter molecules. A second screen based on separation of acidified and non-acidified phagosomes by flow cytometry identified genes involved in mycobacterial control of early acidification. This included the KefB potassium/proton antiport. Mutants unable to control early acidification were significantly attenuated for growth during 6-d infections of macrophages. Early acidification of the phagosome is associated with reduced survival of BCG in macrophages. A strong correlation exists between genes required for intracellular survival of BCG and those required for growth of M. tuberculosis in mice. In contrast, very little correlation exists between genes required for intracellular survival of BCG and those that are up-regulated during intracellular adaptation of M. tuberculosis. This study has identified targets for interventions to promote immune clearance of tuberculosis infection. The screening technologies demonstrated in this study will be useful to the study of pathogenesis in many other intracellular microorganisms.

Journal Article↗
PubMed2000

Identification of Streptococcus agalactiae virulence genes in the neonatal rat sepsis model using signature-tagged mutagenesis.

Group B streptococcal (GBS) infections are the most common cause of bacterial sepsis in the immediate newborn period. Apart from the capsule, the factors required for survival of GBS in the host are not well defined. In this study, signature-tagged transposon mutagenesis (STM) was used to identify genes required for growth and survival of GBS in a neonatal rat sepsis infection model. Approximately 1600 transposon mutants were screened in pools of 80 mutants, and approximately 120 mutants defective for survival in the animal host were identified. We successfully cloned and sequenced DNA flanking the transposon insertions from 92 of the mutants. Fifty per cent of the mutants had transposon insertions in genes with homologues in the public databases, whereas the remaining 50% had transposon insertions in genes with unknown function. A significant proportion of the avirulent mutants had transposon insertions in genes encoding transport-associated or regulatory proteins or in genes involved in cell surface metabolism, emphasizing the significance of these functions for in vivo survival of GBS. Overall, STM analysis revealed GBS genomic loci that encode a wide variety of functional gene classes, underscoring the diversity of bacterial processes required for the infection process. Currently, the function of the genes identified during the screening can only be inferred by homology to previously described genes. However, a number of the genes identified in this study have been shown to correlate with virulence in other pathogens. A virulence of a subset of mutants identified during the screening was confirmed by performing competitive index assays and lethal dose assays. This represents the first report of a genome-wide scan for virulence factors in GBS. The identified genes will further our understanding of the pathogenesis of GBS infections and may represent targets for intervention or lead to the development of novel therapies.

Animals↗
PubMed2001

Transposon mutagenesis reveals novel loci affecting tolerance to salt stress and growth at low temperature.

Using transposon mutagenesis in the haploid Saccharomyces cerevisiae strain W303-1A we have identified genes required for growth in high salt medium, survival of a hypo-osmotic shock and growth at 15 degrees C. Screening 25,000 transposon insertions revealed a total of 61 insertions that caused salt-sensitivity; and those insertions affected 31 genes. Only 12 of those genes were previously known to be required for salt-tolerance. Among the 61 insertions, three caused general osmo-sensitivity. We identified one single insertion mutant in the already-known gene, FPS1, required for survival of hypo-osmotic shock. A total of 31 insertions caused failure to grow at low temperature. Those identified ten different genes, three of which had previously been reported to affect cold-tolerance. Four genes were identified in both the salt and the cold-sensitivity screen. We found several unusual insertion mutations: (1) insertions in or close to essential genes, (2) insertion in an intergenic region and (3) insertions causing stress-sensitivity in W303-1A, while the deletion mutant in BY4741 did not show such a phenotype. Surprisingly, our mutant set and that reported in the large-scale transposon insertion project (TRIPLES, http://ygacmed.yale.edu/triples/triples.htm) only marginally overlap. We discuss some of the features of transposon mutagenesis in light of the availability of the complete set of yeast deletion mutants and we discuss the possible roles of the genes we identified.

Base Sequence↗
PubMed1994

Recovery of heritable, transposon-induced, mutant alleles of the rf 2 nuclear restorer of T-cytoplasm maize.

T (Texas) cytoplasm is associated with a mitochondrial disruption that is phenotypically expressed during microsporogenesis resulting in male sterility. Restoration of pollen fertility in T-cytoplasm maize is controlled by dominant alleles at two unlinked, complementary, nuclear-encoded genes, rf1 and rf2. As a first step in the molecular isolation of the rf2 gene, 178,300 gametes derived from plants that carried the Mutator, Cy or Spm transposon families were screened for rf2 mutant alleles (rf2-m) via their inability to restore pollen fertility to T-cytoplasm male-sterile maize. Seven heritable rf2-m alleles were recovered from these transposon populations. Pedigrees and restriction fragment length polymorphism (RFLP)-based analyses indicated that all seven rf 2-m alleles were derived independently. The ability to obtain rf 2-m derivatives from Rf2 suggests that Rf2 alleles produce a functional product necessary to restore pollen fertility to cmsT. Molecular markets flanking the rf1 and rf2 loci were used to decipher segregation patterns in progenies segregating for the rf2-m alleles. These analyses provided preliminary evidence of a weak, third restorer gene of cmsT that can substitute for Rf1.

Alleles↗
PubMed1997

Random shuttle mutagenesis: gonococcal mutants deficient in pilin antigenic variation.

Shuttle mutagenesis has been adapted to randomly mutate the genome of Neisseria gonorrhoeae (gonococcus; Gc). A size-restricted plasmid library of Gc strain FA1090 was mutated with the mini-transposon mTnEGNS. Radomness was tested by checking for transposon insertion bias between vector and insert DNA, Gc transformation efficiency of individual mutated clones, and representation of unique clones before and after Gc transformation with a mutated pool of DNA. Mutants created by random shuttle mutagenesis were screened, using a colony-based polymerase chain reaction assay, for the ability to undergo pilin antigenic variation. Out of 8,064 mutants screened, 22 unique transposon insertion mutants were found to be antigenic variation deficient (Avd). The Avd mutants were separated into five types according to recombination defect-associated phenotypes, including colony growth, natural DNA transformation competence, and repair of DNA damage caused by ultraviolet radiation.

Antigenic Variation↗
PubMed2003

The Delta subunit of RNA polymerase is required for virulence of Streptococcus agalactiae.

Group B streptococci (GBS) remain the most significant bacterial pathogen causing neonatal sepsis, pneumonia, and meningitis in the United States despite the chemoprophylaxis strategies for preventing infection recommended by the Centers for Disease Control and Prevention. Using signature-tagged transposon mutagenesis to screen for novel virulence factors, we identified the rpoE gene as essential for development of sepsis in a neonatal rat model of GBS infection. An rpoE allelic replacement mutant displayed attenuated virulence in the sepsis model of infection identical to that of the transposon mutant, confirming linkage of the phenotype to the mutation in rpoE. The rpoE mutants also displayed increased sensitivity to killing in whole-blood bactericidal assays, which may explain the attenuated virulence. The mutants were otherwise phenotypically identical to the wild-type strain, including growth rate in plasma, indicating that a growth defect is not responsible for the attenuated virulence. rpoE is found only in gram-positive bacterial species and encodes the delta peptide, a subunit of RNA polymerase. Previous in vitro studies in other bacteria suggest that the delta peptide plays a role in maintaining transcriptional fidelity by blocking RNA polymerase binding at all but the strongest promoters, thereby inhibiting initiation of transcription. Despite the availability of rpoE mutants for several gram-positive bacterial species, a role for the peptide in vivo has not been defined, though it has been postulated that the delta peptide may be important for long-term survival in vitro or during growth phase transitions. Our data represent the first report of a phenotype relevant to virulence for rpoE mutants.

Alleles↗
PubMed2006

Attenuated Francisella novicida transposon mutants protect mice against wild-type challenge.

Francisella tularensis is the bacterial pathogen that causes tularemia in humans and a number of animals. To date, there is no approved vaccine for this widespread and life-threatening disease. The goal of this study was to identify F. tularensis mutants that can be used in the development of a live attenuated vaccine. We screened F. novicida transposon mutants to identify mutants that exhibited reduced growth in mouse macrophages, as these cells are the preferred host cells of Francisella and an essential component of the innate immune system. This approach yielded 16 F. novicida mutants that were 100-fold more attenuated for virulence in a mouse model than the wild-type parental strain. These mutants were then tested to determine their abilities to protect mice against challenge with high doses of wild-type bacteria. Five of the 16 attenuated mutants (with mutations corresponding to dsbB, FTT0742, pdpB, fumA, and carB in the F. tularensis SCHU S4 strain) provided mice with protection against challenge with high doses (>8 x 10(5) CFU) of wild-type F. novicida. We believe that these findings will be of use in the design of a vaccine against tularemia.

Animals↗