# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 9196 | 0 | 1.0000 | Lessons from gene knockouts. The authors describe the technique for the application of homologous recombination in embryonic stem cells, which is now widely used to engineer mice which carry specific knockouts of genes. A summary is given of some of the knowledge of the pathogenesis of and resistance to infections with parasites, bacteria, or viruses which has accumulated during recent years, based on the investigation of knockout mice. Special emphasis is placed on knockout animals which lack components of the cytokine network, lack genes which are critical for the correct presentation of antigens or are deficient in different immune cell subsets. In addition, a brief explanation is offered of the possibilities for inducing targeted deletions or mutations in genes of livestock species (e.g., by nuclear transfer or by mutagenesis using the alkylating agent N-ethyl-N-nitrosourea) which could lead to the breeding of animals which are resistant to infectious diseases in the future. | 1998 | 9638823 |
| 9206 | 1 | 0.9998 | Susceptibility reversed: modified plant susceptibility genes for resistance to bacteria. Plants have evolved complex defence mechanisms to avoid invasion of potential pathogens. Despite this, adapted pathogens deploy effector proteins to manipulate host susceptibility (S) genes, rendering plant defences ineffective. The identification and mutation of plant S genes exploited by bacterial pathogens are important for the generation of crops with durable and broad-spectrum resistance. Application of mutant S genes in the breeding of resistant crops is limited because of potential pleiotropy. New genome editing techniques open up new possibilities for the modification of S genes. In this review, we focus on S genes manipulated by bacteria and propose ways for their identification and precise modification. Finally, we propose that genes coding for transporter proteins represent a new group of S genes. | 2022 | 34400073 |
| 9205 | 2 | 0.9997 | Resistance induction based on the understanding of molecular interactions between plant viruses and host plants. BACKGROUND: Viral diseases cause significant damage to crop yield and quality. While fungi- and bacteria-induced diseases can be controlled by pesticides, no effective approaches are available to control viruses with chemicals as they use the cellular functions of their host for their infection cycle. The conventional method of viral disease control is to use the inherent resistance of plants through breeding. However, the genetic sources of viral resistance are often limited. Recently, genome editing technology enabled the publication of multiple attempts to artificially induce new resistance types by manipulating host factors necessary for viral infection. MAIN BODY: In this review, we first outline the two major (R gene-mediated and RNA silencing) viral resistance mechanisms in plants. We also explain the phenomenon of mutations of host factors to function as recessive resistance genes, taking the eIF4E genes as examples. We then focus on a new type of virus resistance that has been repeatedly reported recently due to the widespread use of genome editing technology in plants, facilitating the specific knockdown of host factors. Here, we show that (1) an in-frame mutation of host factors necessary to confer viral resistance, sometimes resulting in resistance to different viruses and that (2) certain host factors exhibit antiviral resistance and viral-supporting (proviral) properties. CONCLUSION: A detailed understanding of the host factor functions would enable the development of strategies for the induction of a new type of viral resistance, taking into account the provision of a broad resistance spectrum and the suppression of the appearance of resistance-breaking strains. | 2021 | 34454519 |
| 9200 | 3 | 0.9997 | Application of the CRISPR/Cas System for Generation of Pathogen-Resistant Plants. The use of the CRISPR/Cas9 prokaryotic adaptive immune system has led to a breakthrough in targeted genome editing in eukaryotes. The CRISPR/Cas technology allows to generate organisms with desirable characteristics by introducing deletions/insertions into selected genome loci resulting in the knockout or modification of target genes. This review focuses on the current state of the CRISPR/Cas use for the generation of plants resistant to viruses, bacteria, and parasitic fungi. Resistance to DNA- and RNA-containing viruses is usually provided by expression in transgenic plants of the Cas endonuclease gene and short guide RNAs (sgRNAs) targeting certain sites in the viral or the host plant genomes to ensure either direct cleavage of the viral genome or modification of the plant host genome in order to decrease the efficiency of virus replication. Editing of plant genes involved in the defense response to pathogens increases plants resistance to bacteria and pathogenic fungi. The review explores strategies and prospects of the development of pathogen-resistant plants with a focus on the generation of non-transgenic (non-genetically modified) organisms, in particular, by using plasmid (DNA)-free systems for delivery of the Cas/sgRNA editing complex into plant cells. | 2018 | 30878030 |
| 9419 | 4 | 0.9997 | Genes required for mycobacterial growth defined by high density mutagenesis. Despite over a century of research, tuberculosis remains a leading cause of infectious death worldwide. Faced with increasing rates of drug resistance, the identification of genes that are required for the growth of this organism should provide new targets for the design of antimycobacterial agents. Here, we describe the use of transposon site hybridization (TraSH) to comprehensively identify the genes required by the causative agent, Mycobacterium tuberculosis, for optimal growth. These genes include those that can be assigned to essential pathways as well as many of unknown function. The genes important for the growth of M. tuberculosis are largely conserved in the degenerate genome of the leprosy bacillus, Mycobacterium leprae, indicating that non-essential functions have been selectively lost since this bacterium diverged from other mycobacteria. In contrast, a surprisingly high proportion of these genes lack identifiable orthologues in other bacteria, suggesting that the minimal gene set required for survival varies greatly between organisms with different evolutionary histories. | 2003 | 12657046 |
| 9207 | 5 | 0.9997 | Genetically engineered resistance to bacterial and fungal pathogens. In the past 10 years, different strategies have been used to produce transgenic plants that are less susceptible to diseases caused by phytopathogenic fungi and bacteria. Genes from different organisms, including bacteria, fungi and plants, have been successfully used to develop these strategies. Some strategies have been shown to be effective against different pathogens, whereas others are specific to a single pathogen or even to a single pathovar or race of a given pathogen. In this review, we present the strategies that have been employed to produce transgenic plants less susceptible to bacterial and fungal diseases and which constitute an important area of plant biotechnology. | 1995 | 24414746 |
| 9336 | 6 | 0.9997 | Molecular dissection of nutrient exchange at the insect-microbial interface. Genome research is transforming our understanding of nutrient exchange between insects and intracellular bacteria. A key characteristic of these bacteria is their small genome size and gene content. Their fastidious and inflexible nutritional requirements are met by multiple metabolites from the insect host cell. Although the bacteria have generally retained genes coding the synthesis of nutrients required by the insect, some apparently critical genes have been lost, and compensated for by shared metabolic pathways with the insect host or supplementary bacteria with complementary metabolic capabilities. | 2014 | 28043404 |
| 9131 | 7 | 0.9997 | How do antibiotic-producing bacteria ensure their self-resistance before antibiotic biosynthesis incapacitates them? Acquired antibiotic resistance among dangerous bacterial pathogens is an increasing medical problem. While in Mycobacterium tuberculosis this occurs by mutation in the genes encoding the targets for antibiotic action, other pathogens have generally gained their resistance genes by horizontal gene transfer from non-pathogenic bacteria. The ultimate source of many of these genes is almost certainly the actinomycetes that make the antibiotics and therefore need self-protective mechanisms to avoid suicide. How do they ensure that they are resistant at the time when intracellular antibiotic concentrations reach potentially lethal levels? In this issue of Molecular Microbiology, Tahlan et al. describe a solution to this problem in which an antibiotically inactive precursor of a Streptomyces coelicolor antibiotic induces resistance -- in this example by means of a trans-membrane export pump -- so that the organism is already primed for resistance at the time when it is needed. The authors generalize their interpretation to other cases where antibiotic resistance depends on export, but it will be interesting to find out whether it could in fact apply more widely, to include the other major mechanisms of resistance: target modification and the synthesis of antibiotics via a series of chemically modified intermediates, with removal of the protective group at the time of secretion into the outside medium. | 2007 | 17238916 |
| 9198 | 8 | 0.9997 | Recognition of bacterial avirulence proteins occurs inside the plant cell: a general phenomenon in resistance to bacterial diseases? One of the recent exciting developments in the research area of plant-microbe interactions is a breakthrough in understanding part of the initial signalling between avirulent Gram-negative bacteria and resistant plants. For resistance to occur, both interacting organisms need to express matching genes, the plant resistance gene and the bacterial avirulence gene. The biochemical function of bacterial avirulence genes and the nature of the signal molecules recognized by the plant have been a mystery for a long time. Recently, several laboratories have shown that bacterial avirulence proteins function as elicitors that are perceived within the plant cell. | 1997 | 9263447 |
| 9281 | 9 | 0.9997 | Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells. Prophages are quiescent viruses located in the chromosomes of bacteria. In the human pathogen, Staphylococcus aureus, prophages are omnipresent and are believed to be responsible for the spread of some antibiotic resistance genes. Here we demonstrate that release of phages from a subpopulation of S. aureus cells enables the intact, prophage-containing population to acquire beneficial genes from competing, phage-susceptible strains present in the same environment. Phage infection kills competitor cells and bits of their DNA are occasionally captured in viral transducing particles. Return of such particles to the prophage-containing population can drive the transfer of genes encoding potentially useful traits such as antibiotic resistance. This process, which can be viewed as 'auto-transduction', allows S. aureus to efficiently acquire antibiotic resistance both in vitro and in an in vivo virulence model (wax moth larvae) and enables it to proliferate under strong antibiotic selection pressure. Our results may help to explain the rapid exchange of antibiotic resistance genes observed in S. aureus. | 2016 | 27819286 |
| 9204 | 10 | 0.9997 | Susceptibility Genes in Bacterial Diseases of Plants. Plant susceptibility (S) genes exploited by pathogenic bacteria play critical roles in disease development, collectively contributing to symptoms, pathogen proliferation, and spread. S genes may support pathogen establishment within the host, suppress host immunity, regulate host physiology or development, or function in other ways. S genes can be passive, e.g., involved in pathogen attraction or required for pathogen effector localization or activity, or active, contributing directly to symptoms or pathogen proliferation. Knowledge of S genes is important for understanding disease and other aspects of plant biology. It is also useful for disease management, as nonfunctional alleles can slow or prevent disease and, because they are often quantitative, can exert less selection on pathogens than dominant resistance genes, allowing greater durability. In this review, we discuss bacterial exploitation of S genes, S-gene functional diversity, approaches for identifying S genes, translation of S-gene knowledge for disease control, and future perspectives on this exciting area of plant pathology. | 2025 | 40446167 |
| 9232 | 11 | 0.9997 | CRISPR interference can prevent natural transformation and virulence acquisition during in vivo bacterial infection. Pathogenic bacterial strains emerge largely due to transfer of virulence and antimicrobial resistance genes between bacteria, a process known as horizontal gene transfer (HGT). Clustered, regularly interspaced, short palindromic repeat (CRISPR) loci of bacteria and archaea encode a sequence-specific defense mechanism against bacteriophages and constitute a programmable barrier to HGT. However, the impact of CRISPRs on the emergence of virulence is unknown. We programmed the human pathogen Streptococcus pneumoniae with CRISPR sequences that target capsule genes, an essential pneumococcal virulence factor, and show that CRISPR interference can prevent transformation of nonencapsulated, avirulent pneumococci into capsulated, virulent strains during infection in mice. Further, at low frequencies bacteria can lose CRISPR function, acquire capsule genes, and mount a successful infection. These results demonstrate that CRISPR interference can prevent the emergence of virulence in vivo and that strong selective pressure for virulence or antibiotic resistance can lead to CRISPR loss in bacterial pathogens. | 2012 | 22901538 |
| 9470 | 12 | 0.9997 | Practical Method for Isolation of Phage Deletion Mutants. The growing concern about multi-drug resistant pathogenic bacteria has led to a renewed interest in the study of bacteriophages as antimicrobials and as therapeutic agents against infectious diseases (phage therapy). Phages to be used for this purpose have to be subjected to in-depth genomic characterization. It is essential to ascribe specific functions to phage genes, which will give information to unravel phage biology and to ensure the lack of undesirable genes, such as virulence and antibiotic resistance genes. Here, we describe a simple protocol for the selection of phage mutants carrying random deletions along the phage genome. Theoretically, any DNA region might be removed with the only requirement that the phage particle viability remains unaffected. This technique is based on the instability of phage particles in the presence of chelating compounds. A fraction of the phage population naturally lacking DNA segments will survive the treatment. Within the context of phages as antimicrobials, this protocol is useful to select lytic variants from temperate phages. In terms of phage efficiency, virulent phages are preferred over temperate ones to remove undesirable bacteria. This protocol has been used to obtain gene mutations that are involved in the lysogenic cycle of phages infecting Gram-positive bacteria (Staphylococcus and Lactobacillus). | 2018 | 31164553 |
| 9202 | 13 | 0.9997 | Microbial avirulence determinants: guided missiles or antigenic flak? SUMMARY Avirulence (avr) determinants are incompatibility factors which elicit host plant defence responses in a gene-for-gene manner. They are produced by fungi, bacteria and viruses, and their recognition by resistance genes has been extensively studied for decades. But why should a microbe keep a molecule that allows it to be recognized? One argument is that avr genes perform some essential function and must be kept despite giving the pathogen away. Many bacterial avr determinants have been shown to be effectors, which contribute to virulence and aggressiveness. If this were always the case, mutants lacking these essential molecules would be at a serious disadvantage. Some disadvantage has been shown for a small number, but for the majority there is no effect on virulence. This has been explained by functional redundancy for bacterial and fungal avr determinants, with other molecules compensating for the deletion of these essential genes. However, this argument is counter-intuitive because by definition these individual genes are no longer essential; so why keep them? With increasing numbers of avr genes being identified, efforts to elucidate their function are increasing. In this review, we take stock of the accumulating literature, and consider what the real function of avr determinants might be. | 2005 | 20565679 |
| 9356 | 14 | 0.9997 | The expression of antibiotic resistance genes in antibiotic-producing bacteria. Antibiotic-producing bacteria encode antibiotic resistance genes that protect them from the biologically active molecules that they produce. The expression of these genes needs to occur in a timely manner: either in advance of or concomitantly with biosynthesis. It appears that there have been at least two general solutions to this problem. In many cases, the expression of resistance genes is tightly linked to that of antibiotic biosynthetic genes. In others, the resistance genes can be induced by their cognate antibiotics or by intermediate molecules from their biosynthetic pathways. The regulatory mechanisms that couple resistance to antibiotic biosynthesis are mechanistically diverse and potentially relevant to the origins of clinical antibiotic resistance. | 2014 | 24964724 |
| 9137 | 15 | 0.9997 | Virulence- and antibiotic resistance-associated two-component signal transduction systems of Gram-positive pathogenic bacteria as targets for antimicrobial therapy. Two-component signal transduction systems are central elements of the virulence and antibiotic resistance responses of opportunistic bacterial pathogens. These systems allow the bacterium to sense and respond to signals emanating from the host environment and to modulate the repertoire of genes expressed to allow invasion and growth in the host. The integral role of two-component systems in virulence and antibiotic sensitivity, and the existence of essential two-component systems in several pathogenic bacteria, suggests that these systems may be novel targets for antimicrobial intervention. This review discusses the potential use of two-component systems as targets for antimicrobial therapy against Gram-positive pathogens and the current status in the development of inhibitors specific for these systems. | 2002 | 12191621 |
| 9417 | 16 | 0.9997 | General aspects of virus drug resistance with special reference to herpes simplex virus. The features of virus drug resistance are reviewed with examples from studies of herpes simplex virus drug-resistant mutants. Virus drug resistance, compared with drug resistance of bacteria or eukaryotes, is distinguished by its ability to provide information on drug selectivity. Identification of genes in which mutations arise to confer drug resistance defines gene products which contribute to antiviral selectivity. The gene products can then be dissected functionally with the aid of these mutations. Laboratory studies of the frequency of mutation to drug resistance and the features of drug-resistant mutants may have predictive value for the clinic. | 1986 | 3025148 |
| 9423 | 17 | 0.9997 | Integrated evolutionary analysis reveals antimicrobial peptides with limited resistance. Antimicrobial peptides (AMPs) are promising antimicrobials, however, the potential of bacterial resistance is a major concern. Here we systematically study the evolution of resistance to 14 chemically diverse AMPs and 12 antibiotics in Escherichia coli. Our work indicates that evolution of resistance against certain AMPs, such as tachyplesin II and cecropin P1, is limited. Resistance level provided by point mutations and gene amplification is very low and antibiotic-resistant bacteria display no cross-resistance to these AMPs. Moreover, genomic fragments derived from a wide range of soil bacteria confer no detectable resistance against these AMPs when introduced into native host bacteria on plasmids. We have found that simple physicochemical features dictate bacterial propensity to evolve resistance against AMPs. Our work could serve as a promising source for the development of new AMP-based therapeutics less prone to resistance, a feature necessary to avoid any possible interference with our innate immune system. | 2019 | 31586049 |
| 9197 | 18 | 0.9997 | Temperature-sensitive bacterial pathogens generated by the substitution of essential genes from cold-loving bacteria: potential use as live vaccines. Temperature-sensitive (TS) viruses have been used for decades as vaccines capable of limited replication in their hosts. Although attenuated bacteria, such as the Bacille Calmette-Guérin anti-tuberculosis vaccine, have been used for almost a century, it is only recently that there has been progress in using TS bacterial strains as live vaccines. Decades of work on essential bacterial genes and the recent explosion in the number of available bacterial genomic sequences set the groundwork for the identification of essential genes from diverse bacteria. This knowledge has allowed for the substitution of essential genes from cold-loving bacteria into the chromosomes of pathogenic bacteria. Many of these gene substitutions generated TS pathogenic bacterial strains, and some were demonstrated to provide protective immunity in mice. This work opens the possibility of engineering many pathogenic bacteria to create TS strains that can be used as vaccines. | 2011 | 21229224 |
| 9282 | 19 | 0.9997 | Could DNA uptake be a side effect of bacterial adhesion and twitching motility? DNA acquisition promotes the spread of resistance to antibiotics and virulence among bacteria. It is also linked to several natural phenomena including recombination, genome dynamics, adaptation and speciation. Horizontal DNA transfer between bacteria occurs via conjugation, transduction or competence for natural transformation by DNA uptake. Among these, competence is the only mechanism of transformation initiated and entirely controlled by the chromosome of the recipient bacteria. While the molecular mechanisms allowing the uptake of extracellular DNA are increasingly characterized, the function of competence for natural transformation by DNA uptake, the selective advantage maintaining it and the reasons why bacteria take up DNA in the first place are still debated. In this synthesis, I review some of the literature and discuss the four hypotheses on how and why do bacteria take up DNA. I argue that DNA uptake by bacteria is an accidental by-product of bacterial adhesion and twitching motility. Adhesion and motility are generally increased in stressful conditions, which may explain why bacteria increase DNA uptake in these conditions. In addition to its fundamental scientific relevance, the new hypothesis suggested here has significant clinical implications and finds further support from the fact that antibiotics sometimes fail to eliminate the targeted bacterium while inevitably causing stress to others. The widespread misuse of antibiotics may thus not only be selecting for resistant strains, but may also be causing bacteria to take up more DNA with the consequent increase in the chances of acquiring drug resistance and virulence-a scenario in full concordance with the previously reported induction of competence genes by antibiotics in Streptococcus pneumoniae and Legionella pneumophila. | 2013 | 23381940 |