{"id":165,"date":"2024-04-26T10:09:43","date_gmt":"2024-04-26T10:09:43","guid":{"rendered":"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/?page_id=165"},"modified":"2026-01-08T14:45:02","modified_gmt":"2026-01-08T14:45:02","slug":"key-publications","status":"publish","type":"page","link":"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/key-publications\/","title":{"rendered":"Key Publications"},"content":{"rendered":"\n<p class=\"has-text-align-center\"><a href=\"https:\/\/scholar.google.co.uk\/citations?user=jMi2d0UAAAAJ&amp;hl=en&amp;oi=ao\" data-type=\"URL\">Please click here for a full list of publications.<\/a><\/p>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/doi.org\/10.1101\/2023.07.23.550022\">Antibiotics of the future are prone to resistance in Gram-negative pathogens. <\/a>(Daruka et al., preprint 2024)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>Despite the ongoing development of new antibiotics, the future evolution of bacterial resistance may render them ineffective. We demonstrate that antibiotic candidates currently under development are as prone to resistance evolution in Gram-negative pathogens as clinically employed antibiotics. Resistance generally stems from both genomic mutations and the transfer of antibiotic resistance genes from microbiomes associated with humans, both factors carrying equal significance. The molecular mechanisms of resistance overlap with those found in commonly used antibiotics. Therefore, these mechanisms are already present in natural populations of pathogens, indicating that resistance can rapidly emerge through selection of pre-existing bacterial variants. However, certain combinations of antibiotics and bacterial strains are less prone to developing resistance, emphasizing the potential of narrow-spectrum antibacterial therapies that could remain effective. Our comprehensive framework allows for predicting future health risks associated with bacterial resistance to new antibiotics.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/doi.org\/10.7554\/eLife.99752.1\">Heterogeneous efflux pump expression underpins phenotypic resistance to antimicrobial peptides. <\/a>(Maestri et al., Cell Host &amp; Microbe 2024)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>Antimicrobial resistance threatens the viability of modern medical interventions. There is a dire need of developing novel approaches to counter resistance mechanisms employed by starved or slow-growing pathogens that are refractory to conventional antimicrobial therapies. Antimicrobial peptides have been advocated as potential therapeutic solutions due to low levels of genetic resistance observed in bacteria against these compounds. However, here we show that subpopulations of stationary phase\u00a0<em>Escherichia coli<\/em>\u00a0and\u00a0<em>Pseudomonas aeruginosa<\/em>\u00a0survive tachyplesin treatment without genetic mutations. These phenotypic variants induce efflux, outer membrane vesicles secretion and membrane modifications in response to tachyplesin exposure, sequestering the peptide in their membranes where it cannot exert its antimicrobial activity. We discovered that formation of these phenotypic variants could be prevented by administering tachyplesin in combination with sertraline, a clinically used antidepressant, suggesting a novel approach for combatting antimicrobial-refractory stationary phase bacteria.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/doi.org\/10.1016\/j.chom.2024.07.005\">The bacterial defense system MADS interacts with CRISPR-Cas to limit phage infection and escape.<\/a><a href=\"https:\/\/www.sciencedirect.com\/science\/article\/pii\/S1369527424000122\"> <\/a>(Maestri et al., Cell Host &amp; Microbe 2024)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Summary: <\/em>The constant arms race between bacteria and their parasites has resulted in a large diversity of bacterial defenses, with many bacteria carrying multiple systems. Here, we report the discovery of a phylogenetically widespread defense system, coined methylation-associated defense system (MADS), which is distributed across gram-positive and gram-negative bacteria. MADS interacts with a CRISPR-Cas system in its native host to provide robust and durable resistance against phages. While phages can acquire epigenetic-mediated resistance against MADS, co-existence of MADS and a CRISPR-Cas system limits escape emergence. MADS comprises eight genes with predicted nuclease, ATPase, kinase, and methyltransferase domains, most of which are essential for either self\/non-self discrimination, DNA restriction, or both. The complex genetic architecture of MADS and MADS-like systems, relative to other prokaryotic defenses, points toward highly elaborate mechanisms of sensing infections, defense activation, and\/or interference.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/www.sciencedirect.com\/science\/article\/pii\/S1369527424000122\">Multi-layered genome defences in bacteria. <\/a>(Agapov et al., Current Opinion in Microbiology 2024)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Summary<\/em>: Bacteria have evolved a variety of defence mechanisms to protect against\u00a0mobile genetic elements, including restriction-modification systems and CRISPR\u2013Cas. In recent years, dozens of previously unknown defence systems (DSs) have been discovered. Notably, diverse DSs often coexist within the same genome, and some co-occur at frequencies significantly higher than would be expected by chance, implying potential synergistic interactions. Recent studies have provided evidence of defence mechanisms that enhance or complement one another. Here, we review the interactions between DSs at the mechanistic, regulatory, ecological\u00a0and evolutionary levels.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/www.nature.com\/articles\/d41586-023-03796-8\">Viruses wrap up bacterial defences. <\/a>(Blower and van Houte, Nature 2024)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Summary: <\/em>Bacteria use diverse defences against viral predators called bacteriophages. A method to identify antibacterial counter-defences in viral genomes has revealed striking modes of defence inhibition.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/38366022\/\"><strong>CRISPR-Cas in Pseudomonas aeruginosa provides transient population-level immunity against high phage exposures<\/strong>.<\/a> <strong>(Watson et al., ISME J. 2024)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>The prokaryotic adaptive immune system, CRISPR-Cas (clustered regularly interspaced short palindromic repeats; CRISPR-associated), requires the acquisition of spacer sequences that target invading mobile genetic elements such as phages. Previous work has identified ecological variables that drive the evolution of CRISPR-based immunity of the model organism Pseudomonas aeruginosa PA14 against its phage DMS3vir, resulting in rapid phage extinction. However, it is unclear if and how stable such acquired immunity is within bacterial populations, and how this depends on the environment. Here, we examine the dynamics of CRISPR spacer acquisition and loss over a 30-day evolution experiment and identify conditions that tip the balance between long-term maintenance of immunity versus invasion of alternative resistance strategies that support phage persistence. Specifically, we find that both the initial phage dose and reinfection frequencies determine whether or not acquired CRISPR immunity is maintained in the long term, and whether or not phage can coexist with the bacteria. At the population genetics level, emergence and loss of CRISPR immunity are associated with high levels of spacer diversity that subsequently decline due to invasion of bacteria carrying pilus-associated mutations. Together, these results provide high resolution of the dynamics of CRISPR immunity acquisition and loss and demonstrate that the cumulative phage burden determines the effectiveness of CRISPR over ecologically relevant timeframes.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/www.nature.com\/articles\/s41396-023-01487-w\">Interspecific competition can drive plasmid loss from a focal species in a microbial community. <\/a>(S\u00fcnderhauf et al., Nature 2023)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>Plasmids are key disseminators of antimicrobial resistance genes and virulence factors, and it is therefore critical to predict and reduce plasmid spread within microbial communities. The cost of plasmid carriage is a key metric that can be used to predict plasmids&#8217; ecological fate, and it is unclear whether plasmid costs are affected by growth partners in a microbial community. We carried out competition experiments and tracked plasmid maintenance using a model system consisting of a synthetic and stable five-species community and a broad host-range plasmid, engineered to carry different payloads. We report that both the cost of plasmid carriage and its long-term maintenance in a focal strain depended on the presence of competitors, and that these interactions were species specific. Addition of growth partners increased the cost of a high-payload plasmid to a focal strain, and accordingly, plasmid loss from the focal species occurred over a shorter time frame. We propose that the destabilising effect of interspecific competition on plasmid maintenance may be leveraged in clinical and natural environments to cure plasmids from focal strains.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/www.microbiologyresearch.org\/content\/journal\/micro\/10.1099\/mic.0.001334\">Removal of AMR plasmids using a mobile, broad host-range, CRISPR-Cas9 delivery tool. <\/a>(S\u00fcnderhauf et al., Microbiology 2023)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>Antimicrobial resistance (AMR) genes are widely disseminated on plasmids. Therefore, interventions aimed at blocking plasmid uptake and transfer may curb the spread of AMR. Previous studies have used CRISPR-Cas-based technology to remove plasmids encoding AMR genes from target bacteria, using either phage- or plasmid-based delivery vehicles that typically have narrow host ranges. To make this technology feasible for removal of AMR plasmids from multiple members of complex microbial communities, an efficient, broad host-range delivery vehicle is needed. We engineered the broad host-range IncP1-plasmid pKJK5 to encode cas9 programmed to target an AMR gene. We demonstrate that the resulting plasmid pKJK5::csg has the ability to block the uptake of AMR plasmids and to remove resident plasmids from <em>Escherichia coli<\/em>. Furthermore, due to its broad host range, pKJK5::csg successfully blocked AMR plasmid uptake in a range of environmental, pig- and human-associated coliform isolates, as well as in isolates of two species of <em>Pseudomonas<\/em>. This study firmly establishes pKJK5::csg as a promising broad host-range CRISPR-Cas9 delivery tool for AMR plasmid removal, which has the potential to be applied in complex microbial communities to remove AMR genes from a broad range of bacterial species.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/doi.org\/10.1073\/pnas.2216084120\">Antibiotics that affect translation can antagonize phage infectivity by interfering with the deployment of counter-defences.<\/a> (Pons et al., PNAS 2023)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>It is becoming increasingly clear that antibiotics can both positively and negatively impact the infectivity of bacteriophages (phage), but the underlying mechanisms often remain unclear. Here we demonstrate that antibiotics that target the protein translation machinery can fundamentally alter the outcome of bacteria-phage interactions by interfering with the production of phage-encoded counter-defense proteins. Specifically, using <em>Pseudomonas aeruginosa<\/em> PA14 and phage DMS3vir as a model, we show that bacteria with Clustered Regularly Interspaced Short Palindromic Repeat, CRISPR associated (CRISPR-Cas) immune systems have elevated levels of immunity against phage that encode anti-CRISPR (acr) genes when translation inhibitors are present in the environment. CRISPR-Cas are highly prevalent defense systems that enable bacteria to detect and destroy phage genomes in a sequence-specific manner. In response, many phages encode&nbsp;<em>acr<\/em>&nbsp;genes that are expressed immediately following the infection to inhibit key steps of the CRISPR-Cas immune response. Our data show that while phage-carrying&nbsp;<em>acr<\/em>&nbsp;genes can amplify efficiently on bacteria with CRISPR-Cas immune systems in the absence of antibiotics, the presence of antibiotics that act on protein translation prevents phage amplification, while protecting bacteria from lysis.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><strong><a href=\"https:\/\/royalsocietypublishing.org\/doi\/10.1098\/rstb.2020.0464\">CRISPR-Cas is associated with fewer antibiotic resistance genes in bacterial pathogens. <\/a>(Pursey et al., Phil Trans B 2022)<\/strong><\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>The acquisition of antibiotic resistance (ABR) genes via horizontal gene transfer (HGT) is a key driver of the rise in multidrug resistance amongst bacterial pathogens. Bacterial defence systems per definition restrict the influx of foreign genetic material, and may therefore limit the acquisition of ABR. CRISPR-Cas adaptive immune systems are one of the most prevalent defences in bacteria, found in roughly half of bacterial genomes, but it has remained unclear if and how much they contribute to restricting the spread of ABR. We analysed approximately 40 000 whole genomes comprising the full RefSeq dataset for 11 species of clinically important genera of human pathogens, including <em>Enterococcus, Staphylococcus, Acinetobacter <strong>and <\/strong>Pseudomonas<\/em>. We modelled the association between CRISPR-Cas and indicators of HGT, and found that pathogens with a CRISPR-Cas system were less likely to carry ABR genes than those lacking this defence system. Analysis of the mobile genetic elements (MGEs) targeted by CRISPR-Cas supports a model where this host defence system blocks important vectors of ABR. These results suggest a potential &#8216;immunocompromised&#8217; state for multidrug-resistant strains that may be exploited in tailored interventions that rely on MGEs, such as phages or phagemids, to treat infections caused by bacterial pathogens. This article is part of the theme issue &#8216;The secret lives of microbial mobile genetic elements&#8217;.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p><a href=\"https:\/\/doi.org\/10.1016\/j.cell.2018.05.058\"><strong>Anti-CRISPR phages cooperate to overcome CRISPR-Cas immunity.<\/strong> <\/a>(<strong>Landsberger et al., Cell 2018<\/strong>)<\/p>\n\n\n\n<ul>\n<li><em>Abstract: <\/em>Some phages encode anti-CRISPR (<em>acr<\/em>) genes, which antagonize bacterial CRISPR-Cas immune systems by binding components of its machinery, but it is less clear how deployment of these&nbsp;<em>acr<\/em>&nbsp;genes impacts phage replication and epidemiology. Here, we demonstrate that bacteria with CRISPR-Cas resistance are still partially immune to Acr-encoding phage. As a consequence, Acr-phages often need to cooperate in order to overcome CRISPR resistance, with a first phage blocking the host CRISPR-Cas immune system to allow a second Acr-phage to successfully replicate. This cooperation leads to epidemiological tipping points in which the initial density of Acr-phage tips the balance from phage extinction to a phage epidemic. Furthermore, both higher levels of CRISPR-Cas immunity and weaker Acr activities shift the tipping points toward higher initial phage densities. Collectively, these data help elucidate how interactions between phage-encoded immune suppressors and the CRISPR systems they target shape bacteria-phage population dynamics.<\/li>\n<\/ul>\n\n\n\n<div style=\"height:30px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<figure class=\"wp-block-gallery has-nested-images columns-default is-cropped wp-block-gallery-1 is-layout-flex wp-block-gallery-is-layout-flex\">\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"1024\" height=\"768\" data-id=\"143\" src=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0719-1024x768.jpg\" alt=\"\" class=\"wp-image-143\" srcset=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0719-1024x768.jpg 1024w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0719-300x225.jpg 300w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0719-768x576.jpg 768w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0719-1536x1152.jpg 1536w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0719.jpg 2016w\" sizes=\"(max-width: 1024px) 100vw, 1024px\" \/><\/figure>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"1024\" height=\"768\" data-id=\"139\" src=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0717-1024x768.jpg\" alt=\"\" class=\"wp-image-139\" srcset=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0717-1024x768.jpg 1024w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0717-300x225.jpg 300w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0717-768x576.jpg 768w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0717-1536x1152.jpg 1536w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0717.jpg 2016w\" sizes=\"(max-width: 1024px) 100vw, 1024px\" \/><\/figure>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"1024\" height=\"768\" data-id=\"137\" src=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0716-1024x768.jpg\" alt=\"\" class=\"wp-image-137\" srcset=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0716-1024x768.jpg 1024w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0716-300x225.jpg 300w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0716-768x576.jpg 768w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0716-1536x1152.jpg 1536w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0716.jpg 2016w\" sizes=\"(max-width: 1024px) 100vw, 1024px\" \/><\/figure>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"1024\" height=\"768\" data-id=\"127\" src=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0707-1024x768.jpg\" alt=\"\" class=\"wp-image-127\" srcset=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0707-1024x768.jpg 1024w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0707-300x225.jpg 300w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0707-768x576.jpg 768w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0707-1536x1152.jpg 1536w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0707.jpg 2016w\" sizes=\"(max-width: 1024px) 100vw, 1024px\" \/><\/figure>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"1024\" height=\"768\" data-id=\"129\" src=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0708-1024x768.jpg\" alt=\"\" class=\"wp-image-129\" srcset=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0708-1024x768.jpg 1024w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0708-300x225.jpg 300w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0708-768x576.jpg 768w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0708-1536x1152.jpg 1536w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0708.jpg 2016w\" sizes=\"(max-width: 1024px) 100vw, 1024px\" \/><\/figure>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"1024\" height=\"768\" data-id=\"131\" src=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0711-1024x768.jpg\" alt=\"\" class=\"wp-image-131\" srcset=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0711-1024x768.jpg 1024w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0711-300x225.jpg 300w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0711-768x576.jpg 768w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0711-1536x1152.jpg 1536w, https:\/\/sites.exeter.ac.uk\/vanhoutelab\/wp-content\/uploads\/sites\/399\/2024\/04\/IMG_0711.jpg 2016w\" sizes=\"(max-width: 1024px) 100vw, 1024px\" \/><\/figure>\n<\/figure>\n","protected":false},"excerpt":{"rendered":"<p>Please click here for a full list of publications. Antibiotics of the future are prone to resistance in Gram-negative pathogens. (Daruka et al., preprint 2024) Heterogeneous efflux pump expression underpins phenotypic resistance to antimicrobial peptides. (Maestri et al., Cell Host &amp; Microbe 2024) The bacterial defense system MADS interacts with CRISPR-Cas to limit phage infection [&hellip;]<\/p>\n","protected":false},"author":1575,"featured_media":125,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"page-sidebar-boxed-feature-img.php","meta":{"_acf_changed":false,"footnotes":""},"categories":[],"tags":[],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v23.0 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Key Publications - Van Houte Lab<\/title>\n<meta name=\"description\" content=\"A selection of literature published by Stineke Van Houte and colleagues, with focus on bacterial defenses and phage therapy.\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/sites.exeter.ac.uk\/vanhoutelab\/key-publications\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Key Publications - 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