Showing papers by "James J. Collins published in 2022"
TL;DR: Clinicians should test patients with rash consistent with monkeypox,† regardless of whether the rash is disseminated or was preceded by prodrome, and public health efforts should prioritize gay, bisexual, and other men who have sex with men, who are currently disproportionately affected for prevention and testing.
Abstract: Monkeypox, a zoonotic infection caused by an orthopoxvirus, is endemic in parts of Africa. On August 4, 2022, the U.S. Department of Health and Human Services declared the U.S. monkeypox outbreak, which began on May 17, to be a public health emergency (1,2). After detection of the first U.S. monkeypox case), CDC and health departments implemented enhanced monkeypox case detection and reporting. Among 2,891 cases reported in the United States through July 22 by 43 states, Puerto Rico, and the District of Columbia (DC), CDC received case report forms for 1,195 (41%) cases by July 27. Among these, 99% of cases were among men; among men with available information, 94% reported male-to-male sexual or close intimate contact during the 3 weeks before symptom onset. Among the 88% of cases with available data, 41% were among non-Hispanic White (White) persons, 28% among Hispanic or Latino (Hispanic) persons, and 26% among non-Hispanic Black or African American (Black) persons. Forty-two percent of persons with monkeypox with available data did not report the typical prodrome as their first symptom, and 46% reported one or more genital lesions during their illness; 41% had HIV infection. Data suggest that widespread community transmission of monkeypox has disproportionately affected gay, bisexual, and other men who have sex with men and racial and ethnic minority groups. Compared with historical reports of monkeypox in areas with endemic disease, currently reported outbreak-associated cases are less likely to have a prodrome and more likely to have genital involvement. CDC and other federal, state, and local agencies have implemented response efforts to expand testing, treatment, and vaccination. Public health efforts should prioritize gay, bisexual, and other men who have sex with men, who are currently disproportionately affected, for prevention and testing, while addressing equity, minimizing stigma, and maintaining vigilance for transmission in other populations. Clinicians should test patients with rash consistent with monkeypox,† regardless of whether the rash is disseminated or was preceded by prodrome. Likewise, although most cases to date have occurred among gay, bisexual, and other men who have sex with men, any patient with rash consistent with monkeypox should be considered for testing. CDC is continually evaluating new evidence and tailoring response strategies as information on changing case demographics, clinical characteristics, transmission, and vaccine effectiveness become available.§.
197 citations
TL;DR: This work combines AlphaFold2 with molecular docking simulations to predict protein‐ligand interactions between 296 proteins spanning Escherichia coli's essential proteome and 218 active antibacterial compounds and 100 inactive compounds, pointing to widespread compound and protein promiscuity.
Abstract: Efficient identification of drug mechanisms of action remains a challenge. Computational docking approaches have been widely used to predict drug binding targets; yet, such approaches depend on existing protein structures, and accurate structural predictions have only recently become available from AlphaFold2. Here, we combine AlphaFold2 with molecular docking simulations to predict protein‐ligand interactions between 296 proteins spanning Escherichia coli's essential proteome, and 218 active antibacterial compounds and 100 inactive compounds, respectively, pointing to widespread compound and protein promiscuity. We benchmark model performance by measuring enzymatic activity for 12 essential proteins treated with each antibacterial compound. We confirm extensive promiscuity, but find that the average area under the receiver operating characteristic curve (auROC) is 0.48, indicating weak model performance. We demonstrate that rescoring of docking poses using machine learning‐based approaches improves model performance, resulting in average auROCs as large as 0.63, and that ensembles of rescoring functions improve prediction accuracy and the ratio of true‐positive rate to false‐positive rate. This work indicates that advances in modeling protein‐ligand interactions, particularly using machine learning‐based approaches, are needed to better harness AlphaFold2 for drug discovery.
47 citations
TL;DR: Oral supplementation with the engineered live biotherapeutic minimized gut dysbiosis without affecting the ampicillin concentration in serum, precluded the enrichment of antimicrobial resistance genes in the gut microbiome and prevented the loss of colonization resistance against Clostridioides difficile.
28 citations
TL;DR: A nonribosomal peptide synthetase that is induced in male worms upon pairing with a female and find that it is essential for the ability of male worms to stimulate female development was found in this paper .
20 citations
TL;DR: In this article , the authors identify a mechanism of tolerance evolution in E. coli involving deletion of the sodium-proton antiporter gene nhaA, which results in downregulated metabolism and upregulated stress responses, and find that cycling of antibiotics with different metabolic dependencies interrupts evolution of tolerance in vitro, increasing the lifetime of treatment efficacy.
Abstract: Antibiotic tolerance, or the ability of bacteria to survive antibiotic treatment in the absence of genetic resistance, has been linked to chronic and recurrent infections. Tolerant cells are often characterized by a low metabolic state, against which most clinically used antibiotics are ineffective. Here, we show that tolerance readily evolves against antibiotics that are strongly dependent on bacterial metabolism, but does not arise against antibiotics whose efficacy is only minimally affected by metabolic state. We identify a mechanism of tolerance evolution in E. coli involving deletion of the sodium-proton antiporter gene nhaA, which results in downregulated metabolism and upregulated stress responses. Additionally, we find that cycling of antibiotics with different metabolic dependencies interrupts evolution of tolerance in vitro, increasing the lifetime of treatment efficacy. Our work highlights the potential for limiting the occurrence and extent of tolerance by accounting for antibiotic dependencies on bacterial metabolism.
14 citations
TL;DR: In this article , the authors highlight the challenge that transgene silencing poses to the robust engineering of mammalian cells, outline potential molecular mechanisms of silencing, and present approaches for preventing transgogene silencing.
Abstract: To elucidate principles operating in native biological systems and to develop novel biotechnologies, synthetic biology aims to build and integrate synthetic gene circuits within native transcriptional networks. The utility of synthetic gene circuits for cell engineering relies on the ability to control the expression of all constituent transgene components. Transgene silencing, defined as the loss of expression over time, persists as an obstacle for engineering primary cells and stem cells with transgenic cargos. In this review, we highlight the challenge that transgene silencing poses to the robust engineering of mammalian cells, outline potential molecular mechanisms of silencing, and present approaches for preventing transgene silencing. We conclude with a perspective identifying future research directions for improving the performance of synthetic gene circuits.
11 citations
TL;DR: Lummertz da Rocha et al. as discussed by the authors developed and applied CellComm to investigate how the aorta-gonad-mesonephros microenvironment dictates haematopoietic stem and progenitor cell emergence.
Abstract: Intercellular communication orchestrates a multitude of physiologic and pathologic conditions. Algorithms to infer cell–cell communication and predict downstream signalling and regulatory networks are needed to illuminate mechanisms of stem cell differentiation and tissue development. Here, to fill this gap, we developed and applied CellComm to investigate how the aorta–gonad–mesonephros microenvironment dictates haematopoietic stem and progenitor cell emergence. We identified key microenvironmental signals and transcriptional networks that regulate haematopoietic development, including Stat3, Nr0b2, Ybx1 and App, and confirmed their roles using zebrafish, mouse and human models. Notably, CellComm revealed extensive crosstalk among signalling pathways and convergence on common transcriptional regulators, indicating a resilient developmental programme that ensures dynamic adaptation to changes in the embryonic environment. Our work provides an algorithm and data resource for the scientific community. Lummertz da Rocha et al. present CellComm, an algorithm that analyses cell–cell communication to predict signalling and regulatory networks, and identify regulators of haematopoietic development in the aorta–gonad–mesonephros region.
8 citations
TL;DR: A novel classification of three distinct types of mutations identifiable by muscle RNA analysis is proposed: deep intronic point mutations, deletions or insertions, and translocations that differ in potential treatment approaches.
Abstract: DMD pathogenic variants for Duchenne and Becker muscular dystrophy are detectable with high sensitivity by standard clinical exome analyses of genomic DNA. However, up to 7% of DMD mutations are deep intronic and analysis of muscle‐derived RNA is an important diagnostic step for patients who have negative genomic testing but abnormal dystrophin expression in muscle. In this study, muscle biopsies were evaluated from 19 patients with clinical features of a dystrophinopathy, but negative clinical DMD mutation analysis. Reverse transcription‐polymerase chain reaction or high‐throughput RNA sequencing methods identified 19 mutations with one of three pathogenic pseudoexon types: deep intronic point mutations, deletions or insertions, and translocations. In association with point mutations creating intronic splice acceptor sites, we observed the first examples of DMD pseudo 3ʹ‐terminal exon mutations causing high efficiency transcription termination within introns. This connection between splicing and premature transcription termination is reminiscent of U1 snRNP‐mediating telescripting in sustaining RNA polymerase II elongation across large genes, such as DMD. We propose a novel classification of three distinct types of mutations identifiable by muscle RNA analysis, each of which differ in potential treatment approaches. Recognition and appropriate characterization may lead to therapies directed toward full‐length dystrophin expression for some patients.
7 citations
TL;DR: Lummertz da Rocha et al. as discussed by the authors developed and applied CellComm to investigate how the aorta-gonad-mesonephros microenvironment dictates haematopoietic stem and progenitor cell emergence.
Abstract: Intercellular communication orchestrates a multitude of physiologic and pathologic conditions. Algorithms to infer cell–cell communication and predict downstream signalling and regulatory networks are needed to illuminate mechanisms of stem cell differentiation and tissue development. Here, to fill this gap, we developed and applied CellComm to investigate how the aorta–gonad–mesonephros microenvironment dictates haematopoietic stem and progenitor cell emergence. We identified key microenvironmental signals and transcriptional networks that regulate haematopoietic development, including Stat3, Nr0b2, Ybx1 and App, and confirmed their roles using zebrafish, mouse and human models. Notably, CellComm revealed extensive crosstalk among signalling pathways and convergence on common transcriptional regulators, indicating a resilient developmental programme that ensures dynamic adaptation to changes in the embryonic environment. Our work provides an algorithm and data resource for the scientific community. Lummertz da Rocha et al. present CellComm, an algorithm that analyses cell–cell communication to predict signalling and regulatory networks, and identify regulators of haematopoietic development in the aorta–gonad–mesonephros region.
6 citations
TL;DR: It is shown that CRISPR-Cas12a can be used to quickly and cheaply delete or insert genes into the E. faecium genome and this substantial improvement over current methods should speed up research on this important opportunistic pathogen.
Abstract: Enterococcus faecium is increasingly associated with hard-to-treat antibiotic-resistant infections. The ability to generate clean genomic alterations is the first step in generating a complete mechanistic understanding of how E. faecium acquires pathogenic traits and causes disease. ABSTRACT Considered a serious threat by the Centers for Disease Control and Prevention, multidrug-resistant Enterococcus faecium is an increasing cause of hospital-acquired infection. Here, we provide details on a single-plasmid CRISPR-Cas12a system for generating clean deletions and insertions. Single manipulations were carried out in under 2 weeks, with successful deletions/insertions present in >80% of the clones tested. Using this method, we generated three individual clean deletion mutations in the acpH, treA, and lacL genes and inserted codon-optimized unaG, enabling green fluorescent protein (GFP)-like fluorescence under the control of the trehalase operon. The use of in vivo recombination for plasmid construction kept costs to a minimum. IMPORTANCE Enterococcus faecium is increasingly associated with hard-to-treat antibiotic-resistant infections. The ability to generate clean genomic alterations is the first step in generating a complete mechanistic understanding of how E. faecium acquires pathogenic traits and causes disease. Here, we show that CRISPR-Cas12a can be used to quickly (under 2 weeks) and cheaply delete or insert genes into the E. faecium genome. This substantial improvement over current methods should speed up research on this important opportunistic pathogen.
5 citations
TL;DR: Examining the function of two different P53 homologs in the parasitic flatworm Schistosoma mansoni found that Smed-p53 does not seem to play any role in the planarian response to genotoxic stress, implying that the ability to respond to genOToxic stress in parasitic flatworms may have arisen from convergent evolution.
Abstract: Significance P53 is an important tumor suppressor that is found throughout metazoans, including invertebrates that do not develop malignancies. The prevailing theory for why these invertebrates possess a tumor suppressor is that P53 originally evolved to protect the germline of early metazoans from genotoxic stress such as ultraviolet radiation. Here, we examine the function of two P53 homologs in the parasitic flatworm Schistosoma mansoni. The first is orthologous to canonical P53 and regulates flatworm stem cell maintenance and differentiation. The second P53 gene is a parasite-specific paralog that is required for the normal response to genotoxic stress. The existence of this parasite-specific paralog implies that the ability to respond to genotoxic stress in parasitic flatworms may have arisen from convergent evolution.
TL;DR: The ASCGE guideline for infection control during GI endoscopy as mentioned in this paper provides a comparative view of various organizational reprocessing guidelines with respect to the differences in the organizations' practices and practices.
TL;DR: It was found that SETDB1-Cohesin co-regulate target gene expression and genome topology at these DiSCs, which unravels a unique topological and transcriptional axis of control regulated chiefly bySETDB1.
Abstract: Abstract SETDB1 is a key regulator of lineage-specific genes and endogenous retroviral elements (ERVs) through its deposition of repressive H3K9me3 mark. Apart from its H3K9me3 regulatory role, SETDB1 has seldom been studied in terms of its other potential regulatory roles. To investigate this, a genomic survey of SETDB1 binding in mouse embryonic stem cells across multiple libraries was conducted, leading to the unexpected discovery of regions bereft of common repressive histone marks (H3K9me3, H3K27me3). These regions were enriched with the CTCF motif that is often associated with the topological regulator Cohesin. Further profiling of these non-H3K9me3 regions led to the discovery of a cluster of non-repeat loci that were co-bound by SETDB1 and Cohesin. These regions, which we named DiSCs (domains involving SETDB1 and Cohesin) were seen to be proximal to the gene promoters involved in embryonic stem cell pluripotency and lineage development. Importantly, it was found that SETDB1-Cohesin co-regulate target gene expression and genome topology at these DiSCs. Depletion of SETDB1 led to localized dysregulation of Cohesin binding thereby locally disrupting topological structures. Dysregulated gene expression trends revealed the importance of this cluster in ES cell maintenance as well as at gene ‘islands’ that drive differentiation to other lineages. The ‘unearthing’ of the DiSCs thus unravels a unique topological and transcriptional axis of control regulated chiefly by SETDB1.
TL;DR: For example, this article found that people who perceived local COVID-19 transmission levels as high were more likely to report having made behavioral changes, such as wearing a mask in public, limiting travel, and avoiding crowded places or events.
Abstract: During the early stages of the COVID-19 pandemic, use of preventive behaviors was associated with perceived risk for contracting SARS-CoV-2 infection (1,2). Over time, perceived risk has declined along with waning COVID-19-related media coverage (3,4). The extent to which communities continue to be aware of local COVID-19 transmission levels and are implementing recommended preventive behaviors is unknown. During June 1-July 31, 2022, health departments in DuPage County, Illinois and metropolitan Detroit, Michigan surveyed a combined total of 4,934 adults who had received a positive test result for SARS-CoV-2 during the preceding 3 weeks. The association between awareness of local COVID-19 transmission and use of preventive behaviors and practices was assessed, both in response to perceived local COVID-19 transmission levels and specifically during the 2 weeks preceding SARS-CoV-2 testing. Both areas had experienced sustained high COVID-19 transmission during the study interval as categorized by CDC COVID-19 transmission levels.* Overall, 702 (14%) respondents perceived local COVID-19 transmission levels as high, 987 (20%) as substantial, 1,902 (39%) as moderate, and 581 (12%) as low; 789 (16%) reported they did not know. Adjusting for geographic area, age, gender identity, and combined race and ethnicity, respondents who perceived local COVID-19 transmission levels as high were more likely to report having made behavioral changes because of the level of COVID-19 transmission in their area, including wearing a mask in public, limiting travel, and avoiding crowded places or events. Continued monitoring of public perceptions of local COVID-19 levels and developing a better understanding of their influence on the use of preventive behaviors can guide COVID-19 communication strategies and policy making during and beyond the pandemic.
TL;DR: In this paper , the authors colonized the nematode Caenorhabditis elegans gut with cellulolytic bacteria that enabled C. elegans to utilize cellulose, an otherwise indigestible substrate, as a carbon source.
Abstract: The gut microbiome is essential for processing complex food compounds and synthesizing nutrients that the host cannot digest or produce, respectively. New model systems are needed to study how the metabolic capacity provided by the gut microbiome impacts the nutritional status of the host, and to explore possibilities for altering host metabolic capacity via the microbiome. Here, we colonized the nematode Caenorhabditis elegans gut with cellulolytic bacteria that enabled C. elegans to utilize cellulose, an otherwise indigestible substrate, as a carbon source. Cellulolytic bacteria as a community component in the worm gut can also support additional bacterial species with specialized roles, which we demonstrate by using Lactobacillus plantarum to protect C. elegans against Salmonella enterica infection. This work shows that engineered microbiome communities can be used to endow host organisms with novel functions, such as the ability to utilize alternate nutrient sources or to better fight pathogenic bacteria.
TL;DR: Preliminary data is provided on the clinical feasibility, acceptability of dosing, outcome measures, and staff/patient participation obtained from the initial open-label portion of clinical trial NCT04811339 of SARS-CoV-2.
TL;DR:
Abstract: Schistosoma mansoni is a flatworm that causes schistosomiasis, a neglected tropical disease that affects over 200 million people worldwide. New therapeutic targets are needed with only one drug available for treatment and no vaccine. Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides with low or no protein-coding potential. In other organisms, they have been shown as involved with reproduction, stem cell maintenance and drug resistance, and they tend to exhibit tissue-specific expression patterns. S. mansoni expresses thousands of lncRNA genes; however, the cell type expression patterns of lncRNAs in the parasite remain uncharacterized. Here, we have re-analyzed publicly available single-cell RNA-sequencing (scRNA-seq) data obtained from adult S. mansoni to identify the lncRNAs signature of adult schistosome cell types. A total of 8023 lncRNAs (79% of all lncRNAs) were detected. Analyses of the lncRNAs expression profiles in the cells using statistically stringent criteria were performed to identify 74 lncRNA gene markers of cell clusters. Male gamete and tegument progenitor lineages clusters contained most of the cluster-specific lncRNA markers. We also identified lncRNA markers of specific neural clusters. Whole-mount in situ hybridization (WISH) and double fluorescence in situ hybridization were used to validate the cluster-specific expression of 13 out of 16 selected lncRNA genes (81%) in the male and female adult parasite tissues; for one of these 16 gene loci, probes for two different lncRNA isoforms were used, which showed differential isoform expression in testis and ovary. An atlas of the expression profiles across the cell clusters of all lncRNAs detected in our analysis is available as a public website resource (http://verjolab.usp.br:8081). The results presented here give strong support to a tissue-specific expression and to a regulated expression program of lncRNAs in S. mansoni. This will be the basis for further exploration of lncRNA genes as potential therapeutic targets.
TL;DR: In this paper , the authors explore how their research expanded beyond free-living planarians to their gruesome parasitic cousins, Schistosoma mansoni, and the rat tapeworm Hymenolepis diminuta, a model that had been largely forgotten by the molecular biology revolution.
Abstract: Platyhelminthes can perhaps rightly be described as a phylum of the good, the bad, and the ugly: remarkable free-living worms that colonize land, river, and sea, which are often rife with color and can display extraordinary regenerative ability; parasitic worms like schistosomes that cause devastating disease and suffering; and monstrous tapeworms that are the stuff of nightmares. In this chapter, we will explore how our research expanded beyond free-living planarians to their gruesome parasitic cousins. We start with Schistosoma mansoni, which is not a new model; however, approaching these parasites from a developmental perspective required a reinvention that may hold generalizable lessons to basic biologists interested in pivoting to disease models. We then turn to our (re)establishment of the rat tapeworm Hymenolepis diminuta, a once-favorite model that had been largely forgotten by the molecular biology revolution. Here we tell our stories in three, first-person narratives in order to convey personal views of our experiences. Welcome to the dark side.
TL;DR: This investigation demonstrates the successful implementation of a genomically-informed outbreak response which can be extended to university campuses and other settings at high risk for rapid emergence of new variants.
Abstract: The first cluster of SARS-CoV-2 cases with lineage B.1.1.7 in the state of Michigan was identified through intensive university-led surveillance sampling and targeted sequencing. A collaborative investigation and response was conducted by the local and state health departments, and the campus and athletic medicine COVID-19 response teams, using S-gene target failure screening and rapid genomic sequencing to inform containment strategies. A total of 50 cases of B.1.1.7-lineage SARS-CoV-2 were identified in this outbreak, which was due to three coincident introductions of B.1.1.7-lineage SARS-CoV-2, all of which were genetically distinct from lineages which later circulated in the broader community. This investigation demonstrates the successful implementation of a genomically-informed outbreak response which can be extended to university campuses and other settings at high risk for rapid emergence of new variants.
TL;DR: Drug use was prevalent among person-to-person hepatitis A outbreak-associated patients, and more likely among younger patients and patients experiencing homelessness or incarceration and increased hepatitis A vaccination coverage is critical to prevent similar outbreaks in the future.
Abstract: Background People who use drugs are at increased risk for hepatitis A virus infection. Since 1996, the Advisory Committee on Immunization Practices has recommended hepatitis A vaccination for people who use drugs. Since 2016, the U.S. has experienced widespread hepatitis A outbreaks associated with person-to-person transmission. Purpose To describe the prevalence of drug use, route of use, and drugs used among hepatitis A outbreak-associated patients. Methods State outbreak and medical records were reviewed to describe the prevalence, type, and route of drug use among a random sample of 812 adult outbreak-associated hepatitis A patients from Kentucky, Michigan, and West Virginia during 2016–2019. Differences in drug-use status were analyzed by demographic and risk-factor characteristics using the X2 test. Results Among all patients, residents of Kentucky (55.6%), Michigan (51.1%), and West Virginia (60.1%) reported any drug use, respectively. Among patients that reported any drug use, methamphetamine was the most frequently reported drug used in Kentucky (42.3%) and West Virginia (42.1%); however, opioids were the most frequently reported drug used in Michigan (46.8%). Hepatitis A patients with documented drug use were more likely (p<0.05) to be experiencing homelessness/unstable housing, have been currently or recently incarcerated, and be aged 18–39 years compared to those patients without documented drug use. Implications Drug use was prevalent among person-to-person hepatitis A outbreak-associated patients, and more likely among younger patients and patients experiencing homelessness or incarceration. Increased hepatitis A vaccination coverage is critical to prevent similar outbreaks in the future.
TL;DR: It was found that SETDB1-Cohesin co-regulate target gene expression and genome topology at these DiSCs, which unravels a unique topological and transcriptional axis of control regulated chiefly bySETDB1.
Abstract: SETDB1 is a key regulator of lineage-specific genes and endogenous retroviral elements (ERVs) through its deposition of repressive H3K9me3 mark. Apart from its H3K9me3 regulatory role, SETDB1 has seldom been studied in terms of its other potential regulatory roles. To investigate this, a genomic survey of SETDB1 binding in mouse embryonic stem cells across multiple libraries was conducted, leading to the unexpected discovery of regions bereft of common repressive histone marks (H3K9me3, H3K27me3). These regions were enriched with the CTCF motif that is often associated with the topological regulator Cohesin. Further profiling of these non-H3K9me3 regions led to the discovery of a cluster of non-repeat loci that were co-bound by SETDB1 and Cohesin. These regions, which we named DiSCs (Domains involving SETDB1 and Cohesin) were seen to be proximal to the gene promoters involved in embryonic stem cell pluripotency and lineage development. Importantly, it was found that SETDB1-Cohesin co-regulate target gene expression and genome topology at these DiSCs. Depletion of SETDB1 led to localized dysregulation of Cohesin binding thereby locally disrupting topological structures. Dysregulated gene expression trends revealed the importance of this cluster in ES cell maintenance as well as at gene ‘islands’ that drive differentiation to other lineages. The ‘unearthing’ of the DiSCs thus unravels a unique topological and transcriptional axis of control regulated chiefly by SETDB1.
TL;DR: In this paper , the authors investigate how ideas of the right relationships among science, the public, and collective decision-making about science and technology come to be envisioned in constructions of public engagement.
Abstract: : This dissertation investigates how ideas of the right relationships among science, the public, and collective decision-making about science and technology come to be envisioned in constructions of public engagement. In particular, it explores how public engagement has come to be constructed in discourse around gene editing to better understand how it holds together with visions for good, democratic governance of those technologies and with what effects. Using a conceptual idiom of the co-production of science and the social order, I investigate the mutual formation of scientific expertise, responsibility, and democracy through constructions of public engagement. I begin by tracing dominant historical narratives of contemporary public engagement as a continuation of public understanding of science’s projects of social order for democratic society. I then analyze collections of prominent expert meetings, publications, discussions, and interventions about development, governance, and societal implications human heritable germline gene editing and gene drives that developed in tandem with commitments to public engagement around those technologies. Synthesizing the evidence from across gene editing discourse, I offer a constructive critique of constructions of public engagement as expressions and evidence of scientific responsibility as ultimately reasserting and reinforcing of scientific experts' authority in gene editing decision-making, despite intentions for public engagement to extend decision-making participation and power to the public. Such constructions of public engagement go unrecognized in gene editing discourse and thereby subtly reinforce broader visions of scientific expertise as essential to good governance by underwriting the legitimacy and authority of scientific experts to act on behalf of public interests. I further argue that the reinforcement of scientific expert authority in gene editing discourse through public engagement also centers scientific experts in a sociotechnical imaginary that I call “not for science alone.” This sociotechnical imaginary envisions scientific experts as guardians and guarantors of good, democratic governance. I then propose possible alternatives to public engagement alone to improve gene editing governance by orienting discourse around notions of public accountability for potential shared benefits and collective harms of gene editing.