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Choi, E.

Publications and source records attributed to Choi, E..

At least 19 recordsLinked to original sources

Predicting conformational changes induced by biomolecular interactions

Biomolecular interactions trigger structural changes of protein complexes essential for cellular signaling, regulation, and drug action. Modern co-folding models can now generate detailed structures of multi-component complexes directly from sequence. However, recent evaluations reveal that they frequently fail to capture specific conformational states induced by a ligand or partner. Here, we show that explicitly modeling the structural transition from an unbound to a bound state, rather than generating the bound complex alone, better resolves these interaction-induced states. Our generative learning framework, K-Fold, transforms independently predicted unbound component priors into an assembled complex through an ultrafast diffusion bridge, operating entirely without multiple sequence alignments. By eliminating co-evolutionary dependencies, K-Fold accurately recovers non-coevolved interfaces in antibody-antigen and targeted-degrader complexes, as well as ligand-directed regulatory states in GPCRs and kinases. Furthermore, by coupling this diffusion bridge with diverse monomeric equilibrium ensembles, K-Fold provides a computationally tractable foundation for sampling complex multi-state landscapes without retraining. These results demonstrate that formulating molecular assembly as an explicit structural transition moves structure prediction beyond static geometries toward capturing biomolecular dynamics.

molecular biology↗

Manganese availability determines insulin sensitivity by enhancing Akt activity

Insulin signaling is a critical determinant of metabolic health, and impairments in insulin action contribute to the development of type 2 diabetes. The kinase Akt is a central mediator of insulin signaling and is required for insulin's suppression of hepatic glucose output. Although the regulation of Akt by the insulin receptor-PI3K pathway is well understood, there are instances in which signaling downstream of Akt is dissociated from proximal insulin signaling, for example in insulin resistance. Nonetheless, little is known about PI3K-independent mechanisms of Akt regulation. Here, we discovered that hepatocyte manganese concentrations are a key determinant of PI3K-independent Akt function in vivo. We further demonstrated that manganese increases Akt's catalytic efficiency, and quantitative phosphoproteomics revealed that manganese and insulin act additively to enhance Akt activity. Moreover, we uncovered that hepatic manganese concentrations fluctuate during fasting and feeding via carbohydrate-dependent transcriptional regulation of the manganese efflux transporter Slc30a10. This dynamic metal-signaling axis provides a mechanistic link between nutrient status and Akt activation, and suggests a molecular explanation for the glucose-lowering effects of manganese observed in humans. Our findings establish manganese as a physiologically regulated cofactor for Akt and position metal bioavailability as a previously unrecognized layer of insulin signaling control.

physiology↗

Heritable morphology-environment correlations among lake populations of threespine stickleback

Phenotypic differences among populations can arise through heritable genetic divergence, phenotypic plasticity, or both, making it difficult to determine whether trait-environment correlations observed in nature reflect adaptive evolution. Within threespine stickleback (Gasterosteus aculeatus) studies, numerous document morphological differences among allopatric-, parapatric-, and even sympatric populations. These phenotypic differences among populations are often correlated with diet and lake habitat (e.g., lake size), suggesting an adaptive value to the population differences. However, many studies of ecomorphological divergence in stickleback use wild-caught stickleback, which may differ due to evolution or plasticity. Although common garden experiments have confirmed that population differences can be heritable, such experiments typically entail small numbers of populations. Consequently, we still do not know to what extent well-known trait-environment correlations in stickleback are a result of evolution. To address this gap, we reared stickleback embryos from 27 lake populations on Vancouver Island, in a laboratory environment. Morphological differences among populations persist in common-garden fish, confirming a large role for divergent evolution. These heritable differences were associated with environmental variation among lakes, implying an adaptive value. However, some well-known trait-environment relationships in stickleback did not persist in common-garden fish and may be primarily plastic.

evolutionary biology↗

Immune variation and host ontogeny constrain pathogen virulence and transmission in a helminth parasite

Host immune strategies vary widely, yet how this variation shapes parasite virulence and transmission in natural systems remains unresolved. We tested whether host immune strategy governs macroparasite transmission timing and magnitude in Schistocephalus solidus, a cestode with a three-host life cycle. Over 13 months, we surveyed infection and immune activation (fibrosis) in second-intermediate host populations (threespine stickleback) from eight lakes. Host immune strategy (ranging from resistance to tolerance) strongly influenced whether and when parasites reached transmissible sizes, and shifted the synchrony between transmissible-stage peaks and definitive host availability. Across populations, transmission potential peaked at intermediate parasite burdens, consistent with virulence-transmission trade-off theory. These findings demonstrate that host immune phenotype alters epidemiological outcomes in complex life cycle parasites, by shifting both the magnitude and phenology of parasite growth to structure the effective transmission window.

ecology↗

Linking land-use change, water quality, and host-parasite dynamics with droplet digital PCR and Bayesian path analyses

Global changes in land use and nutrient cycling are transforming ecosystems at unprecedented rates, with significant consequences for infectious disease dynamics. Aquatic environments are particularly vulnerable because the interplay of habitat modification, nutrient enrichment, and biodiversity loss can drive pronounced changes in the community composition of food webs, including hosts and parasites. Yet, despite well-documented effects of habitat modification on aquatic communities and food webs, the mechanisms through which these changes influence infectious disease dynamics remain poorly resolved. This gap arises, in part, because it remains challenging to disentangle how multiple stressors interact to shape disease outcomes and quantify parasite levels and host densities from field-collected samples. Here, we illustrate two tools that might help address these challenges. First, highly sensitive droplet digital PCR can quantify infection loads even when the signal:noise ratio is low. Second, stepwise Bayesian path analyses can identify the direct and indirect pathways connecting land-use changes to infectious disease dynamics. As a case study, we examined cyclopoid copepods and their helminth parasite, Schistocephalus solidus, across 47 freshwater lakes on Vancouver Island, a region strongly shaped by commercial logging, including widespread clear-cutting of old-growth forests. Our results reveal a positive correlation between copepod density and deforestation, potentially mediated by associated changes in water quality and calanoid copepods, key competitors of the focal host. ddPCR enabled sensitive detection of extremely low parasite signals in field-collected copepods. We detected positive infections in only 19.5% of the lakes surveyed, highlighting the difficulty of assessing disease dynamics in natural populations. Nonetheless, this study highlights the challenges of linking land-use change to disease outcomes, while also demonstrating that sensitive molecular and statistical tools offer new ways to reveal these hidden connections.

ecology↗

A Multi-Scale Ecological Approach to Assessing Antimicrobial Resistance in a Freshwater Fish

Antimicrobial resistance (AMR) genes are increasingly recognized as an emerging environmental contaminant. Yet, the ecological mechanisms shaping their distribution across natural landscapes remain poorly understood. Here, we quantified AMR gene abundances in microbial communities sampled from wild fish from eight freshwater lakes on Vancouver Island and paired these gene-level measurements with fine-scale limnological and land-use data. Using droplet digital PCR, field surveys, and an iterative spatial forecasting framework that integrates Random Forest models with regression kriging, we explored how watershed-scale processes relate to variation in AMR genes across lakes. Our analyses reveal potential associations between elevated AMR gene levels, changes in water quality, deforestation, and geographic proximity to salmon aquaculture. By integrating data across biological and spatial scales, from genes within microbial communities to lake-level conditions and landscape patterns, this study illustrates the value of combining quantitative molecular measurements with geospatial modeling to identify environmental factors that may promote antimicrobial resistance in natural systems. Our approach provides a proof-of-concept and a general predictive framework for generating hypotheses and informing future monitoring efforts aimed at understanding, managing, and forecasting environmental reservoirs of resistance. SignificanceAntimicrobial resistance (AMR) genes are ancient components of environmental microbiomes. Yet, the mechanisms that generate modern hotspots of resistance across natural landscapes remain unclear. Here, we reveal how watershed-scale environmental change, including water quality metrics linked with deforestation and proximity to salmon aquaculture, predicts elevated AMR gene levels in the microbiomes of wild fish populations. By combining quantitative droplet digital PCR with ecological data and geospatial modeling, we move beyond isolated surveillance data to identify ecological mechanisms that promote antimicrobial resistance in freshwater ecosystems. This integrative approach provides mechanistic insight into why certain habitats, and the organisms within them, become reservoirs of resistance while others do not. Our findings highlight the importance of ecological context in understanding resistance evolution and offer a predictive tool for informing proactive monitoring and management strategies.

ecology↗

Reprogramming insulin receptor activation with a de novo agonist to overcome severe insulin resistance

Computational protein engineering provides a powerful approach to address longstanding clinical challenges. Severe insulin resistance syndromes caused by mutations in the insulin receptor (IR) are life-threatening disorders for which effective long-term therapies remain lacking. Here, we define the in vivo activity and therapeutic potential of RF-409, a de novo-designed IR agonist that activates the receptor through a mechanism distinct from insulin. RF-409 exhibits markedly prolonged circulation compared to insulin and produces sustained improvements in glucose homeostasis without detectable adverse effects on body composition or liver function. In a patient-derived IR D707A mouse model of severe insulin resistance, RF-409--but not insulin--activates the mutant receptor, restoring glucose regulation and ameliorating hyperglycemia, hyperinsulinemia, lipoatrophy, and pancreatic atrophy. Mechanistically, RF-409 engages the IR through a noncanonical binding geometry while stabilizing an active conformation resembling that induced by insulin. Phosphoproteomic profiling shows that RF-409 elicits broadly insulin-like signaling with distinct temporal features in receptor-proximal regulation. Together, these findings establish a framework for reactivating dysfunctional receptors and suggest broader applications beyond rare receptoropathies, including diabetes and liver disease.

pharmacology and toxicology↗

Constitutive and inducible fibrosis explain immune variation among threespine stickleback populations

Understanding how immune variation arises in natural populations requires disentangling the relative contributions of host genetic differences, environmental variation, and parasite effects, which is rarely possible in wild systems. Threespine stickleback populations vary in their use of intraperitoneal fibrosis as a defense against the helminth parasite Schistocephalus solidus, providing a natural system to study the genetic and ecological drivers of immune variation. We combined a 46-lake field survey with common garden experiments on 20 representative populations exposed to multiple parasite genotypes to test whether population differences in fibrosis persist under controlled conditions and whether they depend on parasite genotype or lake ecology. Fibrosis variation was strongly heritable, with both constitutive and inducible components persisting under common garden conditions. In contrast, parasite genotype had only a weak effect on fibrosis responses. Moreover, inducible fibrosis covaried with lake environmental conditions, with populations from more eutrophic-like lakes exhibiting stronger responses than those from more oligotrophic-like lakes. Together, these results reveal ecologically structured divergence in heritable immune responses among natural populations.

evolutionary biology↗

Efficient and scalable modelling of cotranscriptional RNA folding with deterministic and iterative RNA structure sampling

AO_SCPLOWBSTRACTC_SCPLOWRNA structure sampling is central to modelling RNA ensembles, yet stochastic sampling methods are non-exhaustive, scale poorly, and are biased towards low-free-energy structures, while current suboptimal folding approaches generate an unpredictable exponential number of structures. These limitations are particularly problematic for modelling cotranscriptional folding, where vectorial synthesis continuously reshapes the energy landscape during transcription, stabilising transient out-of-equilibrium structures. Here we introduce iterative sampling, a deterministic framework that enumerates unique RNA secondary structures in strict order of increasing free energy, enabling progressive and exhaustive exploration of the structure space up to an arbitrary stopping criterion. To implement this approach, we developed two scalable algorithms, iterative deepening and a persistent data structure approach, that incrementally traverse the expansion tree by evolving partial structures in place, avoiding redundant recomputation and fixed energy windows. Implemented in memerna, this approach achieves orders-of-magnitude speedups over existing tools (10x over ViennaRNA; 100x over RNAstructure). Integration within the sample-and-select framework (R2D2) improves structural diversity and identifies conformations with greater agreement with experimental data. Comprehensive sampling further enables direct comparison of equilibrium and cotranscriptionally restrained ensembles. Analysis of the resulting structural probability distributions uncovers kinetic traps and putative transcriptional pause sites, supporting an intuitive cotranscriptional folding mechanism in which local 3'-hairpin formation transiently stabilises upstream structure to delay large-scale rearrangement. Together, these results establish iterative sampling as a scalable and general framework for resolving out-of-equilibrium RNA cotranscriptional folding. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/720041v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@dee200org.highwire.dtl.DTLVardef@c7af12org.highwire.dtl.DTLVardef@1b6f54dorg.highwire.dtl.DTLVardef@a2c97a_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗

The brain architecture of punishment learning

Learning which actions cause harm is essential for survival, yet how the brain transforms this knowledge into adaptive control of behavior remains unclear. We combined whole-brain analysis, multisite chemogenetic silencing, spatial transcriptomics, and longitudinal calcium imaging to map how punishment learning reorganizes brain networks across scales. Learning reshaped mesoscale community organization into a network anchored by the amygdala, subthalamic-hypothalamic zone, and ventral midbrain tegmentum. These regions contributed distinct components of adaptive avoidance and engaged diverse transcriptional programs across multiple neuronal subclasses. Within this network, the amygdala acted as a hub, partitioning action and outcome information and remapping neural geometry to segregate punished from safe actions. Together, these results identify a multiscale neural architecture through which aversive experience can be transformed into flexible behavioral control.

neuroscience↗

Comparative analysis of whole genome amplification kits for single cell genome analysis

Whole genome amplification (WGA) enables detailed analysis of genomic heterogeneity at the cellular level. Here, we systematically compare two commercially available WGA technologies on single cells; Multiple Displacement Amplification in the Qiagen REPLI-g kit (MDA/REPLI-g) and Primary Template-directed Amplification in the BioSkryb ResolveDNA kit (PTA/ResolveDNA). Beyond quality control and genomic profiling, we assessed a cost-effective array-based approach as a complement to low-pass sequencing. Consistent with available benchmarks, PTA/ResolveDNA sequencing libraries consistently outperformed MDA/REPLI-g across quality metrics, including genome coverage breadth and uniformity. CNV calls from PTA-cells showed higher accuracy and sensitivity, including reliable detection of small CNVs at low sequencing depth. SNP array-based analysis corroborated sequencing-based findings, and additionally provided allelic information. Notably, CNV detection from SNP arrays matched the performance of low-pass sequencing, supporting its utility as an cost-effective approach for WGA quality control and single-cell CNV profiling.

genomics↗

APOE4 homozygotes have less sleep fragmentation in late adulthood

Background and ObjectivesAPOE4, a genetic risk factor for Alzheimers Disease (AD), is associated with reduced functional connectivity of brain regions that regulate sleep, which may predispose persons to AD via altering sleep architecture. However, little is known about differences in sleep architecture by APOE genotype. MethodsThis cross-sectional study examined the association between APOE genotype and sleep architecture among middle-aged and older adults, using polysomnography (Sleep Heart Health Study, N=3,132). APOE genotype included: APOE4 heterozygotes, APOE4 homozygotes, APOE2 carriers, and APOE3 homozygotes. Macro sleep architecture was quantified using the percentage of time spent in rapid eye movement sleep (%REM), N1 (N1%), N2 (%N2), N3 (%N3), and arousal index. Micro sleep architecture was quantified as odds ratio product (ORP; a continuous measure of sleep depth) for overall sleep and each sleep stage, and spindle characteristics (power, density, and frequency). Linear regression was used, adjusting for covariates. ResultsThe mean age was 67, 53 percent were female, 24% were APOE4 heterozygotes, 2% were APOE4 homozygotes, 14% were APOE2 carriers, and 60% were APOE3 homozygotes. Macro sleep architecture did not vary across genotypes. Compared with APOE3 homozygotes, APOE4 homozygotes exhibited fewer arousals with age ({beta}=-0.33 per hour/year, p=0.04), resulting in significantly fewer arousals at age 70+. ORP decreased in a dose-response pattern with the number of APOE4 alleles during overall sleep and across all sleep stages (ORPAPOE3/3=0.94, ORPAPOE3/4=0.91, ORPAPOE4/4=0.87), and these group difference widened with each year of age. Finally, there was a trend for lower spindle density and power in APOE4 homozygotes relative to APOE3 homozygotes (ps=0.06). ConclusionsArousal threshold increased in a dose-response manner with each APOE4 allele, as evidenced by the findings on ORP. The differences in ORP between APOE3 homozygotes and APOE4 carriers widened further with age, paralleling age-related declines in arousal index among APOE4 homozygotes. Despite these indications of elevated arousal thresholds that might suggest less sleep fragmentation in APOE4 carriers, APOE4 homozygotes exhibited poorer sleep micro architecture, including trends toward reduced sleep spindle activity. Taken together, reduced arousability in APOE4 carriers may reflect abnormalities in cortical activation that blunt arousal rather than an indicator of healthier sleep.

physiology↗

Needle in a haystack: A droplet digital polymerase chain reaction assay to detect rare helminth parasites infecting natural host populations

Helminths infect humans, livestock, and wildlife, yet remain understudied despite their significant impact on public health and agriculture. Because many of the most prevalent helminth-borne diseases are zoonotic, the health of diverse host species are closely interconnected. Therefore, understanding helminth transmission among wildlife could improve predictions and management of infection risks across species. A key challenge to understanding helminth transmission dynamics in wildlife is accurately and quantitatively tracking infection levels across hosts and environments. Traditional methods, such as visual parasite identification from environmental samples or infected hosts, are time-consuming, while standard molecular techniques (e.g., PCR and qPCR) often lack the sensitivity to reliably detect lower parasit burdens. These limitations often underestimate the prevalence and severity of infection, hindering efforts to manage infectious diseases. Here, we developed a multiplexed droplet digital PCR (ddPCR) assay to quantify helminth levels in aquatic habitats using 18S rRNA target genes. Using Schistocephalus solidus and their copepod hosts as a case study, we demonstrate ddPCRs sensitivity and precision. By establishing a 1:1 infection standard in the lab, we contextualize ddPCR gene concentration data to quantify both host and parasite numbers in field samples. The assay is highly reproducible, reliably detecting target genes at concentrations as low as 1 picogram of DNA in lab standards and field samples (multi-species and eDNA). Thus, we provide a toolkit for quantifying infection loads in intermediate hosts and monitoring infection dynamics across spatio-temporal scales in multiple helminth systems of concern for public health, agriculture, and conservation biology. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=139 SRC="FIGDIR/small/634533v1_ufig1.gif" ALT="Figure 1"> View larger version (66K): org.highwire.dtl.DTLVardef@1bc2e40org.highwire.dtl.DTLVardef@180822eorg.highwire.dtl.DTLVardef@1e2c2c8org.highwire.dtl.DTLVardef@621909_HPS_FORMAT_FIGEXP M_FIG Applications of ddPCR probe-primer design to parallel systems. Cyclopoid copepods serve as initial hosts for diverse helminthic diseases distributed globally. The primers designed in this assay are suitable for other systems, with minimal work required for probe design specific to each helminth species. C_FIG

molecular biology↗

Epigenetic trajectory predicts development of clinical rheumatoid arthritis in ACPA+ individuals: Targeting Immune Responses for Prevention of Rheumatoid Arthritis (TIP-RA)

The presence of anti-citrullinated protein antibodies (ACPAs) in the absence of clinically-apparent inflammatory arthritis (IA) identifies individuals "at-risk" for developing future clinical rheumatoid arthritis (RA). However, it is unclear why some ACPA+ individuals convert to clinical RA while others do not. We explored the possibility that epigenetic remodeling is part of the trajectory from an at-risk state to clinical disease. Cross-sectional differential methylation analysis at baseline revealed DMLs that distinguish the Pre-RA methylome from ACPA+ Non-converters. Genes overlapping these DMLs correspond to aberrant NOTCH signaling and DNA repair pathways in B cells. Longitudinal analysis showed that ACPA-Control and ACPA+ Non-converter methylomes are relatively constant. In contrast, the Pre-RA methylome remodeled along a dynamic "RA methylome trajectory" characterized by epigenetic changes in active regulatory elements. Machine learning revealed individual loci predictive of RA conversion. DNA methylation is a dynamic process in ACPA+ individuals at-risk for developing RA that later transition to clinical disease. In contrast, non-converters and controls have stable methylomes. The accumulation of epigenetic marks over time prior to conversion to clinical RA conforms to pathways that are associated with immunity and can be used to identify potential pathogenic pathways for therapeutic targeting and/or use as prognostic biomarkers.

immunology↗

Tuning Insulin Receptor Signaling Using De Novo Designed Agonists

Binding of insulin to the insulin receptor (IR) induces conformational changes in the extracellular portion of the receptor that lead to activation of the intracellular kinase domain and the AKT and MAPK pathways, and downstream modulation of glucose metabolism and cell proliferation. We reasoned that designed agonists that induce different conformational changes in the receptor might induce different downstream responses, which could be useful both therapeutically and to shed light on how extracellular conformation is coupled to intracellular signaling. We used de novo protein design to first generate binders to individual IR extracellular domains, and then to fuse these together in different orientations and with different conformational flexibility. We describe a series of synthetic agonists that signal through the IR that differ from insulin and from each other in the induction of receptor autophosphorylation, MAPK activation, intracellular trafficking, and cell proliferation. We identify designs that are more potent than insulin causing much longer lasting reductions in glucose levels, and that retain signaling activity on disease-causing receptor mutants that do not respond to insulin. These results inform our understanding of how changes in receptor conformation and dynamics are transmitted to downstream signaling, and our synthetic agonists have considerable therapeutic potential for diabetes and severe insulin resistance syndromes. HighlightsO_LIComputational design yielded super agonists, partial agonists, and antagonists of IR. C_LIO_LIDe novo agonists induce a distinct IR active conformation. C_LIO_LIDesigned agonists tune IR signaling by modulating conformational dynamics of activated IR. C_LIO_LIDesigned agonists are more potent than insulin, reducing glucose levels longer and activating disease-causing IR mutants. C_LI

bioengineering↗

Elongation factor P controls ribosomal frameshift of a Salmonella antimicrobial resistance gene

Ribosomes translate mRNAs by matching every 3-nucleotide sequence in mRNA, producing the corresponding proteins. As the amino acid sequence directly dictates the activity of the protein, frameshifts often lead to unexpected effects. Here, ribosome profiling reveals that the intracellular pathogen Salmonella Typhimurium suppresses frameshift in the ugtL antimicrobial resistance gene during translation. This suppression of frameshift is mediated by a ribosome pause occurring in a newly-identified overlapping gene, serving as a non-slip bump. Given that the pause site contains a poly-proline motif and can be resolved by elongation factor P, the removal of the ribosome pause by substituting the motif induces ribosome slippage in ugtL, resulting in UgtL frameshifted protein production. This renders Salmonella sensitive to antimicrobial peptides but, in turn, protects the MgtC virulence factor from the FtsH-mediated proteolysis, indicating that elongation factor P-dependent ribosome pause is required for controlling both full antimicrobial resistance and mouse virulence. These findings reveal a new regulatory mechanism in which ribosome pause controls the production of two different protein isoforms by suppressing ribosome slippage-mediated frameshift.

microbiology↗

SLC4A11 mediates ammonia import and promotes cancer stemness in hepatocellular carcinoma

End stage liver disease is marked by portal hypertension, systemic elevations in ammonia, and development of hepatocellular carcinoma (HCC). While these clinical consequences of cirrhosis are well described, it remains poorly understood whether hepatic insufficiency and the accompanying elevations in ammonia contribute to HCC carcinogenesis. Using preclinical models, we discovered that ammonia entered the cell through the transporter SLC4A11 and served as a nitrogen source for amino acid and nucleotide biosynthesis. Elevated ammonia promoted cancer stem cell properties in vitro and tumor initiation in vivo. Enhancing ammonia clearance reduced HCC stemness and tumor growth. In patients, elevations in serum ammonia were associated with an increased incidence of HCC. Taken together, this study forms the foundation for clinical investigations using ammonia lowering agents as potential therapies to mitigate HCC incidence and aggressiveness.

cancer biology↗

A HigB-like toxin promotes non-replicating Salmonella inside macrophages by inhibiting ribonuclease III

Many bacteria are often resistant to antibiotic treatment because they can slow down their growth rate, thereby attenuating the drugs effectiveness. A similar growth-rate control is observed in pathogens that infect and persist inside their hosts. The bacterial toxin-antitoxin (TA) system serves as a non-heritable phenotypic switch by slowing down growth through the expression of a toxin component. Here, we investigated a HigB-like type II toxin from the intracellular bacterial pathogen Salmonella Typhimurium. Unlike other HigB-like toxins that cleave ribosome-bound mRNAs, it does not exhibit endoribonuclease activity. Instead, it inhibits ribonuclease III, which mediates the initial cleavage for rRNA processing, by directly binding to the dsRNA-binding domain of RNase III, thereby decreasing ribosome assembly and bacterial growth. Given that the formation of HigB-like toxin-mediated non-replicating Salmonella within macrophages is RNase III-dependent, persister formation by inhibiting RNase III is a newly identified strategy for pathogens to survive within host cells.

microbiology↗