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bioRxiv2024

Phosphorylation-dependent tuning of mRNA deadenylation rates

mRNA decay is a major determinant of gene regulation that is controlled through shortening of mRNA poly(A) tails by the Ccr4-Not complex. The specificity of deadenylation can be mediated through RNA adaptors - RNA-binding proteins that tether substrate mRNAs to Ccr4-Not in a regulated and context-specific manner. Interaction with Ccr4-Not is mediated by intrinsically disordered regions (IDRs) within the RNA adaptors. Due to the difficulty in studying large IDR-containing complexes, the determinants of specificity and their regulation remain unclear. Here we use structural biology and biochemical reconstitution to show that dispersed segments within IDRs of RNA adaptors bind to several distinct binding sites on Ccr4-Not through multivalent interactions. We further demonstrate that binding can be modulated by phosphorylation, altering the consequent deadenylation rate in a continuously tunable manner. This mechanism is broadly applicable in evolutionarily divergent IDRs from multiple RNA adaptors including fission yeast Puf3, and human Pumilio/PUM1 and Tristetraprolin/TTP. Together, our work suggests that multivalent interactions and phosphorylation represent conserved strategies for regulating gene expression. Thus, in response to cellular cues, mRNA decay can be regulated by a graded mechanism, rather than a bistable on/off switch, rationalizing how post-transcriptional gene expression is fine-tuned.

molecular biology↗

bioRxiv2019

Pyruvate Kinase M Links Glucose Availability to Protein Synthesis

How human cells coordinate various metabolic processes, such as glycolysis and protein translation, remains unclear. One key insight is that various metabolic enzymes have been found to associate with mRNAs, however whether these enzymes regulate mRNA biology in response to changes in cellular metabolic state remains unknown. Here we report that the glycolytic enzyme, pyruvate kinase M (PKM), inhibits the translation of 7% of the transcriptome in response to elevated levels of glucose and pyruvate. Our data suggest that in the presence of glucose and pyruvate, PKM associates with ribosomes that are synthesizing stretches of polyacidic nascent polypeptides and stalls the elongation step of translation. PKM-regulated mRNAs encode proteins required for the cell cycle and may explain previous results linking PKM to cell cycle regulation. Our study uncovers an unappreciated link between glycolysis and the ribosome that likely coordinates the intake of glycolytic metabolites with the regulation of protein synthesis and the cell cycle.

molecular biology↗

bioRxiv2026

Highly resolved tumor architecture via matched spatial and nucleus transcriptomics from a single tissue section

Spatial transcriptomics often relies on reference-based deconvolution to infer cell types in a tissue context; however, public single-cell datasets can miss patient-specific biology. Here we introduce SIMPlex, a method that generates matched spatial and single-nucleus gene-expression profiles from the same 5 um FFPE section. We demonstrate context-matched profiles across mouse brain, breast cancer and prostate cancer tissues, resolving fine-grained cell-states with distinct spatial signatures. By extracting both spatial and nuclear layers, SIMPlex maximises the information recovered from a single tissue section, an advantage for scarce archival and clinical specimens.

molecular biology↗

bioRxiv2020

The cellular modifier MOAG-4/SERF drives amyloid formation through charge complementation

While aggregation-prone proteins are known to accelerate ageing and cause age-related diseases, the cellular mechanisms that drive their cytotoxicity remain unresolved. The orthologous proteins MOAG-4, SERF1A and SERF2 have recently been identified as cellular modifiers of such cytotoxicity. Using a peptide array screening approach on human amyloidogenic proteins, we found that SERF2 interacted with specific patterns of negatively charged and hydrophobic, aromatic amino acids. The absence of such patterns, or the neutralization of the positive charge in SERF2, prevented these interactions and abolished the amyloid-promoting activity of SERF2. In a protein aggregation model in the nematode C. elegans, protein aggregation was suppressed by mutating the endogenous locus of MOAG-4 to neutralize charge. Our data indicate that charge interactions are required for MOAG-4 and SERF2 to promote aggregation. Such charged interactions might accelerate the primary nucleation of amyloid by initiating structural changes and by decreasing colloidal stability. Our finding that negatively charged segments are overrepresented in amyloid-forming proteins suggests that inhibition of charge interactions deserves exploration as a strategy to target age-related protein toxicity. Significance StatementHow aging causes relatively common diseases such as Alzheimers and Parkinsons is still a mystery. Since toxic structural changes in proteins are likely to be responsible, we investigated biological mechanisms that could drive such changes. We made use of a modifying factor called SERF2, which accelerates structural changes and aggregation of several disease-related proteins. Through a peptide-binding screen, we found that SERF2 acts on negatively charged protein regions. The abundance of such regions in the disease-related proteins explains why SERF has its effect. Removing positive charge in SERF was sufficient to suppress protein aggregation in models for disease. We propose that blocking charge-interactions with SERF or other modifiers could serve as a general approach to treat age-related protein toxicity.

molecular biology↗

bioRxiv2021

Xrn1 is a deNADding Enzyme Modulating Mitochondrial NAD Levels

The existence of non-canonical nicotinamide adenine diphosphate (NAD) 5-end capped RNAs is now well established. Nevertheless, the biological function of this nucleotide metabolite cap remains elusive. Here, we show that the yeast Saccharomyces cerevisiae cytoplasmic 5-end exoribonuclease Xrn1 is also a NAD cap decapping (deNADding) enzyme that releases intact NAD and subsequently degrades the RNA. The significance of Xrn1 deNADding is evident in a deNADding deficient Xrn1 mutant that still retains its 5-monophosphate exonuclease activity. This mutant reveals Xrn1 deNADding is necessary for normal growth on non-fermenting sugar and is involved in modulating mitochondrial NAD-capped RNA levels and in turn intramitochondrial NAD levels. Our findings uncover a functional role for mitochondrial NAD-capped RNAs as a reservoir to maintain overall NAD homeostasis. We propose NAD-capped RNAs function as a cistern for mitochondrial NAD with Xrn1 serving as a rheostat for NAD-capped RNAs.

molecular biology↗

bioRxiv2025

Inhibition of lysine deacetylase activity impacts formation of the vitamin D receptor activation complex.

The vitamin D endocrine system is responsible for the regulation of many biological processes including bone metabolism, calcium homeostasis, cell proliferation and cell differentiation. Alterations to the vitamin D signaling pathway are associated with several diseases including bone diseases, diabetes, cardiovascular diseases, autoimmune diseases, and cancer. Vitamin D precursors are obtained through diet or synthesized in the skin and must be further chemically modified to become the biologically active hormone, calcitriol. Calcitriol binds to the vitamin D receptor (VDR), a member of the nuclear hormone receptor (NHR) superfamily. VDR forms a heterodimer with retinoid X receptor (RXR) and together they bind to promoters containing vitamin D response elements (VDREs) to activate transcription of target genes. Other NHRs have been shown to accept post-translational modifications that can either increase or decrease their transcriptional output through alterations in protein-protein or protein-DNA interactions. We have generated evidence that two lysines on VDR may be targets of post-translational modifications, and alterations to lysine deacetylase activity will impact VDR transcriptional output through changes in co-activator and co-repressor binding. Together, these data suggest a novel way for the cell to modulate the response of VDR to available vitamin D.

molecular biology↗

bioRxiv2019

Natural diversity in the predatory behavior facilitates the establishment of a new robust model strain for nematode-trapping fungi

Nematode-trapping fungi (NTF) are a group of specialized microbial predators that consume nematodes when food sources are limited. Predation is initiated when conserved nematode ascaroside pheromones are sensed, followed by the development of complex trapping devices. To gain insights into the co-evolution of this inter-kingdom predator-prey relationship, we investigated natural populations of nematodes and NTF, that we found to be ubiquitous in soils. Arthrobotrys species were sympatric with various nematode species and behaved as generalist predators. The ability to sense prey amongst wild isolates of A. oligospora varied greatly, as determined by the number of traps after exposure to Caenorhabditis elegans. While some strains were highly sensitive to C. elegans and the nematode pheromone ascarosides, others responded only weakly. Furthermore, strains that were highly sensitive to the nematode prey also developed traps faster. The polymorphic nature of trap formation correlated with competency in prey killing, as well as with the phylogeny of A. oligospora natural strains, calculated after assembly and annotation of the genomes of twenty isolates. A chromosome level genome assembly and annotation was established for one of the most sensitive wild isolate, and deletion of the only G protein {beta} subunit-encoding gene of A. oligospora nearly abolished trap formation, implicating G protein signaling in predation. In summary, our study establishes a highly responsive A. oligospora wild isolate as a novel model strain for the study of fungal-nematode interactions and demonstrates that trap formation is a fitness character in generalist predators of the NTF family. Significance statementNematode-trapping fungi (NTF) are carnivorous microbes that hold potential to be used as biological control agents due to their ability to consume nematodes. In this work we show that NTF are ubiquitous generalist predators found in sympatry with their prey in soil samples. Wild isolates of NTF displayed a naturally diverse ability to execute their predatory lifestyle. We generated a large whole genome sequencing dataset for many of the fungal isolates that will serve as the basis of future projects isolates. In particular, we establish TWF154, a highly responsive strain of Arthrobotrys oligospora, as a model strain to study the genetics of NTF. Lastly, we provide evidence that G-protein signaling is necessary for trap induction in NTF.

molecular biology↗

bioRxiv2024

Overloading And unpacKing (OAK) - droplet-based combinatorial indexing for ultra-high throughput single-cell multiomic profiling

Multiomic profiling of single cells by sequencing is a powerful technique for investigating cellular diversity in complex biological systems. Although the existing droplet-based microfluidic methods have advanced single-cell sequencing, they produce a plethora of cell-free droplets and underutilize barcoding capacities due to their low cell concentration prerequisites. Meanwhile, combinatorial indexing on microplates can index cells in a more effective way; however, it requires time-consuming and laborious protocols involving multiple splitting and pooling steps. Addressing these constraints, we have developed "Overloading And unpacKing" (OAK). With reduced labor intensity, OAK can provide cost-effective multiomic profiling for hundreds of thousands of cells, offering detection sensitivity on par with commercial droplet-based methods. To demonstrate OAKs versatility, we conducted single-cell RNA sequencing (scRNA-Seq) as well as joint single-nucleus RNA sequencing (snRNA-Seq) and single-nucleus Assay for Transposase Accessible Chromatin with sequencing (snATAC-Seq) using cell lines. We further showcased OAKs performance on more complex samples, including in vitro differentiated bronchial epithelial cells and primary retinal tissues. Finally, we examined transcriptomic responses of 408,000 melanoma cells across around 1,000 starting lineages over a 90-day treatment with a RAF inhibitor, belvarafenib. We discovered a rare cell population (0.12%) that underwent a sequence of transcriptomic changes, resulting in belvarafenib resistance. Ultra-high throughput, broad compatibility with diverse molecular modalities, high detection sensitivity, and simplified experimental procedures distinguish OAK from previous methods, and render OAK a powerful tool for large-scale analysis of molecular signatures, even for rare cells.

molecular biology↗

bioRxiv2021

Genetic tools for the stable overexpression of circular RNAs

Circular RNAs (circRNAs) are a class of non-coding RNAs that feature a covalently closed ring structure formed through backsplicing. circRNAs are broadly expressed and contribute to biological processes through a variety of functions. Standard gain-of-function and loss-of-function approaches to study gene functions have significant limitations when studying circRNAs. Overexpression studies in particular suffer from the lack of efficient genetic tools. While mammalian expression plasmids enable transient overexpression of circRNAs in cultured cells, most cell biological studies require long-term ectopic expression. Here we report the development and characterization of genetic tools enabling stable circRNA overexpression in vitro and in vivo. We demonstrated that circRNA expression constructs can be delivered to cultured cells via transposons, whereas lentiviral vectors have limited utility for the delivery of circRNA constructs. We further showed that circRNA transposons can be supplied to mouse livers via hydrodynamic tail vein injection, resulting in ectopic circRNA expression in a hepatocellular carcinoma mouse model. Furthermore, we generated genetically engineered mice harboring circRNA expression constructs. We demonstrate that this approach enables constitutive, global circRNA overexpression as well as inducible circRNA expression directed specifically to melanocytes in a melanoma mouse model. Overall, these tools expand the genetic toolkit available for the functional characterization of circRNAs of interest.

molecular biology↗

bioRxiv2025

Proteomic analysis of bronchoalveolar lavage fluid after lung transplantation associates stable allograft function with less lung damage at 12 months

IntroductionFreedom from chronic lung allograft dysfunction (CLAD) is a key objective after lung transplantation, yet predicting its onset remains challenging. This study investigated whether early proteomic changes in bronchoalveolar lavage fluid (BALF) can differentiate between patients maintaining stable graft function at 36 months and those developing CLAD within the first year. Additionally, findings were compared to proteomic data from non-transplanted individuals. MethodsBALF samples were collected at one and twelve months post-transplant from 43 lung transplant recipients together with clinical parameters. Proteomic analysis was performed using mass spectrometry with label-free quantification for global protein profiling and heavy-labelled peptides for absolute quantification of mucins and related proteins. Differentially expressed proteins were identified and analyzed through pathway enrichment to explore biological mechanisms associated with CLAD. ResultsNo significant proteomic differences were detected at one month. By twelve months, 63 proteins were differentially expressed between patients who developed early CLAD and those with stable function. Mucin levels declined in stable patients but remained elevated in both groups compared to healthy controls. Cartilage acidic protein 1 was significantly higher in stable patients at twelve months and correlated with better pulmonary function. Pathway analysis linked several altered proteins in CLAD patients to networks associated with lung injury and remodelling. ConclusionProtein profiles in BALF that resemble those of healthy lungs are associated with sustained graft function, while persistent expression of lung injury markers is associated with early CLAD. This suggests an adaptive process is needed for long-term post-transplant success.

molecular biology↗

bioRxiv2023

Deep quantitative glycoproteomics reveals gut microbiome induced remodeling of the brain glycoproteome

HighlightsO_LIHigh throughput glycoproteomics method with multiplexed quantification C_LIO_LI25-fold improvement of the mouse brain glycoproteome coverage C_LIO_LIStructural features dictate level of glycosite micro-heterogeneity C_LIO_LIGut microbiome composition extensively impacts the brain glycoproteome C_LIO_LIModulation of glycosylation is site-specific C_LI Protein glycosylation is a highly diverse post-translational modification, modulating key cellular processes such as cell signaling, adhesion and cell-cell interactions. Its deregulation has been associated with various pathologies, including cancer and neurological diseases. Methods capable of quantifying glycosylation dynamics are essential to start unraveling the biological functions of protein glycosylation. Here we present Deep Quantitative Glycoprofiling (DQGlyco), a method that combines high-throughput sample preparation, high-sensitivity detection, and precise multiplexed quantification of protein glycosylation. We used DQGlyco to profile the mouse brain glycoproteome, in which we identify 158,972 and 15,056 unique N- and O-glycopeptides localized on 3,199 and 2,365 glycoproteins, respectively - this amounts to 25-fold more glycopeptides identified compared to previous studies. We observed extensive heterogeneity of glycoforms and determined their functional and structural preferences. The presence of a defined gut microbiota resulted in extensive remodeling of the brain glycoproteome when compared to that of germ-free animals, exemplifying how the gut microbiome may affect brain protein functions.

molecular biology↗

bioRxiv2024

Plasma proteomics in the UK Biobank reveals youthful brains and immune systems promote healthspan and longevity

Organ-derived plasma protein signatures derived from aptamer protein arrays track organ-specific aging, disease, and mortality in humans, but the robustness and clinical utility of these models and their biological underpinnings remain unknown. Here, we estimate biological age of 11 organs from 44,526 individuals in the UK Biobank using an antibody-based proteomics platform to model disease and mortality risk. Organ age estimates are associated with future onset of heart failure (heart age HR=1.83), chronic obstructive pulmonary disease (lung age HR=1.39), type II diabetes (kidney age HR=1.58), and Alzheimers disease (brain age HR=1.81) and sensitive to lifestyle factors such as smoking and exercise, hormone replacement therapy, or supplements. Remarkably, the accrual of aged organs progressively increases mortality risk while a youthful brain and immune system are uniquely associated with disease-free longevity. These findings support the use of plasma proteins for monitoring organ health and the efficacy of drugs targeting organ aging disease.

molecular biology↗

bioRxiv2025

Tetramerisation governs SALL transcription factor function in development and disease

Spalt-like (SALL) proteins are C2H2 zinc-finger transcription factors important for embryogenesis, with mutations in SALL1 and SALL4 causing rare congenital disorders Townes-Brocks and Okihiro syndromes, respectively. While SALL proteins are known to associate with one another, the biological significance of the resulting complexes is unknown. Here we define a conserved glutamine-rich region that mediates SALL1/4 homo- and heterotetramerisation and find that complex formation is indispensable for DNA binding. Modelling a patient mutation that abolishes SALL4 multimerisation led to gene misregulation and, in mice, embryonic lethality, therefore phenocopying a complete Sall4 knockout. Furthermore, a common disease-causing SALL1 truncation, which retains multimerisation but lacks DNA-binding domains, sequesters SALL4 into heterotetramers that are defective in DNA binding, thereby providing a mechanistic explanation for the dominant-negative effects of many Townes-Brocks mutations. Together, our findings establish tetramerisation as a prerequisite for SALL function, linking complex formation to developmental gene regulation and human disease.

molecular biology↗

bioRxiv2022

Zika virus NS4A hijacks host ANKLE2 to promote viral replication

Zika virus (ZIKV) is infamous among flaviviruses for its unique association with congenital birth defects, notably microcephaly. We previously mapped ZIKV-host protein interactions and identified the interaction between ZIKV NS4A and host ANKLE2, which itself has established ties to congenital microcephaly. In fruit flies, NS4A induces microcephaly phenotypes in an ANKLE2-dependent manner. This suggests that NS4A interacts with ANKLE2 to dysregulate cell behavior and contributes to abnormal host neurodevelopment. Here, we explore the role of ANKLE2 in ZIKV replication to understand the biological significance of the interaction from the viral perspective. We show that knockdown of ANKLE2 reduces replication of two ZIKV strains, across multiple MOIs and timepoints. We observe that localization of ANKLE2 is drastically shifted to sites of NS4A accumulation during infection. We investigate which domains of ANKLE2 mediate this behavior and the interaction with NS4A. Using co-immunoprecipitation, we show that deletion of either the transmembrane or LEM domain has little impact on the interaction, but deletion of both significantly reduces interaction with NS4A. We show that the C-terminal transmembrane domains of NS4A stabilize the interaction with ANKLE2. Finally, we explore this interaction in other flaviviruses and observe ANKLE2 interacts with NS4A across four additional mosquito-borne flaviviruses. Together, these results suggest NS4A interacts with ANKLE2 through a combination of its transmembrane and LEM domains, bringing it to sites of ZIKV replication to promote replication through an unknown mechanism. Taken together with our previous results, our findings indicate that, in the process of hijacking ANKLE2 for replication, ZIKV disrupts its physiological function to cause disease. ImportanceThe ZIKV epidemic led to the astonishing revelation that congenital ZIKV infection is associated with devastating birth defects, including microcephaly. Microcephaly is the condition in which head and brain size are severely reduced, and is often accompanied by intellectual disability. The molecular mechanisms by which ZIKV replicates and causes microcephaly are still incompletely understood. We previously identified the protein interaction between ZIKV NS4A and host ANKLE2, which is associated with congenital microcephaly. In flies, NS4A induces microcephaly in an ANKLE2-dependent manner, suggesting this interaction is crucial for ZIKV pathogenesis. Here, we explore the relevance of this physical interaction for virus replication. We find that ANKLE2 promotes ZIKV replication, concentrates at sites of NS4A accumulation during infection, and interacts with NS4A via its N-terminal domain. Thus, this represents a rare example of a ZIKV-host protein interaction that impacts both disease and virus replication.

molecular biology↗

bioRxiv2013

Water and the biology of prions and plaques

This is an attempt to account for the insolubility and/or aggregation of prions and plaques in terms of a model of water consisting of an equilibrium between high density and low density microdomains. Hydrophobic molecules, including proteins, accumulate selectively into stable populations, enriched in high density water, at charged sites on biopolymers. In enriched high density water, proteins are probably partially unfolded and may precipitate out when released. All extracellular matrices contain such charged polymers. Prions, which have been shown to accumulate in soils and clays containing silicates and aluminates also probably accumulate in extracellular matrices.\n\nRelease of proteins follows hydrolysis of the charged groups by highly reactive high density water. This is normally a slow process but is greatly accelerated by urea. Plaques may form with age and disease because of accumulation of urea and, perhaps, glucose in the blood. This favours precipitation of proteins emerging from matrices, rather than refolding and solution. Dialysis should, therefore, interfere with plaque formation and impede the development of some age-related diseases.

Molecular Biology↗

bioRxiv2020

Protease Activity Profiling Via Programmable Phage Display

Endopeptidases catalyze the internal cleavage of proteins, playing pivotal roles in protein turnover, substrate maturation and the activation of signaling cascades. A broad range of biological functions in health and disease are controlled by proteases, yet assays to characterize their activities at proteomic scale do not yet exist. To address this unmet need, we have developed SEPARATE (Sensing EndoPeptidase Activity via Release and recapture using flAnking Tag Epitopes), which uses monovalent phage display of the entire human proteome at 90-aa peptide resolution. We demonstrate that SEPARATE is compatible with several human proteases from distinct catalytic classes, including Caspase-1, ADAM17, and Thrombin. Both well-characterized and newly identified substrates of these enzymes were detected in the assay. SEPARATE was used to discover a non-canonical Caspase-1 substrate, the E3 ubiquitin ligase HUWE1, a key mediator of apoptotic cell death. SEPARATE is a novel methodology to enable efficient, unbiased assessment of endopeptidase activity using a phage-displayed proteome.

molecular biology↗

bioRxiv2020

Pharmacophore-based peptide biologics neutralize SARS-CoV-2 S1 and deter S1-ACE2 interaction in vitro

Effective therapeutics and stable vaccine are the urgent need of the day to combat COVID-19 pandemic. SARS-CoV-2 spike protein has a pivotal role in cell-entry and host immune response, thus regarded as potential drug- and vaccine-target. As the virus utilizes the S1 domain of spike to initiate cell-attachment and S2 domain for membrane fusion, several attempts have been made to design viral-receptor and viral-fusion blockers. Here, by deploying interactive structure-based design and pharmacophore-based approaches, we designed short and stable peptide-biologics i.e. CoV-spike-neutralizing peptides (CSNPs) including CSNP1, CSNP2, CSNP3, CSNP4. We could demonstrate in cell culture experiments that CSNP2 binds to S1 at submicromolar concentration and abrogates the S1-hACE2 interaction. CSNP3, a modified and downsized form of CSNP2, could neither interfere with the S1-hACE2 interaction nor bind to S1. CSNP4 exhibited dose-dependent binding to both S1 and hACE2 and abolished the S1-hACE2 interaction in vitro. CSNP4 possibly enhance the mAb-based S1 neutralization by limiting the spontaneous movement of spike receptor-binding domain (RBD), whereas CSNP2 allowed RBD-mAb binding without any steric hindrance. Taken together, we suggest that CSNP2 and CSNP4 are potent and stable candidate peptides that can neutralize the SARS-CoV-2 spike and possibly pose the virus to host immune surveillance.

molecular biology↗

bioRxiv2021

Sialoglycan microarray encoding reveals differential sialoglycan binding of phylogenetically-related bacterial AB5 toxin B subunits

Vertebrate sialic acids (Sias) display much diversity in modifications, linkages and underlying glycans. Slide microarrays allow high-throughput explorations of sialoglycan-protein interactions. A microarray presenting [~]150 structurally-defined sialyltrisaccharides with various Sias linkages and modifications still poses challenges in planning, data sorting, visualization and analysis. To address these issues, we devised a simple 9-digit code for sialyltrisaccharides with terminal Sias and underlying two monosaccharides assigned from the non-reducing end, with three digits assigning a monosaccharide, its modifications, and linkage. Calculations based on the encoding system reveals >113,000 likely linear sialyltrisaccharides in nature. Notably a biantennary N-glycan with two terminal sialyltrisaccharides could thus have >1010 potential combinations and a triantennary N-glycan with three terminal sequences, >1015 potential combinations. While all possibilities likely do not exist in nature, sialoglycans encode enormous diversity. While glycomic approaches are used to probe such diverse sialomes, naturally-occurring bacterial AB5 toxin B subunits are simpler tools to track the dynamic sialome in biological systems. Sialoglycan microarray was utilized to compare sialoglycan-recognizing bacterial toxin B subunits. Unlike the poor correlation between B subunits and species phylogeny, there is stronger correlation with Sia-epitope preferences. Further supporting this pattern, we report a B subunit (YenB) from Yersinia enterocolitica (broad host range) recognizing almost all sialoglycans in the microarray, including 4-O-acetylated-Sias not recognized by a Y. pestis orthologue (YpeB). Differential Sia-binding patterns were also observed with phylogenetically-related B subunits from Escherichia coli (SubB), Salmonella Typhi (PltB), S. Typhimurium (ArtB), extra-intestinal E.coli (EcPltB), Vibrio cholera (CtxB), and cholera family homologue of E. coli (EcxB).

molecular biology↗

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