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Bryant, C.

Publications and source records attributed to Bryant, C..

15 recordsLinked to original sources

Combinatorial docking and molecular generation to navigate over 100-billion molecules for prospective ligand discovery

Commercially available make-on-demand libraries now exceed 100 billion compounds, requiring over 50 years to screen on 2,000 CPU cores using conventional docking. We present two complementary approaches to address this challenge. CombiDOCK, a combinatorial docking framework, enables exhaustive screening at the 100-billion scale within 40 days. MINT-Dock, a generative framework, accelerates navigation of this space by integrating CombiDOCK with Monte Carlo Tree Search. Benchmarked on 46 diverse targets, CombiDOCK matched full-molecule docking accuracy, and MINT-Dock achieved a 4,800-fold enrichment over random selection. Compared with prior billion-scale brute-force campaigns against {sigma}2, VMAT2, and VAChT, prospective CombiDOCK screens of the 100-billion-molecule library yielded higher hit rates and more potent ligands, while MINT-Dock achieved comparable outcomes across single- and multi-target objectives with >20-fold computational cost reductions. Docking-predicted poses of the best VAChT-binding compounds were confirmed by cryo-EM structures. These methods provide exhaustive and generative paths for navigating the trillion-molecule frontier of drug discovery.

bioinformatics↗

AlphaFold3 for Structure-guided Ligand Discovery

Deep-learning methods for protein structure prediction, such as AlphaFold2 (AF2) and RosettaFold (RF), have transformed structural biology and accelerated downstream biological discovery. More recent models, including AlphaFold3 (AF3) and RosettaFold All-Atom (RFAA), extend this capability to protein-ligand co-folding, enabling direct prediction of bound complexes from sequence and ligand inputs. This advance has raised the possibility that such models could function not only as structure predictors but also as AI-based molecular docking engines for virtual screening. Yet their true impact on ligand discovery remains unclear and, in many cases, controversial. Here, we systematically assess AF3 co-folding across tasks central to small-molecule discovery compared to conventional molecular docking. First, retrospective enrichment of actives over decoys showed that AF3 outperforms the physics-based docking program DOCK3 across 43 drug targets in DUDE-Z; however, this advantage is largely driven by hidden ligand-only biases inherent to computational decoy sets. In contrast, in three large experimental datasets (the sigma-2 receptor ({sigma}2), the D4 dopamine receptor (D4), AmpC {beta}-lactamase (AmpC)) with over 2,500 tested molecules that lack such biases, DOCK3 achieved stronger overall enrichment, while AF3 contributed mainly to early enrichment. Second, out-of-sample pose reproduction on >8,000 protein-ligand complexes deposited after the AF3 training and validation cutoff showed that AF3 accuracy is strongly dependent on training-set similarity, indicating that the model memorizes atomic positions more than learning general principles of molecular recognition. Finally, in the first prospective head-to-head screen against the {sigma}2 receptor, novel to AF3s training set, AF3 achieved a 13% hit rate and identified a 13 nM binder directly from the screen. However, compared with the parallel DOCK3 campaign, AF3 delivered a two-fold lower hit rate, despite yielding a similar affinity distribution among the top five hits. A crystal structure of the {sigma}2 receptor bound to the most potent AF3-derived hit confirmed that AF3 produced a near-native ligand pose. AF3 therefore represents the beginning of deep-learning-based structure-guided ligand discovery: a complementary tool rather than a replacement for conventional docking, with practical applications both as a screening engine and as a post-docking filter that improves hit rates. More broadly, this work establishes a framework for evaluating next-generation deep-learning co-folding models and quantifying their impact on small-molecule discovery.

pharmacology and toxicology↗

LubriShieldTM - a unique permanent coating for indwelling urinary catheters that impedes surface-associated uropathogens from forming biofilm

Catheter-associated urinary tract infection (CAUTI) is one of the most common healthcare-associated infections and biofilm formation plays a key role in its pathogenesis. Indwelling medical devices introduce ideal pathways inside the body for invading pathogens and feature surfaces conducive to biofilm development. These devices are the root cause of severe clinical infections often recalcitrant to antimicrobials. When bacteria and fungi switch to biofilm mode of growth, they produce a matrix in the form of extracellular polymeric substances (EPS). This creates a unique environment for growing virulent colonizers and persisting cells while also forming a shielding barrier against immune system attacks, antimicrobial agents and mechanical removal by fluid shear forces. To address this challenge, LubriShield TM - a novel permanent coating was invented, and evenly applied to both the internal and external surfaces of indwelling urinary Foley catheters. Without releasing active substances, it effectively prevented pathogens from producing biofilm. The coating was superhydrophilic and incorporated a proprietary anti-fouling ligand, which created a surface that significantly inhibited up to 99% of colonizing uropathogens from forming biofilm for the duration of use without any microbial killing (p< 0.001). The predominant uropathogens, including Gram-positive and Gram-negative as well as Candida albicans, were inhibited from forming biofilm on the LubriShieldTM coated surfaces for up to 14 days in artificial urine medium. After challenging the adhering bacteria in a glass bladder flow model, the coating still significantly reduced biofilm formation by 83% (p<0.001). The growth mode and emergent properties of adhering bacteria on uncoated silicone catheter surfaces were compared with those on LubriShieldTM coated surfaces. RNA-seq analysis revealed that gene expression associated with microbial EPS formation was significantly downregulated on the coated surfaces. Additionally, microorganisms adhering to LubriShieldTM coated catheters were 46% more susceptible to antibiotics compared to those on uncoated silicone catheters (p<0.01).

microbiology↗

Alternative mRNA Splicing and Polyadenylation Events are Synchronous with Podocyte Injury and Slit Diaphragm Dysregulation in Glomerular Disease Models

BackgroundGlomerular disease, characterized by podocyte injury and proteinuria, can lead to chronic kidney disease and end stage kidney disease. We hypothesized that the glomerular pathophysiology is associated with mRNA alternative splicing and polyadenylation of glomerular genes and of critical podocyte and slit diaphragm components that regulate the filtration barrier. MethodsGlomerular damage, accompanied by proteinuria, was induced by puromycin-aminonucleoside or adriamycin to mimic human minimal change disease or focal segmental glomerulosclerosis (FSGS), respectively, and RNA-seq analyses was performed. Alternatively spliced and alternatively polyadenylated events through differential exon and poly(A) site usage were queried in JunctionSeq and APATrap pipelines. These events were further mapped on podocyte and glomerular landscape, analyzed and modulated for slit diaphragm components, and cis- and trans-regulatory elements were identified. ResultsAltered glomerular mRNA processing by alternative splicing/polyadenylation was identified in 136/71 and 1875/746 genes in minimal change disease and FSGS models, respectively. Transcript annotation and prioritization of significant alternative splicing and polyadenylation identified key events in several podocyte and slit diaphragm genes with novel and established roles. Alternative splicing of critical slit diaphragm components, the junction protein TJP1/ZO1 and microtubule associating protein ITM2B was further characterized. Alternative polyadenylation of core members of the slit diaphragm, NPHS1, NPHS2 and NEPH1 was analyzed with potential alteration of microRNA binding sites between the proximal vs distal poly (A) site usage in their mRNAs. Concomitantly, dysregulation of trans-regulatory elements (polyadenylation and splicing factors), was discovered in these models of nephropathies. Additionally, beneficial proteinuria-reducing treatments, pioglitazone and GQ16 reversed many alternatively spliced and polyadenylated events. Moreover, GWAS SNPs as potential cis-regulatory elements were identified in several genes from the human nephrotic syndrome database. Finally, we demonstrated proof-of-concept principle of chemically modified splice switching oligonucleotides in modulating TJP1 alternative splicing in podocytes. ConclusionFindings from our studies identified that glomerular pathophysiology and disruption of the filtration barrier is associated with alternative splicing and alternative polyadenylation of glomerular genes, many of which are crucial determinants of podocyte structure and function and the slit diaphragm complex. Key PointsO_LIAlternative mRNA processing adds an important layer of transcriptome complexity in podocyte and slit diaphragm components during glomerular injury. C_LIO_LITrans- and cis-elements may offer potential mechanisms to regulate alternative splicing and polyadenylation during podocyte injury. C_LIO_LIAntisense oligonucleotides can regulate mRNA processing events, thus offering a potential RNA-based therapeutic strategy to treat glomerular disease. C_LI

molecular biology↗

Alpha-synuclein aggregates trigger anti-viral immune pathways and RNA editing in human astrocytes

RNA editing is a post transcriptional mechanism that targets changes in RNA transcripts to modulate innate immune responses. We report the role of astrocyte specific, ADAR1 mediated RNA editing in neuroinflammation in Parkinsons disease. We generated hiPSC-derived astrocytes, neurons and co-cultures and exposed them to small soluble alpha-synuclein aggregates. Oligomeric alpha-synuclein triggered an inflammatory glial state associated with TLR activation, viral responses, and cytokine secretion. This reactive state resulted in loss of neurosupportive functions, and the induction of neuronal toxicity. Notably, interferon response pathways were activated leading to upregulation, and isoform switching of the RNA deaminase enzyme, ADAR1. ADAR1 mediates A-to-I RNA editing, and increases in RNA editing were observed in inflammatory pathways in cells, as well as in post-mortem human PD brain. Aberrant, or dysregulated, ADAR1 responses and RNA editing may lead to sustained inflammatory reactive states in astrocytes triggered by alpha-synuclein aggregation, and this may drive the neuroinflammatory cascade in Parkinsons.

neuroscience↗

Activity of Salmonella SPI-1 inhibits the TLR4-dependent transcriptional but not translational response during macrophage infection

Changes in gene expression during bacterial infection are the combined result of altered transcription and translation, with the latter comparatively understudied. Gram-negative bacteria rapidly trigger cytokine gene transcription in macrophages through the activation of pathogen associated molecular pattern receptors, for example detection of Salmonella lipopolysaccharide (LPS) from the bacterial cell envelope by Toll-like receptor 4 (TLR4). Here, through time-resolved parallel translatomic and transcriptomic profiling, we now show temporal TLR4-specific translational upregulation of cell signalling proteins in macrophages induced by Salmonella. While transcriptional upregulation of these genes is dampened through the activity of the Salmonella SPI-1 type three secretion system, a robust translational response remains. These data reveal an important host-pathogen translational regulatory network that modifies the innate immune response of macrophages to infection.

molecular biology↗

Elevation-dependent patterns of snow-gum dieback are moderated by trait differences between montane and subalpine forests.

Subalpine forests worldwide face the synergistic threats of global warming and increased biotic attack, and the collapse or transition of subalpine forests is predicted in south-eastern Australia under future climates. The recent widespread dieback of subalpine snow gum forests due to increased activity of a native wood-boring longicorn beetle suggests this process may already be underway. We investigated how variation in tree tissue traits and environmental conditions correlated with elevation-dependent spatial patterns of forest mortality. We hypothesised that increased vulnerability of subalpine snow gums to wood-borer-mediated dieback at intermediate elevations was associated with poorly-resolved differences in traits between montane (Eucalyptus pauciflora subsp. pauciflora) and subalpine (E. pauciflora subsp. niphophila) snow-gum subspecies. We first sought to characterise variation and elevation-dependent transitions in 20 structural and drought-related functional traits among 120 healthy trees distributed along a 1000m elevation transect which spanned the subspecies transition zone. Secondly, we surveyed 774 trees across 53 sites between 1280-1980m asl. to explore associations between borer-damage severity, elevation, subspecies, and a subset of traits that differed between subspecies. These snow-gum subspecies exhibited mean differences and/or divergent elevation responses in 25% of traits surveyed, indicating contrasting suites of traits between montane and subalpine subspecies. Increased borer-damage severity across the montane-to-subalpine subspecies transition was correlated with lower bark thickness, whereas reduced borer damage at the highest elevations was associated with greater precipitation and lower temperatures. Our results suggest that due to possessing distinct traits associated with increased borer susceptibility, subalpine snow-gum forests will be subject to increased risk of severe borer-mediated forest dieback under warmer and drier future climates. Identifying traits contributing to species distribution limits and biotic-agent vulnerability remains critical for predicting, monitoring, and possibly mitigating forest and vegetation declines under future climates.

ecology↗

Development of covalent chemogenetic K2P channel activators

K2P potassium channels regulate excitability by affecting cellular resting membrane potential in the brain, cardiovascular system, immune cells, and sensory organs. Despite their important roles in anesthesia, arrhythmia, pain, hypertension, sleep, and migraine, the ability to control K2P function remains limited. Here, we describe a chemogenetic strategy termed CATKLAMP (Covalent Activation of TREK family K+ channels to cLAmp Membrane Potential) that leverages the discovery of a site in the K2P modulator pocket that reacts with electrophile-bearing derivatives of a TREK subfamily small molecule activator, ML335, to activate the channel irreversibly. We show that the CATKLAMP strategy can be used to probe fundamental aspects of K2P function, as a switch to silence neuronal firing, and is applicable to all TREK subfamily members. Together, our findings exemplify a new means to alter K2P channel activity that should facilitate studies both molecular and systems level studies of K2P function and enable the search for new K2P modulators.

biophysics↗

The delayed kinetics of Myddosome formation explains why Aβ aggregates trigger TLR4 less efficiently than LPS

The Myddosome is a key innate immune signalling platform. It forms at the cell surface and contains MyD88 and IRAK proteins which ultimately coordinate the production of pro-inflammatory cytokines. Toll-like receptor 4 signals via the Myddosome when triggered by Lipopolysaccharide (LPS) or Amyloid-Beta (A{beta}) aggregates but the magnitude and time duration of the response are very different for reasons that are unclear. Here we followed the formation of Myddosomes in live macrophages using local delivery of TLR4 agonist to the cell surface and visualisation with 3D rapid light sheet imaging. This was complemented by super-resolution imaging of Myddosomes in fixed macrophages to determine the size of the signalling complex at different times after triggering. Myddosomes formed more rapidly after LPS than in response to sonicated A{beta} 1-42 fibrils (80 seconds vs 372 seconds). The mean lifetimes of the Myddosomes was also shorter when triggered by LPS compared to sonicated A{beta} fibrils (170 and 220 s) respectively. In both cases a range of Myddosome of different sizes (50-500 nm) were formed. In particular, small round Myddosomes around 100 nm in size formed at early time points, then reduced in proportion over time. Collectively our data suggests that compared to LPS the multivalency of A{beta} fibrils leads to the formation of larger Myddosomes which form more slowly and, due to their size, take longer to disassemble. This explains why sonicated A{beta} fibrils results in less efficient triggering of TLR4 signalling and may be a general property of protein aggregates.

biophysics↗

Architectural asymmetry enables DNA transport through the Helicobacter pylori cag type IV secretion system

Structural asymmetry within secretion system architecture is fundamentally important for apparatus diversification and biological function. However, the mechanism by which symmetry mismatch contributes to nanomachine assembly and interkingdom effector translocation are undefined. Here, we show that architectural asymmetry orchestrates dynamic substrate selection and enables trans-kingdom DNA conjugation through the Helicobacter pylori cag type IV secretion system (cag T4SS). Structural analyses of asymmetric units within the cag T4SS periplasmic ring complex (PRC) revealed intermolecular {pi}-{pi} stacking interactions that coordinate DNA binding and license trans-kingdom conjugation without disrupting the translocation of protein and peptidoglycan effector molecules. Additionally, we identified a novel proximal translocation channel gating mechanism that regulates cargo loading and governs substrate transport across the outer membrane. We thus propose a model whereby the organization and geometry of architectural symmetry mismatch exposes {pi}-{pi} interfaces within the PRC to facilitate DNA transit through the cag T4SS translocation channel.

microbiology↗

Salmonella impairs macrophage immunity through effector-independent rapid translational induction in response to membrane puncture by the SPI-1 injectisome

During bacterial infection both the host cell and its invader must divert intracellular resources to synthesise specific proteins in a timely manner. For the host, these factors may be needed for innate immune responses, including programmed cell death, and in the bacteria newly synthesized proteins may be survival factors needed to counteract host responses. Salmonella is an important food-borne bacterial pathogen that invades and multiplies within host cells. It is well established that invasion of epithelial cells is dependent upon the SPI-1 Type III injectisome, a biological needle that penetrates and secretes effectors into host cells to promote internalization. However, the importance of the SPI-1 injectisome in infection of professional phagocytes such as macrophages, which are the predominant host cell type during systemic infection, is less clear. Through time resolved parallel transcriptomic and translatomic studies of macrophage infection, we revealed that SPI-1 injectisome-dependent infection of macrophages triggers rapid translation of transcription factor mRNAs, including Early Growth Response 1 (Egr1). Despite the short half-life of EGR1 protein, its swift synthesis within the initial hour of infection is sufficient to inhibit transcription of pro-inflammatory genes and thereby restrain inflammatory responses and programmed cell death within the first hour of during early infection. This transient period of inflammatory suppression in macrophages is exploited by Salmonella to establish infection and sheds new insight on the importance of translational activation in host-pathogen dynamics during Salmonella infection.

molecular biology↗

Alternatively Spliced Landscape of PPARγ mRNA in Podocytes is Distinct from Adipose Tissue

Podocytes are highly differentiated epithelial cells, and their structural and functional integrity is compromised in a majority of glomerular and renal diseases, leading to proteinuria, chronic kidney disease, and kidney failure. Traditional agonists (e.g., pioglitazone) and selective modulators (e.g., GQ-16) of peroxisome-proliferator-activated-receptor-{gamma} (PPAR{gamma}) reduce proteinuria in animal models of glomerular disease and protect podocytes from injury via PPAR{gamma} activation. This indicates a pivotal role for PPAR{gamma} in maintaining glomerular function through preservation of podocytes distinct from its well-understood role in driving insulin sensitivity and adipogenesis. While its transcriptional role in activating adipokines and adipogenic genes is well-established in adipose tissue, liver and muscle, understanding of podocyte PPAR{gamma} signaling remains limited. We performed a comprehensive analysis of PPAR{gamma} mRNA variants due to alternative splicing, in human podocytes and compared with adipose tissue. We found that podocytes express the ubiquitous PPAR{gamma} Var 1 (encoding {gamma}1) and not Var2 (encoding {gamma}2), which is mostly restricted to adipose tissue and liver. Additionally, we detected expression at very low level of Var4, and barely detectable levels of other variants, Var3, Var11, VartORF4 and Var9, in podocytes. Furthermore, a distinct podocyte vs adipocyte PPAR-promoter-response-element containing gene expression, enrichment and pathway signature was observed, suggesting differential regulation by podocyte specific PPAR{gamma}1 variant, distinct from the adipocyte-specific {gamma}2 variant. In summary, podocytes and glomeruli express several PPAR{gamma} variants, including Var1 ({gamma}1) and excluding adipocyte-specific Var2 ({gamma}2), which may have implications in podocyte specific signaling and pathophysiology. This suggests that new selective PPAR{gamma} modulators can be potentially developed that will be able to distinguish between the two forms, {gamma}1 and {gamma}2, thus forming a basis of novel targeted therapeutic avenues.

molecular biology↗

Levelling out differences in aerobic glycolysis neutralizes the competitive advantage of oncogenic PIK3CA mutant progenitors in the esophagus

Normal human tissues progressively accumulate cells carrying mutations. Activating mutations in PIK3CA generate large clones in the aging human esophagus, but the underlying cellular mechanisms are unclear. Here, we tracked mutant PIK3CA esophageal progenitor cells in transgenic mice by lineage tracing. Expression of an activating heterozygous Pik3caH1047R mutation in single progenitor cells tilts cell fate towards proliferation, generating mutant clones that outcompete their wild type neighbors. The mutation leads to increased aerobic glycolysis through the activation of Hif1 transcriptional targets compared with wild type cells. We found that interventions that level out the difference in activation of the PI3K/HIF1/aerobic glycolysis axis between wild type and mutant cells attenuate the competitive advantage of Pik3caH1047R mutant cells in vitro and in vivo. Our results suggest that clinically feasible interventions that even out signaling imbalances between wild type and mutant cells may limit the expansion of oncogenic mutants in normal epithelia.

cancer biology↗

Small molecule inhibitors of a human recombination-associated ATPase, RAD54

Homologous recombination (HR) is a principal support pathway for DNA replication and for recovery from DNA breaks and interstrand crosslinks, making it a rational target for inhibition in cancer therapy. The ATPase RAD54 functions in molecular events that promote DNA sequence-preservation during HR-mediated damage repair, including homology search, DNA strand exchange, and transition to DNA repair synthesis within a displacement loop intermediate. We developed a high-throughput biochemical screen to identify small-molecule inhibitors of human RAD54, using a phosphate detection assay to monitor RAD54 ATPase activity in the presence of double-stranded DNA (dsDNA). After filtering potential DNA intercalators and frequent hitters, we identified two chemotypes that reproducibly inhibited RAD54 ATPase in vitro. We evaluated these chemotypes for inhibition of RAD54-dsDNA binding and cancer cell survival. A halogenated carbazole/dihydroacridine scaffold inhibited a panel of SWI2/SNF2-related ATPases but not VCP/p97, an unrelated ATPase. Small molecules that interfere with key steps in HR-- such as inhibitors of RAD54--may expose DNA repair-dependent vulnerabilities in cancer cells.

biochemistry↗

Collateral sensitivity is contingent on the repeatability of evolution

Antibiotic resistance represents a growing health crisis that necessitates the immediate discovery of novel treatment strategies. One such strategy is the identification of collateral sensitivities, wherein evolution under a first drug induces susceptibility to a second. Here, we report that sequential drug regimens derived from in vitro evolution experiments may have overstated therapeutic benefit, predicting a collaterally sensitive response where cross resistance ultimately occurs. We quantify the likelihood of this phenomenon by use of a mathematical model parametrised with combinatorially complete fitness landscapes for Escherichia coli. Through experimental evolution we then verify that a second drug can indeed stochastically exhibit either increased susceptibility or increased resistance when following a first. Genetic divergence is confirmed as the driver of this differential response through targeted and whole genome sequencing. Taken together, these results highlight that the success of evolutionarily-informed therapies is predicated on a rigorous probabilistic understanding of the contingencies that arise during the evolution of drug resistance.

evolutionary biology↗