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Using experimental results of protein design to guide biomolecular energy-function development

Computational models of macromolecules have many applications in biochemistry, but physical inaccuracies limit their utility. One class of models uses energy functions rooted in classical mechanics. The standard datasets used to train these models are limited in diversity, pointing to a need for new training data. Here, we sought to explore a new paradigm for training an energy function, where the Rosetta energy function was used to design de novo proteins. Experimental results on these designs were then used to identify failure modes of design, which were subsequently used as a "guiding principle" to retrain the energy function. Specifically, we examined a diverse set of de novo protein designs experimentally tested for their ability to stably fold, identifying unstable designs that were predicted to be stable by the Rosetta energy function. Using deep mutational scanning, we identified single amino-acid mutations that rescued the stability of these designs, providing insight into common failure modes of the energy function. We identified one key failure mode, involving steric clashing in protein cores. We identified similar overpacking when using Rosetta to refine high-resolution protein crystal structures, quantified the degree of overpacking, and refit a small set of energy-function parameters to better recapitulate native-like packing. Following fitting, we largely eliminated the failure mode in the refinement task, while retaining performance on other benchmarks, resulting in an updated version of the Rosetta energy function. This work shows how learning from protein designs can guide energy-function development. Author summaryComputational models of macromolecules have many applications, such as predicting structures, predicting mutational effects, or designing new proteins. One type of model uses an energy function to explicitly model the physical forces at play. These models are trained using experimental data. However, available training data are limited in number and diversity, prompting a need for new sources of training data. In this paper, we explore a new paradigm for training an energy function, which involves using the energy function to design de novo proteins and then learning from which designs succeed and which fail when experimentally tested in the lab. We used experimental data to learn common failure modes in design, identified examples of a failure mode in a high-quality benchmark, and then used this benchmark to retrain the energy function. Using this strategy, we identified and largely resolved a bias in the Rosetta energy function that involved energetically unfavorable steric clashes in protein cores. Overall, this work helps establish a framework for how learning from design can be used to guide the development of macromolecular models.

biochemistry↗

Intracellular aggregation of the transthyretin protein is limited by Hsp70 chaperones

Extracellular amyloid deposits are a hallmark feature of systemic protein aggregation diseases such as transthyretin amyloidosis (ATTR). However, emerging evidence suggests that extracellular transthyretin (TTR) aggregates are internalized and result in an intracellular stress response, including elevated Hsp70 levels. While ATTR research has predominantly focused on extracellular TTR amyloid, our understanding of TTR aggregation inside the cell is poorly explored. To better understand how intracellular chaperones impact intracellular TTR, we used a yeast model that expresses TTR fused eGFP (TTR-eGFP) within the cytoplasm. Since the Hsp70 chaperone family, and co-chaperones the J-domain proteins (JDPs) and Hsp110, act as a disaggregase in vitro, we asked how these molecular chaperones impact TTR aggregation intracellularly in vivo. TTR-eGFP forms detergent-soluble high molecular weight (HMW) aggregates in yeast that have biochemistry profiles similar to human patient TTR. While knockdown of the JDP, Sis1, and deletion of the Hsp110, Sse1, appear to slightly increase TTR-eGFP aggregation, the loss of two major yeast Hsp70s, Ssa1 and Ssa2, lead to a significant increase in the size of HMW species. Taken together, our data suggest that Hsp70s limit the formation of HMW TTR aggregates in the intracellular environment. Based on our results, it is possible that the age-related decline of protein homeostasis, including Hsp70s, may promote the intracellular aggregation of TTR.

biochemistry↗

Discovery of the metalloenzyme IsmB revises a pathway for coprostanol formation by the human gut microbiome

High levels of circulating cholesterol are associated with human cardiovascular diseases and an altered gut microbiome. Still, major gaps exist in our understanding of the interactions of cholesterol with gut microbes. The reductive transformation of cholesterol to the poorly absorbed sterol coprostanol by human gut bacteria has long been known, but the genetic and biochemical basis for this activity is only partially elucidated. Here, we discover and characterize a gut bacterial enzyme that catalyzes the reduction of cholestenone to coprostanone, the second step in the intestinal sterol metabolism (ism) pathway for coprostanol production. We identify a gene encoding a previously unknown 5{beta}-reductase, IsmB, a new member of the Fe-S cluster flavoenzyme superfamily, in the coprostanol producing organism Eubacterium coprostanoligenes. Biochemical characterization of IsmB confirms it is an anaerobic Fe-S cluster flavoenzyme and reveals specificity for reduction of an unanticipated intermediate, 5-cholesten-3-one, to coprostanone, revising the ism pathway. We also identify and characterize homologs of IsmB encoded in uncultured human gut bacteria that also encode the previously identified ism pathway enzyme IsmA, further supporting the role of IsmB in coprostanol formation. Finally, analysis of human stool metagenomics and metabolomics datasets further confirms the relevance of IsmB in the human gut microbiome, and analyses of human serum metabolomics from Framingham Heart Study participants reveal negative correlation between serum cholesterol levels and the presence of IsmA/IsmB encoders in the gut. Together, these results show the utility of combining biochemistry and stool metagenomic analysis for gut microbial enzyme discovery, and suggests IsmA/IsmB-encoding gut bacteria carry potential benefits for cholesterol homeostasis and cardiovascular health.

biochemistry↗

A CK2-FBXW11 kinase-E3 ubiquitin ligase cascade is a metabolic sensor regulating Tryptophan 2,3-dioxygenase stability

Small molecules toggling the ubiquitin-proteasome system (UPS) are powerful regulators of protein degradation. Yet, mechanistic knowledge of how endogenous ligands gate UPS decisions remains rudimentary. Here, we define control of UPS access to Tryptophan-2,3-dioxygenase (TDO2), which converts the essential amino acid tryptophan (Trp) to N-formylkynurenine. When Trp concentrations are limiting, TDO2 is degraded to avert tryptophanemia. Using CRISPRi screening and biochemistry, we identify a CK2-FBXW11 kinase-E3 ligase cascade that generates and recognizes tandem TDO2 phosphodegrons when not protected by Trp. Trp binding to an exosite safeguards TDO2 from phosphorylation-dependent ubiquitylation. Effects of Trp analogs on CK2-FBXW11-dependent ubiquitylation indicated that the indole, amino, and carboxylate groups are necessary for substrate shielding. Cryo-EM reveals how these moieties order a region proximal to the phosphodegrons; without Trp, this segment is flexible, enabling phosphorylation-coupled ubiquitylation. Overall, our data uncovered an endogenous small molecule allosterically stabilizing its own metabolizing enzyme through protection from a phosphorylation-ubiquitylation cascade.

biochemistry↗

Ribosomal Protein bL27 Protects Translating Ribosomes from tmRNA-SmpB

Bacterial ribosomal protein bL27 is universally conserved and its amino terminus is adjacent to the peptidyl transfer center, yet its role in translation remains unclear. Combining genetics, biochemistry and molecular dynamics, we show that bL27 has an unexpected role in preventing trans-translation, the bacterial ribosome rescue mechanism, from interfering with protein synthesis. Deletion of the bL27 gene causes a 10,000-fold decrease in viability and this defect is partially rescued by deletion of the gene encoding tmRNA, a critical molecule for trans-translation. Molecular dynamics simulations also indicate that bL27 can slow the movement of tmRNA on the ribosome. These data link trans-translation and bL27, and support a model in which the amino terminus of bL27 acts as a gatekeeper to prevent tmRNA from sterically interfering with tRNA on the ribosome.

biochemistry↗

Disrupted TRiC allostery and conformational equilibrium by LCA-linked mutations: structural and functional insights

The eukaryotic chaperonin TRiC/CCT is essential for proteostatis, yet the molecular basis of its subunit-specific pathologies remains poorly understood. Here, we elucidate the molecular mechanism of Leber Congenital Amaurosis (LCA), a severe hereditary retinal dystrophy arised from mutations in the CCT2 subunit of TRiC. By integrating cryo-electron microscopy, biochemistry, and proteomics, we demonstrate that LCA-associated mutations (T400P and R516H in CCT2) disrupt TRiCs critical intra-molecular and intra-ring allosteric network and impair its functional cycle, drastically reducing the population of the folding-active closed state. Unexpectedly, we captured a fully folded endogenous -tubulin within the mutant TRiC chamber, revealing a unique CCT8 C-terminal tail involved folding pathway, distinct from {beta}-tubulin. Furthermore, cellular proteomics revealed that TRiC dysfunction causes a specific downregulation of essential SLC membrane transporters. We propose that the loss of these transporters is likely catastrophic for metabolically demanding tissues like the retina and developing embryo. Our work provides a direct mechanistic link between TRiC structural defects and LCA pathology, offering a new framework for understanding etiology of chaperonopathies.

biochemistry↗

Mismatch type impacts interference and priming activities in the type I-E CRISPR-Cas system

Type I-E CRISPR-Cas systems direct RNA-guided interference against foreign nucleic acids using the CRISPR RNA (crRNA)-guided Cascade complex and Cas3 helicase-nuclease. DNA targeting by Cascade-Cas3 promotes priming, a mechanism that allows for rapid acquisition of new spacers within the CRISPR array. Target mutations in the PAM and PAM-proximal seed region can block interference but may still allow priming. Previous studies have suggested that target mutations to T and A are tolerated, but that C and G substitutions are deleterious to interference and priming, respectively. However, the contributions of the crRNA spacer sequence to mutational tolerance remain unclear. Here, we systematically tested the effects of crRNA seed sequences on mutational tolerance. We engineered four E. coli strains with variable spacer sequences and tested CRISPR interference and priming against a plasmid library for each strain. Consistent with prior studies, we observe that mutations to C or G in the seed can be highly deleterious, especially at positions 1, 2 and 4. However, the corresponding crRNA sequence also strongly impacts the level of defect, with rC-dC and rA/G-dG causing the largest defects in our plasmid library experiments. Using in vitro biochemistry, we observe that mismatch type at the first position of the seed affects Cas8 conformation, and results in reduction in the rates of both Cascade-target binding and Cas3 recruitment. Overall, our results reveal that although nucleotide identity of target mutations is an important determinant of type I-E CRISPR immunity, the crRNA sequence also strongly impacts immune outcomes upon target mutation.

biochemistry↗

Chemical control of 2'-hydroxyl-dependent Cas9 target engagement enables CRISPR RNA ribose replacement

Advanced CRISPR-based therapies benefit from CRISPR RNA (crRNA) with high nuclease resistance and enhanced drug-like properties, which is primarily achieved through chemical replacement of the RNA ribose moiety. However, for gene editing enzymes like CRISPR-Cas9 a handful of residues cannot be replaced with chemical ribose analogues, limiting the scope of therapeutic strategies. The mechanism underlying this restriction has remained unclear. Here, using nucleic acid chemistry, biochemistry, cryo-EM, and molecular dynamics simulations, we show that the ribose 2-hydroxyl group at specific crRNA residues is required to achieve a conformational state competent for Cas9 target DNA binding. Based on the mechanistic principles uncovered, we combined site-specific phosphorothioate linkage chemistry with ribose replacement chemistry to restore binding and activity, resulting in high Cas9 editing efficiency and fidelity with a ribose-free crRNA. This study offers novel mechanistic insight and crRNAs with full chemical stabilization, making rational design of guide RNAs with complete nuclease protection for CRISPR-based medicines possible.

biochemistry↗

Coupling high-throughput protease enzymology with viral replication reveals biochemical constraints of viral fitness

Proteases govern essential biological processes and are key drug targets, yet how protease sequence variation quantitatively reshapes biochemical parameters and constrains biological fitness remains poorly understood. Here, we integrate high-throughput in vitro enzymology with cellular assays to link protease sequence, biochemistry, and fitness. We extend a microfluidic platform for high-throughput protease enzymology (HT-MEKpro), which is broadly applicable across protease families and catalytic classes, enabling measurement of catalytic turnover (kcat), Michaelis constant (KM), inhibitor potency (IC50), and relative substrate specificity for 102-103 variants. Applied to the SARS-CoV-2 main protease (Mpro), HT-MEKpro generated parallel catalytic and inhibitory landscapes for >400 variants. Integration with viral replication and in-cell cleavage assays reveals that variants with altered substrate specificity fail to support replication, suggesting imbalanced polyprotein processing as a constraint on viral fitness. More broadly, these data can enable mechanistically grounded modeling of protease sequence-property relationships and inform strategies for pharmacological modulation beyond active-site inhibition.

biochemistry↗

Gene sharing during enzyme recruitment reveals distinct adaptive strategies including massive, sustained duplication without divergence

Organisms expand their metabolism by repurposing enzymes to perform new reactions. To be repurposed, an enzyme must balance its original and new functions if both contribute to fitness. If an enzyme cannot balance its functions, another candidate may take its place. Here, we used adaptive evolution on a glucokinase-deficient Escherichia coli containing four promiscuous surrogates to investigate enzyme recruitment when the preferred candidate, N-acetyl-D-mannosamine kinase (NanK), is under selective pressure to maintain its original function. We find that NanK is still recruited to restore glycolysis under conditions requiring both functions via two distinct mechanisms that leave native activity largely unaltered. In one mechanism, small-scale gene amplification precedes the appearance of two non-synonymous mutations in nanK that increase glucokinase activity but have little or no effect on N-acetyl-D-mannosamine kinase activity. In another mechanism, recruitment occurs via amplification of a [~]1000 base pair fragment that narrowly encompasses nanK and reaches copy numbers as high as 127. Despite maintenance of amplification for hundreds of generations, we observe no persistent mutations in any nanK duplicate at the level of resolution provided by 75X whole genome sequencing coverage. Our results demonstrate that gene sharing can alter the trajectory but not necessarily prevent the recruitment of a preferred promiscuous candidate during adaptive evolution when other, seemingly equal candidates are available. Our findings also reveal that evolution by Innovation-Amplification-Divergence may only be facilitated at moderate levels of gene amplification, and hindered by massive amplification, as increased gene copy number diminishes returns of individual adaptive point mutations. Classification: Evolution, Biochemistry SignificanceThe Innovation-Amplification-Divergence model posits that single multifunctional enzymes evolve into multiple monofunctional enzymes through two events: First, selective pressure on a multifunctional enzyme leads to a duplication of the gene encoding that enzyme in an organisms genome. Second, the duplicate gene copy can freely accumulate mutations that enhance one of the encoded enzymes functions while the original copy can accumulate mutations that enhance the enzymes other encoded function. Intriguingly, our results reveal sequence divergence only in cells that experience mild amplification, and no divergence in cells that experience massive amplification. This suggests that sequence divergence may be suppressed above a certain number of gene copies, providing a new perspective on a widely accepted theory of evolution.

biochemistry↗

Impact of Sequential Processing (Boiling and Fermentation) on the Nutritional, Anti-nutrient, and Antioxidant Profile of Manihot esculenta Tubers.

1.BackgroundManihot esculenta (Cassava) is a vital staple in Sub-Saharan Africa, yet its high levels of cyanogenic glycosides and anti-nutrients pose health risks. While boiling is common, its holistic impact on the nutritional biochemistry and antioxidant profile of the "Farmers Pride" (IBA 961632) variety remains under-characterized. This study evaluated the sequential impact of food processing -boiling and multi-stage fermentation -on cassavas toxicological and bioactive profiles. MethodsFresh tubers were boiled for 10 minutes and fermented for 24, 48, and 72 hours. Proximate composition, vitamins, and anti-nutritional factors (cyanide, oxalate, phytate) were quantified. Linamarase activity and total phenolic and flavonoid contents were measured to assess enzymatic detoxification and phytotherapeutic potential. ResultsBoiling concentrated carbohydrates but created a "nutrient void," leaching 93% of Vitamin C. However, fermentation acted as a biochemical refinery; by 72 hours, total cyanide plummeted from 98.15 to 0.54 mg/100g, meeting WHO safety standards. Concurrently, fermentation triggered a resurgence in bioactives, significantly increasing phenolic and flavonoid levels. ConclusionBoiling alone is insufficient for detoxification. Sequential fermentation beyond 48 hours is essential to "rescue" antioxidant potential and ensure safety. The 72-hour fermented tuber represents an optimized bioactive food vehicle for managing oxidative stress-related pathologies like prostatic hyperplasia

biochemistry↗

Neuronal calcium sensors emerge as novel adenylyl cyclase 8 regulators

Adenylyl cyclase 8 (AC8) is a Ca2+-sensitive membrane adenylyl cyclase highly expressed in the central nervous system. AC8-mediated intracellular cyclic adenosine monophosphate (cAMP) accumulation shapes synaptic function, plasticity, and memory formation and is tightly controlled by intracellular Ca2+ and G protein-coupled receptor signaling. Although it is well known that the effects of Ca2+ on AC8 activity are directly mediated by calmodulin, it has remained unclear until now whether other Ca2+-binding proteins also regulate AC8 function. Here, we identify the neuronal calcium sensor hippocalcin-like protein 1 (HPCAL1) as a direct interaction partner of AC8. Using biochemistry, structural proteomics, integrative modeling, cryo-EM and cell-based FRET approaches, we show that HPCAL1 associates with AC8 in a Ca2+-dependent manner. HPCAL1 shows weak positive modulation of AC8 activity in vitro, with sub micromolar affinity. HPCAL1 interacts with flexible regulatory regions of AC8, including the C1b domain and the N- and C-terminal regions. Interestingly, other members of the neuronal calcium sensor family can bind AC8 via the same sites. Together, our study reveals a previously unrecognized mode of Ca2+-dependent AC8 recognition by a group of neuronal calcium sensor proteins, which may be relevant to context-dependent regulation of cAMP signaling.

biochemistry↗

Structural basis of the two-photon photoactivation mechanism of orange carotenoid protein

Cyanobacteria have produced Earths oxygen for 2.4 billion years by adapting to fluctuating irradiance. This adaptation relies on orange carotenoid protein (OCP), which mediates light-intensity- dependent photoprotective energy dissipation using a unique two-photon absorption mechanism. Photon absorption by ground-state OCP (OCPO) generates a metastable intermediate (OCP1h{nu}) that either relaxes thermally or, upon absorption of a second photon within [~]1 s, converts to the active photoprotective state (OCPR). By integrating static and time-resolved crystallography, cryo-EM, computation, spectroscopy and biochemistry, we assign the structure of OCP1h{nu}, establish its functional relevance and capture structural snapshots along the OCPO[->]OCP1h{nu} and OCP1h{nu}[->]OCPR photochemical pathways. We elucidate the molecular mechanism of OCP, which serves as a unique biological circuit breaker protecting the photosynthetic machinery from high light flux.

biochemistry↗

Schizokinen siderophores in the methylotrophy model organism Methylorubrum extorquens AM1

The facultative methylotroph model organism Methylorubrum extorquens AM1 is a known lanthanide user, which has shed light on the role of rare-earth metals in biochemistry. The characterization of a methanol dehydrogenase (MDH) protein which requires lanthanides as an enzymatic cofactor outlined the question of how these metals are acquired from the environment. It has been proposed that mesophilic organisms as M. extorquens AM1 can produce siderophore-like molecules, which chelate, transport and traffic rare-earth elements into the microbial cell. Therefore, we performed the bioinformatic and chemical investigation of M. extorquens AM1 by using genome mining, the CAS and arsenazo assay, molecular networking and chemical analytical techniques. Our results showed that indeed Methylorubrum extorquens AM1 harbored a gene cluster to produce metal chelators. The chemical analysis confirmed the production of the known hybrid hydroxamate-citrate siderophores schizokinen A and N-deoxyschizokinen A, which are very likely the side products of the transformation of schizokinen and N-deoxyschizokinen. The determination of the lanthanide chelation activity of the schizokinen siderophores series against three different lanthanides (La, Eu and Lu) showed no coordination activity, thus ruling out the involvement of schizokinen siderophores in rare-earth metal transport.

biochemistry↗

Context-dependent peptide recognition shapes tyrosine kinase substrate specificity beyond consensus motifs

Protein tyrosine kinases (PTKs) regulate cellular biochemistry by phosphorylating tyrosine residues that alter protein function; their substrate preferences define the topology of signaling cascades. Previous studies of PTKs have mapped their average preferences for amino acids surrounding phosphorylation sites, but their sensitivity to sequence variation remains poorly understood. Here, we used microbial biosensors for PTK activity to examine the influence of local sequence context on substrate specificity. Across five well-studied PTKs, we identified amino acid substitutions within consensus substrates that could confer sensitivity to substrate length or enhance selectivity for one PTK over others. Using a secondary decoy screen, we found sequence-diverse substrates with unexpectedly orthogonal PTK compatibilities. Our findings show how context-specific sequence features alter PTK substrate specificity far beyond what might be expected from classical consensus models and establish an experimental framework for defining the limits of substrate overlap between closely related kinases.

biochemistry↗

A tunable aqueous architecture modulates functionaloutput in biomolecular condensates

Biomolecular condensates organize cellular biochemistry, yet the principles governing their internal solvent architectures remain poorly understood. Most current models focus on macromolecular scaffolds while treating the solvent as a passive, spatially uniform background. Here, we introduce Condensate Spatial Topography via Emission Lifetimes (ConSTEL) to map the continuous solvent polarity landscape inside biomolecular condensates. Using PopZ as a model system, we show that the condensate interior contains a persistent, tunable mosaic of aqueous environments whose apparent polarity, reported by Nile Red fluorescence lifetimes, is organized by thermodynamic state and chemical cues. This microphase-separated solvent architecture defines distinct mesoscale rheological regimes, with intermediate aqueous niches supporting fast, confined tracer motion and highly polar or non-polar extremes forming a slower, viscoelastic mesh. We further demonstrate that drug-like small molecules partition non-uniformly across this landscape according to their physicochemical properties, and that exceeding local solubility limits drives "reciprocal sculpting", in which mismatched guests remodel the host solvent architecture. Together, these results highlight internal solvent organization as an active, tunable determinant of condensate material properties, molecular transport, and partitioning, and suggest that predictive models of condensate function and pharmacology would benefit from incorporating the spatial arrangement of solvent environments alongside bulk composition.

biochemistry↗

β-Ketoacyl Synthase II Homologs from a Ladderane-Producing Organism Form a Ketosynthase/Chain Length Factor-like functional heterodimer

Ladderanes are extraordinary, highly strained chemical structures consisting of linearly concatenated cyclobutane rings. Ladderane-containing fatty acids are found in the lipids of anaerobic ammonium oxidizing (anammox) bacteria, reducing the proton permeability of their membranes to support their unique metabolism. Almost nothing is known about the biosynthesis of ladderanes, but a gene cluster unique to ladderane-producing bacteria is likely to be involved. This cluster encodes radical SAM enzymes as well as homologs of enzymes known from fatty acid biosynthesis. Amongst these are two homologs of FabF, the enzyme performing chain elongation in canonical fatty acid synthesis. The presence of two chain-elongating enzymes is unexpected; a single one would be expected to suffice, and the fact that one of the two homologs has a mutated, nonfunctional catalytic triad deepens the mystery. Here we present an in-depth characterization of the FabF homologs from anammox organisms, using biochemistry, enzymology, structural biology and computational biology. We show that the two homologs form a heterodimer analogous to the ketosynthase/chain length factor complexes known from polyketide synthases. This heterodimer is capable of performing the decarboxylation of malonate-loaded acyl carrier protein, thus initiating fatty acid biosynthesis. The crystal structure of the heterodimer explains how homodimer formation is avoided, and shows the details of the substrate binding tunnel. Mechanism-based crosslinking studies of wild-type and mutant heterodimers show the influence of residues on both subunits on substrate preference (which differs from canonical FabFs), and, together with computational studies, the crystal structure of the heterodimer in complex with substrate-loaded ACP helps explain its preference for ladderane-specific ACP. The results clearly refute an early proposal for a ladderane biosynthetic mechanism and greatly expand our current knowledge on how anammox bacteria produce their extraordinary lipids.

biochemistry↗

Structural basis of substrate recognition and transport in bacterial ACS transporters

Membrane transporters of the major facilitator superfamily (MFS) mediate uptake of diverse metabolites, yet the molecular basis of substrate recognition within many bacterial families remains unclear. The anion:cation symporter (ACS) family is conserved from bacteria to humans and includes medically relevant solute carrier transporters, but only few bacterial members have been functionally characterized. Here, we combine genetics, biochemistry, transport assays, and structural biology to define the substrate specificity of five ACS transporters from Escherichia coli. Using systematic growth complementation assays in deletion strains, we assign physiological substrates to each transporter, identifying DgoT, LgoT, and ExuT as specific uptake systems for D-galactonate, L-galactonate, and galacturonate/glucuronate, respectively, while revealing overlapping roles for GarP and GudP in C6 sugar acid uptake. NanoDSF ligand binding assays show highly selective recognition of sugar acids but do not predict transport activity. Proton-coupled uptake was directly demonstrated using reconstituted proteoliposomes, defining strict stereoselectivity of LgoT and DgoT. We determined the 2.2 [A] X-ray structure of LgoT in an inward-open conformation, revealing a canonical MFS fold with a conserved but differentially tuned substrate-binding cavity. Comparative structural and sequence analyses across ACS members identify a conserved core for coordination of sugar acid carboxylate and hydroxyl groups, while localized substitutions modulate steric and electrostatic properties to enable discrimination of substrate size and stereochemistry. These results provide a framework for substrate recognition in bacterial ACS transporters and establish LgoT as a structural model for stereo-selective proton-coupled organic anion transport.

biochemistry↗