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Goyal, P.

Publications and source records attributed to Goyal, P..

13 recordsLinked to original sources

A Kinetic Scout Approach Accelerates Targeted Protein Degrader Development

Bifunctional molecules such as targeted protein degraders induce proximity to promote gain-of-function pharmacology. These powerful approaches have gained broad traction across academia and the pharmaceutical industry, leading to an intensive focus on strategies that can accelerate their identification and optimization. We and others have previously used chemical proteomics to map degradable target space, and these datasets have been used to develop and train multiparameter models to extend degradability predictions across the proteome. In this study, we now turn our attention to develop generalizable chemistry strategies to accelerate the development of new bifunctional degraders. We implement lysine-targeted reversible-covalent chemistry to rationally tune the binding kinetics at the protein-of-interest across a set of 25 targets. We define an unbiased workflow consisting of global proteomics analysis, IP/MS of ternary complexes and the E-STUB assay, to mechanistically characterize the effects of ligand residence time on targeted protein degradation and formulate hypotheses about the rate-limiting step of degradation for each target. Our key finding is that target residence time is a major determinant of degrader activity, and this can be rapidly and rationally tuned through the synthesis of a minimal number of analogues to accelerate early degrader discovery and optimization efforts.

pharmacology and toxicology↗

Molecular determinants of Neu5Ac binding to tripartite ATP independent periplasmic (TRAP) transporter

N-Acetylneuraminic acid (Neu5Ac) is a negatively charged nine-carbon amino-sugar that is often the peripheral sugar in human cell-surface glycoconjugates. Some bacteria scavenge, import, and metabolize Neu5Ac or redeploy it on their cell surfaces for immune evasion. The import of Neu5Ac by many bacteria is mediated by tripartite ATP-independent periplasmic (TRAP) transporters. We have previously reported the structures of SiaQM, a membrane-embedded component of the Haemophilus influenzae TRAP transport system, (Currie et al., 2024). However, none of the published structures contain Neu5Ac bound to SiaQM. This information is critical for defining the transport mechanism and for further structure-activity relationship studies. Here, we report the structures of Fusobacterium nucleatum SiaQM with and without Neu5Ac. Both structures are in an inward (cytoplasmic side) facing conformation. The Neu5Ac-bound structure reveals the interactions of Neu5Ac with the transporter and its relationship with the Na+ binding sites. Two of the Na+-binding sites are similar to those described previously. We identify a third metal-binding site that is further away and buried in the elevator domain. Ser300 and Ser345 interact with the C1-carboxylate group of Neu5Ac. Proteoliposome-based transport assays showed that Ser300-Neu5Ac interaction is critical for transport, whereas Ser345 is dispensable. Neu5Ac primarily interacts with residues in the elevator domain of the protein, thereby supporting the elevator with an operator mechanism. The residues interacting with Neu5Ac are conserved, providing fundamental information required to design inhibitors against this class of proteins.

biochemistry↗

A TBX5-dependent compartment boundary patterns the cardiac interventricular septum

Failure of septation of the interventricular septum (IVS) is the most common congenital heart defect (CHD), but mechanisms for patterning the IVS are largely unknown. Here, we show that a Tbx5+/Mef2cAHF+ progenitor lineage forms a compartment boundary bisecting the IVS. This coordinated population originates at a first- and second heart field interface. Ablation of Tbx5+/Mef2cAHF+ progenitors cause IVS disorganization, right ventricular hypoplasia and mixing of IVS lineages. Reduced dosage of the CHD transcription factor TBX5 disrupts boundary position and integrity, resulting in ventricular septation defects (VSDs) and patterning defects, including misexpression of Slit2 and Ntn1, which encode guidance cues. Reducing NTN1 dosage partly rescues cardiac defects in Tbx5 mutant embryos. Loss of Slit2 or Ntn1 causes VSDs and perturbed septal lineage distributions. Thus, we identify Tbx5 as a candidate selector gene, directing progenitors and regulating essential cues, to pattern a compartment boundary for proper cardiac septation, revealing mechanisms for cardiac birth defects.

developmental biology↗

Mosquitoes escape looming threats by actively flying with the bow-wave induced by the attacker

To detect and escape from a looming threat, night-flying insects must rely on other senses than vision alone. Nocturnal mosquitoes have been described to escape looming objects in the dark, but how they achieve this is still unknown. Here, we show how night-active female malaria mosquitoes escape from a rapidly looming object that simulates the defensive action of a blood-host. By combining videography-based automatic tracking with numerical simulations of the attacker-induced airflow, we first show that night-flying mosquitoes use airflow-sensing to detect the danger and trigger their escape. Secondly, by combining these data with mechanistic movement modelling, we unravelled how mosquitoes control their escape manoeuvres: they actively steer away from the danger, and passively travel with the bow-wave produced by the attacker. Our results demonstrate that night-flying mosquitoes escaping from a looming object use the object-induced airflow both to detect the danger, and as fluid medium to move with for avoiding collision. This shows that the escape strategy of flying insects is more complex than previous visually-induces escape flight studies suggest. As mosquitoes are average-sized insects, a combined airflow-induced and visual-induced escape strategy is expected to be common amongst millions of flying insect species. Also, our research helps explain the high escape performance of mosquitoes from counterflow-based odour-baited mosquito traps. It can therefore provide new insights for the development of novel trapping techniques for integrative vector management.

zoology↗

A Biotin Targeting Chimera (BioTAC) System to Map Small Molecule Interactomes in situ

Unbiased chemical biology strategies for direct readout of protein interactome remodelling by small molecules provide advantages over target-focused approaches, including the ability to detect previously unknown targets, and the inclusion of chemical off-compete controls leading to high-confidence identifications. We describe the BioTAC system, a small-molecule guided proximity labelling platform, to rapidly identify both direct and complexed small molecule binding proteins. The BioTAC system overcomes a limitation of current approaches, and supports identification of both inhibitor bound and molecular glue bound complexes.

pharmacology and toxicology↗

Bumblebees actively compensate for the adverse effects of sidewind during visually-guided landings

Flying animals often encounter winds during visually guided landings. However, how winds affect their flight control strategy during landing is unknown. Here, we investigated how sidewind affects the landing strategy, sensorimotor control, and landing performance of foraging bumblebees (Bombus terrestris). For this, we trained a hive of bumblebees to forage in a wind tunnel, and used high-speed stereoscopic videography to record 19,421 landing flight maneuvers in six sidewind speeds (0 to 3.4 m s-1), which correspond to winds encountered in nature. Bumblebees landed less often in higher windspeeds, but the landing duration from free flight was not increased by wind. We then tested how bumblebees adjusted their landing control to compensate for the adverse effects of sidewind on landing. This showed that the landing strategy in sidewind was similar to that in still air, but with important adaptations. In the highest windspeeds, more hover phases occurred than during landings in still air. The rising hover frequency did not increase landing duration because bumblebees flew faster in between hover phases. Hence, they negated the adverse effects of increased hovering in high windspeeds. Using control theory, we revealed how bumblebees integrate information from the wind-mediated mechanosensory modality with their vision-based sensorimotor control loop. The proposed multi-sensory flight control system may be commonly used by insects landing in windy conditions and it may inspire the development of landing control strategies onboard man-made flying systems. Summary statementBumblebees foraging in strong sidewinds can still land precisely on artificial flowers, allowing them to be efficient and robust pollinators in these adverse environmental conditions.

animal behavior and cognition↗

Computational and biochemical analyses reveal that cofilin-2 self assembles into amyloid-like structures and promotes the aggregation of other proteinaceous species: Pathogenic relevance to myopathies

Cofilin-2 is a member of the ADF/cofilin family, expressed extensively in adult muscle cells and involved in muscle maintenance and regeneration. Phosphorylated cofilin-2 is found in pre-fibrillar aggregates formed during idiopathic dilated cardiomyopathy. A recent study shows that phosphorylated cofilin-2, under oxidative distress, forms fibrillar aggregates. However, it remains unknown if cofilin-2 holds an innate propensity to form amyloid-like structures. In the present study, we employed various computational and biochemical techniques to explore the amyloid-forming potential of cofilin-2. We report that cofilin-2 possesses aggregation-prone regions (APRs), and these APRs get exposed to the surface, become solvent-accessible, and are involved in the intermolecular interactions during dimerization, an early stage of aggregation. Furthermore, the cofilin-2 amyloids, formed under physiological conditions, are capable of cross-seeding other monomeric globular proteins and amino acids, thus promoting their aggregation. We further show that Cys-39 and Cys-80 are critical in maintaining the thermodynamic stability of cofilin-2. The destabilizing effect of oxidation at Cys-39 but not that at Cys-80 is mitigated by Ser-3 phosphorylation. Cysteine oxidation leads to partial unfolding and loss of structure, suggesting that cysteine oxidation further induces early events of cofilin-2 aggregation. Overall, our results pose a possibility that cofilin-2 amyloidogenesis might be involved in the pathophysiology of diseases, such as myopathies. We propose that the exposure of APRs to the surface could provide mechanistic insight into the higher-order aggregation and amyloidogenesis of cofilin-2. Moreover, the cross-seeding activity of cofilin-2 amyloids hints towards its involvement in the hetero-aggregation in various amyloid-linked diseases.

biochemistry↗

Mechanistic insights into global suppressors of protein folding defects

Most amino acid substitutions in a protein either lead to partial loss of function or are near neutral. Several studies have shown the existence of second-site mutations that can rescue defects caused by diverse loss of function mutations. Such global suppressor mutations are key drivers of protein evolution. However, the mechanisms responsible for such suppression remain poorly understood. To address this, we characterized multiple suppressor mutations both in isolation and in combination with inactive mutants. We examined six global suppressors of the bacterial toxin CcdB, the known M182T global suppressor of TEM-1 {beta}-lactamase, the N239Y global suppressor of p53-DBD and three suppressors of the SARS-CoV-2 spike Receptor Binding Domain. The suppressors both alone, and in conjunction with inactive mutants, stabilise the protein both thermodynamically and kinetically in-vitro, predominantly through acceleration of the refolding rate. When coupled to inactive mutants they promote increased in-vivo solubilities as well as regain-of-function phenotypes. In the case of CcdB, where novel suppressors were isolated, we determined the crystal structures of three such suppressors to obtain insight into the specific molecular interactions responsible for the observed effects. While most individual suppressors result in small stability enhancements relative to wildtype, which can be combined to yield significant stability increases, thermodynamic stabilisation is neither necessary nor sufficient for suppressor action.

biophysics↗

Computational investigation for modelling the protein-protein interaction of TasA(28-261)with TapA(33-253); a decisive process in biofilm formation by Bacillus subtilis

Biofilms have significant role in microbial persistence, antibiotic resistance and chronic infections; consequently, there is a pressing need for development of novel "anti-biofilm strategies". One of the fundamental mechanisms involved in biofilm formation is protein-protein interactions of amyloid like proteins (ALPs) in extracellular matrix. Such interactions could be potential targets for development of novel anti-biofilm strategies; therefore, assessing the structural features of these interactions could be of great scientific value. Characterization of biomolecular interaction with conventional structure biology tools including X-Ray diffraction and Nuclear Magnetic Resonance is technically challenging, expensive and time-consuming. In contrast, modelling such interactions is time-efficient, economical and might provide deeper understanding of structural basis of interactions. Therefore, during the present study, protein-protein interaction of TasA(28-261)-TapA(33-253) (which is a decisive process for biofilm formation by Bacillus subtilis) was modeled using in silico approaches viz., molecular modelling, protein-protein docking and molecular dynamics simulations. Results identified amino-acid residues present within intrinsically disordered regions of both proteins to be critical for interaction. These results were further supported with PCA and FEL analyses. Results presented here represent novel finding and we hypothesize that aa identified during the present study could be targeted for inhibition of biofilm formation by B. subtilis.

bioinformatics↗

A TBX5 dosage-sensitive gene regulatory network for human congenital heart disease

Haploinsufficiency of transcriptional regulators causes human congenital heart disease (CHD). However, underlying CHD gene regulatory network (GRN) imbalances are unknown. Here, we define transcriptional consequences of reduced dosage of the CHD-linked transcription factor, TBX5, in individual cells during cardiomyocyte differentiation from human induced pluripotent stem cells (iPSCs). We discovered highly sensitive dysregulation of TBX5-dependent pathways-- including lineage decisions and genes associated with cardiomyocyte function and CHD genetics--in discrete subpopulations of cardiomyocytes. GRN analysis identified vulnerable nodes enriched for CHD genes, indicating that cardiac network stability is sensitive to TBX5 dosage. A GRN-predicted genetic interaction between Tbx5 and Mef2c was validated in mouse, manifesting as ventricular septation defects. These results demonstrate exquisite sensitivity to TBX5 dosage by diverse transcriptional responses in heterogeneous subsets of iPSC-derived cardiomyocytes. This predicts candidate GRNs for human CHDs, with implications for quantitative transcriptional regulation in disease.

developmental biology↗

Coiled-coil registry shifts in the F684I mutant of Bicaudal result in cargo-independent dynein recruitment

The dynein adaptor Drosophila Bicaudal D (BicD) is auto-inhibited and activates dynein motility only after cargo is bound, but the underlying mechanism is elusive. In contrast, we show that the full-length BicD/F684I mutant activates dynein processivity even in the absence of cargo. Our X-ray structure of the C-terminal domain of the BicD/F684I mutant reveals a coiled-coil registry shift; in the N-terminal region, the two helices of the homodimer are aligned, whereas they are vertically shifted in the wild-type. One chain is partially disordered and this structural flexibility is confirmed by computations, which reveal that the mutant transitions back and forth between the two registries. We propose that a coiled-coil registry shift upon cargo binding activates BicD for dynein recruitment. Moreover, the human homolog BicD2/F743I exhibits diminished binding of cargo adaptor Nup358, implying that a coiled-coil registry shift may be a mechanism to modulate cargo selection for BicD2-dependent transport pathways.

biophysics↗

Role of coiled-coil registry shifts in activation of human Bicaudal D2 for dynein recruitment upon cargo-binding

Dynein adaptors such as Bicaudal D2 (BicD2) recognize cargo for dynein-dependent transport. BicD2-dependent transport pathways are important for brain and muscle development. Cargo-bound adaptors are required to activate dynein for processive transport, but the mechanism of action is elusive. Here, we report the structure of the cargo-binding domain of human BicD2 that forms a dimeric coiled-coil with homotypic registry, in which both helices are aligned. To investigate if BicD2 can switch to an asymmetric registry, where a portion of one helix is vertically shifted, we performed molecular dynamics simulations. Both registry types are stabilized by distinct conformations of F743. For the F743I variant, which increases dynein recruitment in the Drosophila homolog, and for the human R747C variant, which causes spinal muscular atrophy, spontaneous coiled-coil registry shifts are observed, which may cause the BicD2-hyperactivation phenotype and disease. We propose that a registry shift upon cargo-binding activates auto-inhibited BicD2 for dynein recruitment.\n\nHighlightsO_LIStable, bona fide BicD2 coiled-coils with distinct registries can be formed.\nC_LIO_LIWe provide evidence that a human disease mutation causes a coiled-coil registry shift.\nC_LIO_LIA coiled-coil registry shift could relieve BicD2-autoinhibition upon cargo-binding.\nC_LIO_LIThe ability to undergo registry shifts may be an inherent property of coiled-coils.\nC_LI\n\nIn BriefOur results support that stable coiled-coils of BicD2 with distinct registries can be formed, and suggest a molecular mechanism for such registry switches. We provide evidence that disease-causing mutations in coiled-coils may alter the equilibrium between registry-shifted conformers, which we propose as a general mechanism of pathogenesis for coiled-coils.\n\nGraphical Abstract O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY

biophysics↗

Patterns of Treatment in Patients with Heart Failure with Preserved Ejection Fraction: the REasons for Geographic And Racial Differences in Stroke study

PurposeWe described medication use patterns among REasons for Geographic And Racial Differences in Stroke (REGARDS) participants hospitalized for heart failure with preserved ejection fraction (HFpEF) (152 hospitalizations, 101 unique individuals).\n\nMethodsMedication data were obtained from medical record review and Medicare Part D pharmacy claims. We compared discharge medication prescriptions between patients with and without chronic kidney disease (CKD), coronary heart disease (CHD), chronic obstructive pulmonary disease (COPD), and diabetes.\n\nResultsThe mean age was 74.8 years, 53.3% were black and 73.7% were female. Hypertension (97.2%), diabetes (65.1%), COPD (51.3%), CKD (41.1%) and history of CHD (60.9%) were common. On admission and discharge, respectively, beta-blockers (66.4%, 72.7%), angiotensin converting enzyme inhibitors or angiotensin receptor blockers (42.8%, 51.7%), diuretics (61.2%, 80.9%), loop diuretics (55.9%, 78.3%), calcium channel blockers (41.0%, 41.2%) and statins (44.7%, 50.3%) were commonly used. Spironolactone, digoxin, hydralazine plus isosorbide dinitrate (HISDN), isosorbide dinitrate alone and aldosterone receptor antagonists were used by <20%. For each medication, prescriptions were more common at discharge than admission. Many participants did not have Medicare claims for filled prescriptions in the year following discharge. A higher percentage of patients with versus without CKD, CHD, and diabetes had discharge prescriptions statins. Participants with CKD were also more likely to receive prescriptions for HISDN.\n\nConclusionBeta-blockers and diuretics were commonly prescribed at admission and discharge among HFpEF, but pharmacy claims for these medications within one-year were substantially less common. The comorbidities CHD, CKD, and diabetes were associated with prescriptions of statins at discharge.

epidemiology↗