California Institute Of Technology

NIH Research Projects · FY 2025 · 2016-05

Project Summary A hallmark of living organisms is their ability to adapt to the world around them. Such adaptation takes place across many different scales in both space and time. On cellular time scales, molecules in individual cells enable them to regulate metabolic genes and thrive despite changing carbon sources. Over generations, cells evolve and adapt to stresses such as antibiotics. In the work proposed here, we will uncover principles of such adaptation over the functional hierarchy from molecules to cells to populations. To achieve this goal, our laboratory will use our tradition of integrating precise measurements with biophysical theory on specifically constructed biological systems. Our first research thrust is built on the recognition that despite the amazing successes of molecular biology and genome science over the last half century, we still know next to nothing about how genes are regulated for more than 65% of the genes in the commensal gut bacterium E. coli, which is arguably biology's best-understood organism. With this award we will create a first draft of the regulatory genome for the entire E. coli genome - including the binding energies and identities of every transcription factor and the genes or operons that they regulate. A second thrust focuses on a key way that living organisms respond to intracellular and environmental signals: through conformational changes in individual allosteric proteins and in assemblies of proteins, such as those found in the spindle responsible for chromosome segregation. Using a system we developed to finely control cytoskeleton-motor interactions using light, we seek to discover a predictive theoretical framework that guides and constrains how we view assembly and adaptation. The third thrust in our study of adaptation will build upon the previous two threads by providing a rigorous examination of how genomes and the proteins that interact with them evolve. The specific case studies will focus on the evolution of transcriptional regulation with special emphasis on the response of pathogenic bacteria to antibiotic drugs. The cell is the fundamental organizational unit of living organisms and the work proposed here will provide a far-reaching but detailed view of how cells adapt. The approach we adopt is ultimately biophysical; we insist that our analysis of the cell be at once quantitative and predictive, sharpening our questions and deepening our understanding in a way that can ultimately be parlayed into new strategies for improving human health.

NIH Research Projects · FY 2025 · 2016-05

Project Summary To enable the preparation of bioactive molecules with increased complexity, it is imperative to develop both the synthetic logic (the design concepts) and the synthetic tools (the chemical reactions) to assemble molecules with chiral centers and polycyclic frameworks. The proposed research program seeks to address this need through chemical research in two general areas. The first research area will focus on the synthesis of complex, highly oxidized, biologically active diterpenes. These total synthesis efforts inspire the invention of new reactions and investigate the ability of existing reactions to solve strategic bond constructions in complex settings. Synthetic access to these natural products will transform our ability to use them and their synthetic derivatives as biological probes or as lead compounds for the development of new medicines. The second research area will focus on the development of new Ni-catalyzed cross-electrophile coupling reactions. These reactions have emerged as versatile methods for carbon–carbon bond formation that are increasingly being adopted by chemists in academia and the pharmaceutical sectors. Despite recent advances, several challenges remain, particularly with respect to the development of catalyst-controlled stereoselective cross-electrophile coupling. To address these challenges, this research seeks to 1) identify new modes of electrophile activation to broaden the scope of products that can be prepared by Ni-catalyzed cross-electrophile coupling; 2) develop stereoselective cross-electrophile coupling reactions of small rings for medicinal chemistry and natural product synthesis; and 3) develop enantioselective CEC reactions of feedstock building blocks such as carboxylic acids and olefins. The expected outcomes of this research program are two-fold: it will provide new reactions and strategies for preparing complex polycyclic molecules, and it will provide access to medicinally relevant natural products and their derivatives. This research will be carried out by a team composed of the PI, four chemistry graduate students and one postdoctoral researcher. As part of this project, the graduate students and postdoctoral researchers will receive rigorous training in the theory, methods, and strategies of organic chemistry. The successful execution of this research will provide new tools to enable the synthesis of small molecules for the study and treatment of human disease.

NIH Research Projects · FY 2026 · 2016-02

TITLE Molecular basis of mRNA export ABSTRACT In eukaryotes, the genetic information encoded in the chromatin is stored within the nucleus. For genetic programs to be executed, folded proteins, ribonucleic acids, and assembled macromolecular complexes must be transported across the nuclear envelope. Nuclear pore complexes (NPCs) are exclusive gateways for the regulated bidirectional exchange of macromolecules between the nucleus and cytoplasm. In humans, NPCs are assembled from multiple copies of 35 different proteins known as nucleoporins (nups) that give rise to a ~1,000-protein cylindrical structure spanning the nuclear envelope with a molecular mass of ~120 million Daltons. Due to its size and flexibility, obtaining an atomic structure of the NPC has been a formidable task that we have overcome over the last two decades with a divide-and-conquer approach. This approach relies on biochemical reconstitution and nup-nup interaction mapping, along with high-resolution structure determination of nups and nup complexes, combined with lower resolution cryo-electron tomography (cryoET) and in vivo validation. These efforts have resulted in a near-atomic composite structure accounting for ~90% of the human NPC’s mass. However, critical aspects of both its structure and function remain unexplored. The NPC’s cytoplasmic face harbors nups that mediate interactions between mobile transport factors and their protein or ribonucleic acid cargoes, as well as the machinery that dismantles messenger ribonucleoprotein particles (mRNPs) as they emerge from the NPC’s central transport channel, irreversibly releasing mRNA into the cytoplasm. Notably, genetic variations in these nups are prominently associated with various human diseases, including neurodegenerative and neoplastic disorders, and heightened susceptibility to viral infections. We have previously reconstituted nup complexes of fungal NPCs’ cytoplasmic faces, enabling the systematic dissection of their nup-nup interactome. We now propose to perform an equivalent reconstitution of the human NPC’s cytoplasmic face using recombinantly expressed and highly purified proteins. Our second goal is to expand our high-resolution structural characterization to still unresolved parts of the NPC. Third, we will functionally characterize previously identified RNA-binding events involving cytoplasmic nups and the mobile RNA-transporting machinery by determining high-resolution structures and assessing their functional relevance using in vitro activity assays and cell-based assays for nucleocytoplasmic cargo transport. Finally, we will investigate the mechanism of action of the ORF6 virulence factor from SARS-CoV-2 and related sarbecoviruses. We will employ a multidisciplinary approach to gain atomic-level insights into ORF6's interactions with the NPC and the nucleocytoplasmic transport machinery, as well as the effects these interactions have on nuclear transport, mRNA export, and NPC integrity. Overall, our research will contribute to understanding the NPC’s role in mRNA export and the viral interference mechanisms targeting this process, providing atomic- level detail toward addressing this fundamental cell biological question and the molecular basis for the development of antiviral treatments.

NIH Research Projects · FY 2025 · 2014-06

In the previous grant period, we explored regulatory differences between cranial and trunk neural crest cells. Comparative transcriptomics coupled with functional perturbation revealed a premigratory “cranial-specific” neural crest GRN subcircuit that links anterior identity to ability to differentiate into facial cartilage. Here, we propose to elucidate the gene regulatory network (GRN) downstream of this cranial-specific subcircuit that confers ability to differentiate into facial skeleton. The goal is to understand the program underlying differentiation and pattern formation of craniofacial cartilage. First, we will explore regulatory changes in trunk neural crest cells after introduction of cranial crest subcircuit genes. Next, we will characterize late-migrating cranial crest cells as they condense to form facial cartilage at the single cell level to understand GRN changes as a function of time, at single cell resolution and a functional level. Finally, we propose to identify active enhancers and their direct inputs in late migrating and condensing cranial crest cells by combining in vivo electroporation of reporter constructs in the chick embryo with high throughput genomic approaches. To these ends, we will conduct the following aims: Specific Aim 1: Effects of “reprogramming” trunk neural crest cell identity. Ectopic expression of cranial crest subcircuit genes imbues trunk crest cells with chondrogenic potential after grafting to the head. Here we will: characterize transcriptional changes that occur in reprogrammed trunk crest cells over time; test the ability of reprogrammed trunk neural crest to form ectopic cartilage in their normal environment; test the ability of the cranial subcircuit to confer chondrogenic ability onto ES cells and crestosphere-derived cells. Specific Aim 2: Transcriptional profiling and functional validation of condensing cranial neural crest cells at high cell resolution using single cell RNA-seq and multiplex in situ hybridization. To gain insights into how neural crest-derived cells differentiate and what gene regulatory programs control their progression to facial skeleton, we propose to perform single cell RNA-seq of condensing cranial crest cells in the branchial arches with the goal of identifying candidate GRN components of the cartilage-forming module. We will validate expression of candidate transcription factors at high resolution and test their function using CRISPR-Cas9 knockout. Specific Aim 3: Construction of a cranial cartilage gene regulatory network (GRN) by identifying cis- regulatory elements and direct downstream targets of the cranial crest-specific subcircuit genes. In order to build regulatory linkages in branchial arch neural crest, we will characterize their chromatin landscape using low-input Assay for Transposase-Accessible Chromatin (ATAC-seq) optimized for as few as 1500 cells per replicate and perform CUT&RUN to confirm direct inputs downstream of subcircuit genes.

NIH Research Projects · FY 2026 · 2013-02

PROJECT SUMMARY A central goal in HIV/AIDS vaccine research is the elicitation of broadly neutralizing antibodies (bNAbs). During the previous funding period, the Bjorkman lab used novel design strategies to develop HIV-1 envelope (Env) trimer-based immunogens to elicit bNAbs against single and multiple epitopes, including the V3 glycan patch, CD4 binding site (CD4bs), and triple V3/CD4bs/V1V2 targets. In publications among the 32 supported by the current HIVRAD, the Bjorkman and Nussenzweig labs were the first to show that sequential immunizations with multimerized immunogens on protein nanoparticles elicited heterologous neutralizing antibodies (Abs) in inferred germline (iGL) mice, and more impressively, in wildtype (wt) animals with polyclonal Ab repertoires [mice, rabbits, and rhesus macaques (RMs)]. However, the elicited cross-neutralizing Abs did not confer protection from heterologous viral challenge, due at least in part to increasing off-target responses following multiple boosts and the failure of the cross-neutralizing Abs to affinity mature to achieve high potency, breadth, and durability. This led to the discovery by Nussenzweig of Ab feedback and epitope masking, which attenuate focused B cell responses, a concept now becoming entrenched in the HIV-1 vaccine field. The goal of this renewal application is to build on these fundamental discoveries and design more strategic and effective priming and boosting immunogens. To accomplish this, we added a third collaborating research team (Hahn/Shaw/Weissman) that brings expertise in the SHIV model of bNAb induction and mRNA immunogen design. We will gain unique synergies from these highly collaborative research teams as follows: Project 1 (Bjorkman) will design next-generation prime and boost immunogens based on structural and biophysical analyses of GL-targeted and lineage-based Env-Ab recognition from Project 2; Project 2 (Hahn/Shaw/Weissman) will decipher molecular pathways of Env-Ab coevolution shared among different SHIV- infected RMs that develop neutralization breadth as a “molecular guide” for novel lineage-based immunogen design in Project 1 and will test these new protein nanoparticle and mRNA vaccine platforms for immunogenicity and protection in RMs; and Project 3 (Nussenzweig) will delineate the impacts of Ab feedback, epitope masking, and T follicular helper (Tfh) cell repertoire on enhancing or attenuating on-target B cell responses. These projects will be enabled by a Protein Expression and Automated Assays Core A (Vielmetter) and an Administrative Core B (Bjorkman). Our hypothesis is that by incorporating lineage-based Env “immunotypes” that elicited bNAbs in SHIV infected RMs in novel nanoparticle and mRNA-LNP vaccine designs (Projects 1 and 2) and by modulating epitope masking and Tfh responses in germinal centers (Projects 1 and 3), we can develop new prime and boost immunogens that lead to neutralization breadth, potency, and durability in wt animals. Achieving this goal would represent a major scientific advance directly translatable to vaccine efforts in humans.

NIH Research Projects · FY 2026 · 2002-12

Project Summary/Abstract Carbohydrates (also known as glycans) comprise one of the largest, most diverse collections of biologically active molecules. However, relative to other biomolecules such as nucleic acids and proteins, carbohydrates remain poorly understood due to challenges in their detection, synthesis, and analysis. The broad objective of this program is to develop chemical approaches to advance a fundamental understanding of the roles of carbohydrates in biology and disease. In the last granting period, we developed a novel Networking of Interactors and SubstratEs (NISE) method to study the biological functions of O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation. O-GlcNAc is an abundant, essential post-translational modification that is emerging as a key regulator of many physiological functions, ranging from epigenetic and transcriptional gene regulation to insulin signaling, cancer cell metabolism, and neurodegeneration. Our NISE approach combines new chemoproteomic tools, genetic engineering, mass spectrometry analysis, and bioinformatics methods to quantitatively profile O- GlcNAc sites and O-GlcNAc transferase (OGT) interactors across the proteome and to determine key interconnections between the interactors and substrates. The resulting networks have revealed novel, unexpected functions for O-GlcNAc and highlighted potential mechanisms to explain the unique specificity of OGT. In the coming granting period, we will expand on this approach and investigate the roles of O- GlcNAcylation in neurons and in the context of neurodegenerative diseases as we continue to tackle the next critical barriers in the field. In Aim 1, we will focus on understanding how O-GlcNAcylation within intrinsically disordered, low-complexity domains of proteins affects their functions and alters biomolecular condensate (BMC) formation, composition, and dynamics. These studies should provide new paradigms and methods for understanding the fundamental mechanisms by which O-GlcNAc regulates proteins and its role in aberrant BMC activity linked to Alzheimer’s disease and related dementias (AD/ADRDs). In Aim 2, we will test specific hypotheses revealed by our NISE networks regarding the regulation of OGT activity at neuronal synapses and specifically toward proteins implicated in AD/ADRDs. In Aim 3, we will apply our NISE method to examine directly how O-GlcNAcylation of specific proteins and pathways becomes dysregulated during AD pathogenesis and with disease-specific mutations by using patient-derived induced pluripotent stem cells (iPSCs) and human AD brain samples. Together, the proposed studies will provide a powerful approach to identify and understand physiologically important and/or disease-causing O-GlcNAcylation events. In turn, this information is expected to provide new potential therapeutic targets and/or strategies to combat progressive neurodegeneration and AD/ADRDs.

NIH Research Projects · FY 2025 · 2000-07

Project Summary We will continue to develop WormBase, a broadly and often daily-used knowledgebase of information about the C. elegans genome, genes, sequence features, gene function, gene interactions, and related information. C. elegans is a premier research organism with about 1500 registered laboratories worldwide who use the short generation time, complete genome, efficient genome editing, defined anatomy and neuroanatomy to study a wide range of biomedical and fundamental topics. WormBase also curates, stores, and displays information about nine other nematode genomes of biomedical importance. We will continue to develop necessary ontologies and gene nomenclature to support systematic annotation of the genome and gene function and expression. After 20 years of independent infrastructure development, we will now use the Alliance of Genome Resources infrastructure for data ingest, storage, efficient curation, and presentation via download, API, and web portal. We will complete the migration of the software infrastructure by the second year. This project will focus on curation of genome scale datasets and individual experiments from the literature as well as storage and display of C. elegans- or nematode-specific data. A major challenge is the increased published data and datasets and decreased staff, which we will proactively address by streamlining and making our systems more automated and high throughput. Our main strategies for scaling curation are by increased automation, namely machine learning (ML) and artificial intelligence (AI); and by community input powered by ML/AI, also incentivized by microPublication-based reviews of pathways and genes. As we are trying to scale, while maintaining our very high-quality data collection (which is re-used by many other bioinformatic resources), professional biocurators with a deep understanding of the biology and researchers needs will increasingly focus on data modeling, quality control, development and training of automated systems, and supporting community curation. We will curate information directly tied to nucleic acid sequence including the genome sequence; sequence features such as gene structure models, regulatory regions, variants, sequence-based reagents, genome-scale experiments; and gene expression including reporter gene assays and RNA-seq, sc-RNA-seq. We will curate information centered on gene function including phenotype of variants and perturbations, disease models, genetic and physical interactions, Gene Ontology (GO) annotations, and pathways using GO-Causal Activity Models. After we transition computational infrastructure to the Alliance, we will continue to curate datasets unique to C. elegans and add them to the Alliance infrastructure. We will support researchers by a 24/7 help desk, which provides advice and often analysis; curation, storage, and display of worm-specific datasets; provision of customized analysis tools; and a community forum. For new data, we will specify software requirements for development at the Alliance.

NIH Research Projects · FY 2025 · 1995-02

Project Summary/Abstract Regulated proteolysis by the ubiquitin-proteasome system (ubiquitin system) plays essential roles in a multitude of biological processes and has major ramifications for human health and disease, including illnesses that range from cancer and neurodegeneration to cardiovascular syndromes and defects of immunity. Our studies of the ubiquitin-proteasome system and ubiquitin-dependent N-degron pathways (previously called “N-end rule pathways”) over more than three decades were made possible, to a large extent, by the present grant (DK039520), currently in its 34th year of support. N-degron pathways recognize proteins containing N-terminal (Nt) degradation signals called N-degrons, polyubiquitylate these proteins and thereby cause their degradation by the proteasome or autophagy. Recognition components of N-degron pathways, called N-recognins, are E3 ubiquitin ligases that can target N-degrons. One eukaryotic N-degron pathway, called the Arg/N-degron pathway, targets, in particular, specific unmodified Nt-residues of protein substrates. Another Nt-proteolytic system, called the Pro/N-degron pathway, recognizes, in particular, the Nt-proline (Pro) residue of protein substrates. This DK039520 renewal application stems from our unpublished studies over the last ~2 years, and focuses on the yeast (S. cerevisiae) Pro/N-degron and Arg/N-degron pathways, including the functions of specific aminopeptidases and the recently discovered ability of Ubr1, the E3 of the Arg/N-degron pathway, to target not only N-degrons but also C-degrons. These and related studies, described in Specific Aims of the DK039520 renewal application, will advance the understanding of protein degradation and the universally present (as well as medically significant) N-degron pathways.

NIH Research Projects · FY 2026 · 1992-07

Project Summary/Abstract Regulated proteolysis by the ubiquitin-proteasome system (ubiquitin system) plays essential roles in a multitude of biological processes and has major ramifications for human health and disease, including illnesses that range from cancer and neurodegeneration to cardiovascular syndromes and defects of immunity. Our studies of the ubiquitin-proteasome system and ubiquitin-dependent N-degron pathways (previously called “N-end rule pathways”) over more than three decades were made possible, to a large extent, by the present grant (GM031530), currently in its 41st year of support. N-degron pathways recognize proteins containing N-terminal (Nt) degradation signals called N-degrons, polyubiquitylate these proteins and thereby cause their degradation by the proteasome or autophagy. Recognition components of N-degron pathways, called N-recognins, are E3 ubiquitin ligases that can target N-degrons. One eukaryotic N-degron pathway, called the Arg/N-degron pathway, targets, in particular, specific unmodified Nt-residues of protein substrates. This GM031530 renewal application stems from our unpublished studies over the last ~2 years, and focuses on new, previously unexplored aspects of the Arg/N-degron pathway. Specific proposed studies address a coupling between a C-degron and stability of a protein’s mRNA, the new phenomenon of superchanneling in targeting specific degrons, and a functional (as well as mechanistic) link between human caspases and the Arg/N-degron pathway. Our studies of this universally present proteolytic system will contribute to advances in fundamental biology and may also lead to therapies for specific human diseases.

NIH Research Projects · FY 2026 · 1990-01

Project Summary/Abstract In both invertebrate and vertebrate nervous systems, cell recognition molecules control assembly of synaptic circuits during development. We discovered a network of interacting cell surface proteins (CSPs) through an in vitro binding (“interactome”) screen for interactions among all Drosophila immunoglobulin superfamily (IgSF) proteins. In this network, 11 DIP proteins in one IgSF subfamily interact with 21 Dpr proteins in another subfamily, with affinities ranging from 1 µM to 200 µM. Each DIP and Dpr is expressed by a unique subset of neurons in each area of the developing brain. The connectome of the Drosophila pupal optic lobe (OL) is assembled by activity-independent mechanisms. DIP::Dpr interactions are important for OL and neuromuscular system wiring, and loss of individual DIPs or Dprs can alter synaptic connectivity and cause neuronal death. In this proposal, we address the functions of affinity variation and avidity by examining how changes in DIP::Dpr binding affinity and expression level affect synaptic terminal development in the neuromuscular system and synaptic connectivity in the OL. We also examine other interaction networks that may be involved in determination of the optic lobe connectome. Two such networks are the Beat/Side network of 22 IgSF proteins, which we also discovered in the interactome screen, and a network of ligands for receptor tyrosine phosphatases (RPTPs), which are neuronal signaling receptors that regulate axon guidance and synaptogenesis. We will examine how these three networks work together in vivo to control synaptic connectivity between specific lamina and medulla neurons in the OL. We will generate a comprehensive map of interactions and measure binding affinities for all of the Beat/Side proteins using surface plasmon resonance. To validate interactions in the RPTP network and identify inter-network interactions, we will develop a method for multiplexed interactome screening using high-avidity 60-mer nanoparticles that may be able to identify lower-affinity interactions missed in earlier screens. The objectives of the present application are to define how the affinities of DIP::Dpr interactions affect synaptic connection patterns, to examine how DIPs and Dprs work together with other families of cell recognition molecules, and to develop improved methods to detect and characterize in vitro interactions among CSPs. We plan to attain these objectives through three Specific Aims. Aim 1: Define the functions of DIP::Dpr affinity variation in control of muscle innervation. Aim 2: Examine the roles of DIP::Dpr affinity and of interplay among cell adhesion and signaling molecules in determination of synaptic connectivity in the OL. Aim 3: Map in vitro interactions among Beats, Sides, RPTPs, and other CSPs. The expected outcome of the proposed research will be the acquisition of new insights into the mechanisms by which interactions among cell recognition molecules control the assembly of neural circuits. This will have a significant positive impact by increasing our understanding of conserved mechanisms involved in nervous system development, some of which are affected by disease.

NIH Research Projects · FY 2025 · 1979-05

Oxygenase and oxidase enzymes must coordinate the delivery of four protons and four electrons to O2 to prevent the formation of harmful reactive oxygen species. The risks posed by reactive intermediates are so great that aerobic organisms need mechanisms to protect oxygen-utilizing enzymes from inactivation when primary electron/proton transfer mechanisms are disrupted. Radical transfer pathways that deliver oxidizing equivalents (holes) away from frustrated reactive intermediates in enzyme active sites to the protein surface for reaction with intracellular antioxidants can provide such protection. These radical transfer pathways are constructed from chains of tryptophan (W), tyrosine (Y), cysteine (C), and possibly methionine (M) residues. This research will focus on cytochromes P450 (P450) and Streptomyces coelicolor small laccase (SLAC). The cytochromes P450 are members of a superfamily of heme oxygenases involved in xenobiotic metabolic and biosynthetic pathways. In mammals these functions include drug metabolism, conversion of lipophilic molecules to more polar products for enhanced elimination, steroid biosynthesis, and eicosanoid synthesis and degradation. Cytochromes P450 also are responsible for 66% of enzymatic activation of carcinogens. Elucidating the mechanisms by which P450s avoid inactivation in the presence of diverse substrates can contribute to defining therapeutic drug efficacies and mitigating the risks of adverse drug-drug interactions. Chains of W and Y residues in three bacterial P450s have been characterized for their potential as protective electron transport conduits. The protective roles of individual amino acids in W/Y chains of the three cytochromes P450 will be evaluated in measurements of the total number of turnovers before enzyme deactivation. The mechanism of protection will be elucidated using colorimetric redox indicators bound near the surface termini of W/Y chains. These indicators will report on the arrival of holes at the end of a W/Y chain in single-turnover stopped-flow kinetics measurements. Evidence is emerging from in vitro studies of P. megaterium P450BM3 that hole transport along W/Y chains can extend the functional life of the enzyme. Research in this program aims to establish whether the extended P450BM3 survival resulting from these chains provides any measurable advantage to the bacterium. Preliminary studies of a P450BM3 deletion mutant of P. megaterium have identified a phenotype attributable to the enzyme. Investigations of wild-type and mutant P. megaterium strains aim to determine whether disruption of W/Y chains negatively impacts growth of the organism. The multicopper oxidase SLAC and human ceruloplasmin are structurally homologous enzymes in which a Tyr radical forms during catalysis. SLAC will be used as a surrogate for ceruloplasmin, owing to its efficient heterologous expression in E. coli. Measurements of the total number of turnovers in wild-type and mutant enzymes aim to elucidate the roles of W and Y radicals in SLAC catalysis.

Other NSERC · FY 2024

symbolic dynamics, dynamical systems, amenable groups, mathematical analysis, functional analysis, amenability

Other NSERC · FY 2024

Active metasurfaces, Non-local metasurfaces, Inverse design/optimization, Electromagnetic field simulation, Machine learning

Other NSERC · FY 2024

Organic Synthesis, Catalysis, Asymmetric Catalysis, Cross-coupling

Other NSERC · FY 2024

Atmospheric chemistry, Heterocyclic molecules, Formation mechanism, Spectroscopy, Planetary sciences, Titan, Quantum calculations, Astrochemistry, Resonance stabilized radicals

Other NSERC · FY 2024

Nanophotonics, 2D Materials, Spatial Light Modulators, Nanofabrication, Augmented and Virtual Reality, Optics, Beam Steering, Physics, Communications, Biosensing

Other NSERC · FY 2024

inorganic chemistry, quantum information science, molecular sensing, electron paramagnetic resonance, electrochemistry, surface science, physical chemistry

Other NSERC · FY 2024

dynamic metasurfaces, flat optics, opto-electronics, radio frequency (RF) devices, nanotechnology, plasmonics

Other NSERC · FY 2024

Medical devices, Soft electronics, Biosensors, Molecularly imprinted polymers, Bioelectronic medicine, Implantable device, Inflammation, Hypertension, Heart failure

Other NSERC · FY 2024

cosmology, galaxy surveys, large-scale structure, general relativity, primordial non-Gaussianity, inflation, galactic foregrounds

Other NSERC · FY 2024

aerospace, transpiration cooling, thermal protection system, fluid mechanics, computational fluid dynamics, combustion, turbulence, reactive flow, porous media, multi-physics

Other NSERC · FY 2024

Other NSERC · FY 2024

electrochemistry, thermodynamic physics, chemistry, chemical kinetics

Other NSERC · FY 2024

protein engineering, gas vesicles, acoustic reporter genes, directed evolution, ultrasound imaging, multiplexed imaging, deep tissue imaging, machine learning, genetic engineering, protein binding

Other NSERC · FY 2024

Natural Product Synthesis, Enantioselective Synthesis, Homogenous Catalysis, Synthetic Chemistry, Total Synthesis, Convergent Synthesis, Alkaloids