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Giri, P.

Publications and source records attributed to Giri, P..

5 recordsLinked to original sources

Genetic Code Expansion for Site-Specific Encoding of a Switchable, Intrinsic Fluorophore-Quencher Pair to Monitor Protein Dynamics

Precisely modifying proteins at multiple sites in their native, folded structures offers unique opportunities to answer molecular and cellular-level biological questions. Here, we present a genetic code expansion strategy for site-specific integration of a fluorophore-quencher pair comprising two non-canonical amino acids--acridonylalanine (Acd) and methyltetrazinyl phenylalanine (Tet) -- into a protein expressed in E. coli. The Acd and Tet pair requires no post-translational labeling, and quenching can be switched off by biorthogonal or photochemical reactions of Tet for convenient internal control experiments. Mechanistic studies based on Stern-Volmer quenching, fluorescence lifetime measurements, and "proline ruler" peptides established the distance dependence of quenching. As proof-of-concept, we applied this strategy to study: 1) calmodulin, a calcium-sensing protein, 2) RecA, a DNA damage sensor in bacteria, and 3) LexA, a transcriptional repressor whose activation by RecA governs acquired antibiotic resistance in bacteria. Using these proteins, we demonstrate that dual Acd/Tet labeling provides molecular-level insights into protein dynamics, enables high-throughput drug screening, and advances tools for studying protein structure-function relationships.

biochemistry↗

Cryo-ET reveals nanoscale thick filamentdisorganization in MYH7 P710R hypertrophiccardiomyopathy cardiomyocytes

Hypertrophic cardiomyopathy (HCM) is the most common monogenic inherited heart disease and is a major cause of sudden death in individuals under 35 years of age. HCM is associated with progressive tissue-level disarray and subcellular disorganization in individual cardiomyocytes. Mutations in {beta}-cardiac myosin (MYH7), the second most common genetic cause of HCM, commonly result in changes in sarcomeric force production, but how this leads to altered cell- and tissue-level organization is unclear. Here, we use cryo-electron tomography (cryo-ET) to bridge the molecular and cellular scales by visualizing the nanoscale organization of individual myosin-containing thick filaments within sarcomeres of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Compared to isogenic wild-type controls, hiPSC-CMs expressing P710R MYH7 exhibit pronounced disruption of the hexagonal packing of thick filaments within individual sarcomeres, which would be difficult to visualize using conventional light microscopy or even room-temperature electron microscopy. We also observe ribosome infiltration into areas of sarcomeric disorder for both wild-type and P710R MYH7 hiPSC-CMs, suggesting that disordered regions may be sites of local proteostasis or remodeling. Together, these data illuminate how altered myosin activity can propagate to yield dramatic changes in sarcomeric organization in HCM.

cell biology↗

Identification and functional characterization of LDB3 gene variants in DCM patients from Indian Population

The LIM domain-binding protein 3 (LDB3), also known as Z-band alternatively spliced protein (ZASP), is a key component of the Z-disc, essential for maintaining sarcomeric integrity and transmitting contractile force in cardiomyocytes. Genetic variants in LDB3 have been implicated in cardiomyopathies, including dilated cardiomyopathy (DCM). In this study, we have screened 100 idiopathic DCM cases along with controls by Sanger sequencing and identified nine non-synonymous (p.S184I, p.D193N, p.K204R, p.R229C, p.P295T, p.Q402P, p.F465I, p.F496L, p.P606S), seven synonymous (p.T91=, p.A152=, p.D168=, p.S182=, p.A279=, p.S347=, p.A358=), and seven intronic (c.322-50G>C, c.548+53A>C, c.718+47G>C, c.718+81G>A, c.755+11G>A, c.755+86G>A, c.*30C>G) variants, among which six (p.S184I, p.D193N, p.P295T, p.F465I, p.F496L, p.P606S) missense variants were novel. In-vitro studies demonstrated that p.K204R increased LDB3 expression whereas p.S184I, p.F465I, p.F496L, p.P606S reduced LDB3 expression. Immunostainning revealed cytoplasmic aggregation of the p.K204R-LDB3 protein. The variant p.R229C also over-expressed the mutant protein. In case of variant, p.P295T, Z-disc was severely disrupted indicating impaired Z-disc integrity. Furthermore, synonymous variants showed altered mRNA folding, stability, and codon usage bias, potentially affecting translation efficiency. In-silico analyses predicted p.F465I, p.F496L, p.P606S, and p.S184I variants to be deleterious, significantly altering protein structure. Structural modeling using AlphaFold2 showed high RMSD values, suggesting conformational destabilization. Collectively, these findings highlight LDB3 as a hypermutable candidate gene for DCM in our cohort that may contribute to DCM pathogenesis by perturbing protein structure, expression, and cellular localization, underscoring the critical role of LDB3 in cardiac muscle function and disease.

genetics↗

Cryo-electron tomography reveals the structural diversity of cardiac proteins in their cellular context

Cardiovascular diseases are a leading cause of death worldwide, but our understanding of the underlying mechanisms is limited, in part because of the complexity of the cellular machinery that controls the heart muscle contraction cycle. Cryogenic electron tomography (cryo-ET) provides a way to visualize diverse cellular machinery while preserving contextual information like subcellular localization and transient complex formation, but this approach has not been widely applied to the study of heart muscle cells (cardiomyocytes). Here, we deploy an optimized cryo-ET platform that enables cellular-structural biology in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Using this platform, we reconstructed sub-nanometer resolution structures of the human cardiac muscle thin filament, a central component of the contractile machinery. Reconstructing the troponin complex, a regulatory component of the thin filament, from within cells, we identified previously unobserved conformations that highlight the structural flexibility of this regulatory complex. We next measured the impact of chemical and genetic perturbations associated with cardiovascular disease on the structure of troponin. In both cases, we found changes in troponin structure that are consistent with known disease phenotypes--highlighting the value of our approach for dissecting complex disease mechanisms in the cellular context.

biophysics↗

Interferon-gamma promotes iron export in human macrophages to limit intracellular bacterial replication

Salmonellosis and listeriosis together accounted for more than one third of foodborne illnesses in the United States and almost half the hospitalizations for gastrointestinal diseases in 2018 while tuberculosis afflicted over 10 million people worldwide causing almost 2 million deaths. Regardless of the intrinsic virulence differences among Listeria monocytogenes, Salmonella enterica and Mycobacterium tuberculosis, these intracellular pathogens share the ability to survive and persist inside the macrophage and other cells and thrive in iron rich environments. Interferon-gamma (IFN-{gamma}) is a central cytokine in host defense against intracellular pathogens and has been shown to promote iron export in macrophages. We hypothesize that IFN-{gamma} decreases iron availability to intracellular pathogens consequently limiting replication in these cells. In this study, we show that IFN-{gamma} regulates the expression of iron-related proteins hepcidin, ferroportin, and ferritin to induce iron export from macrophages. Listeria monocytogenes, S. enterica, and M. tuberculosis infections significantly induce iron sequestration in human macrophages. In contrast, IFN-{gamma} significantly reduces hepcidin secretion in S. enterica and M. tuberculosis infected macrophages. Similarly, IFN-{gamma}-activated macrophages express higher ferroportin levels than untreated controls even after infection with L. monocytogenes bacilli; bacterial infection greatly down-regulates ferroportin expression. Collectively, IFN-{gamma} significantly inhibits pathogen-associated intracellular iron sequestration in macrophages and consequently retards the growth of intracellular bacterial pathogens by decreasing iron availability.

cell biology↗