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Umehara, T.

Publications and source records attributed to Umehara, T..

7 recordsLinked to original sources

Temperature vaulting: A method for screening selective, slow- and tight-binding inhibitors targeting kinases in their non-native state

A polypeptide folds into its protein tertiary structure in the native state through a folding intermediate in the non-native state. The transition between these states is thermodynamically driven. A folding intermediate of dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) autophosphorylates intramolecularly, whereas DYRK1A in the native state no longer catalyzes this reaction. The alteration in substrate specificity suggests a conformational transition of DYRK1A during its folding process. Consistent with this hypothesis, we identified FINDY (1), which inhibits the intramolecular autophosphorylation but not the intermolecular phosphorylation, suggesting that the folding intermediate possesses an alternative inhibitor-binding site. Meanwhile, it remains an issue that the methods for approaching the alternative binding site require an intricate assay tailored to the individual target. Here we show a method, designated as "temperature vaulting," for screening the non-native-state-targeted inhibitors of DYRK1A. Transient heating of recombinant DYRK1A protein drove the reversible transition between the native state and the non-native state targeted by FINDY (1). At physiological temperature, FINDY (1) slowly bound to the DYRK1A protein. These results indicate that transient heating accelerates the slow-binding process by assisting the protein to overcome the high-energy barrier leading to the target non-native state. The energy barrier also slowed down the dissociation process, resulting in tight binding between DYRK1A and FINDY (1). Furthermore, this study suggests that the dissociation rate underlies the inhibition selectivity of FINDY (1) between DYRK1A and its family kinase DYRK1B. This method enables the identification of slow- and tight-binding inhibitors that have been missed in conventional assays. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=112 SRC="FIGDIR/small/632643v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@be5661org.highwire.dtl.DTLVardef@1925beorg.highwire.dtl.DTLVardef@fceb5borg.highwire.dtl.DTLVardef@bfbf91_HPS_FORMAT_FIGEXP M_FIG C_FIG HIGHLIGHTSA temperature vaulting method facilitated the screening of a slow- and tight-binding inhibitor targeting DYRK1A in the non-native state. A structure-activity relationship study of FINDY (1) demonstrated that a slight alteration in chemical structure impacts the inhibition kinetics. A molecular dynamics simulation of DYRK1A revealed binding-ready conformations for FINDY (1). The dissociation rate may underlie the inhibition selectivity of FINDY (1) between DYRK1A and DYRK1B in cellular systems.

biophysics↗

Engineered acetylation patterns drive large-scale chromatin organization in vitro

Chromatin organization plays a crucial role in gene regulation [1, 2, 3], but disentangling the contributions of various epigenetic components to gene-scale chromatin structure remains challenging. While in vitro chromatin reconstitution enables controlled studies on the effect of bio-chemical factors on the structure, current methods are either limited to short arrays or lack control over histone modification patterns. Here we directly test how histone modification affects higher-order chromatin architecture by characterizing gene-scale reconstituted chromatin using single-molecule microscopy and in vitro Hi-C. We reconstitute 20-kilobase chromatin arrays with histone modification patterns controlled at 12-nucleosome resolution, achieving complete assembly of 96 nucleosomes in the designed order as confirmed by atomic force microscopy and longread sequencing. Observing end-to-end fluctuations of the reconstituted arrays, we find that increasing the density of acetylated nucleosomes leads to larger structural fluctuations with longer relaxation times, consistent with the predictions of a polymer model with hydrodynamic interactions. We demonstrate through in vitro Hi-C how acetylation reduces contact frequency between nucleosomes and induces open conformations. In heterogeneously modified arrays, differential contact probabilities between acetylated and unmodified regions lead to distinct structural domains. The results establish the physical principles by which histone modifications directly modulate chromatin architecture through altered nucleosome-nucleosome interactions, providing a quantitative framework for understanding and engineering genome organization.

biophysics↗

Testosterone-Induced Metabolic Changes in Seminal Vesicle Epithelial cells Alter Plasma Components to Enhance Sperm Fertility

Male factors account for almost half of the causes of infertility. In rodents and humans, most of the components of semen are supplied by the seminal vesicles, and they support male reproductive ability, but there are many unknown details. In this study, the metabolic changes in the seminal vesicle epithelial cells were focused on, and the mechanisms by which testosterone affected the seminal plasma composition were investigated. A factor improving the linear motility of sperm was secreted from the seminal vesicles, and it was produced in an androgen-dependent manner. Bioassays, gene expression, and flux analysis studies demonstrated that testosterone promotes glucose uptake in seminal vesicle epithelial cells via GLUT4, resulting in fatty acid synthesis. ACLY was a critical factor in this metabolic change, which produced fatty acid, especially oleic acid. In conclusion, the critical role of testosterone-induced metabolic changes in the seminal vesicles is to ensure the synthesis of fatty acid. These findings suggest that testosterone-dependent lipid remodeling may contribute to sperm straight-line motility, and further functional verification is required. One Sentence Summary Testosterone promotes the conversion of glucose to fatty acid by increasing the expression of ACLY in seminal vesicle epithelial cells, thereby regulating the seminal plasma components.

cell biology↗

Epigenetic mechanisms to propagate histone acetylation by p300/CBP

Histone acetylation is important for the activation of gene transcription but little is known about its direct read/write mechanisms. Here, we report cryo-electron microscopy structures in which a p300/CBP multidomain monomer recognizes histone H4 N-terminal tail (NT) acetylation (ac) in a nucleosome and acetylates non-H4 histone NTs within the same nucleosome. p300/CBP not only recognized H4NTac via the bromodomain pocket responsible for reading, but also interacted with the DNA minor grooves via the outside of that pocket. This directed the catalytic center of p300/CBP to one of the non-H4 histone NTs. The primary target that p300 writes by reading H4NTac was H2BNT, and H2BNTac promoted H2A-H2B dissociation from the nucleosome. We propose a model in which p300/CBP replicates histone NT acetylation within the H3-H4 tetramer to inherit epigenetic storage, and transcribes it from the H3-H4 tetramer to the H2B-H2A dimers to activate context-dependent gene transcription through local nucleosome destabilization.

biochemistry↗

Rational design and implementation of a chemically inducible hetero-trimerization system

Chemically inducible dimerization (CID) uses a small molecule to induce binding of two different proteins. CID tools exemplified by the FKBP/FRB/rapamycin system have been widely employed to probe molecular events inside and outside cells. While various CID tools are available, chemically inducible trimerization (CIT) has not been developed, due to inherent challenges in designing or identifying a chemical that simultaneously binds three proteins with high affinity and target specificity. Nevertheless, by introducing a third recruitable component, CIT could enable versatile applications. Here, we devised the CIT by rationally splitting FRB and FKBP. Based on cellular and structural datasets, select split pairs of FRB or FKBP underwent efficient trimerization with full length FKBP or FRB, respectively, upon addition of rapamycin. We also demonstrated its potential for cellular applications by rapidly inducing tri-organellar plasma membrane-ER-mitochondria junctions, and by perturbing intended membrane lipids exclusively at the plasma membrane-ER membrane contact sites. By conferring one additional condition to what is achievable with CID, CIT expands the types of manipulation in single live cells, to address cell biology questions otherwise intractable, and engineer cell functions for future synthetic biology applications.

cell biology↗

Quantification of the effect of site-specific histone acetylation on chromatin remodeling rate

Eukaryotic transcription is epigenetically regulated by chromatin structure and post-translational modifications (PTMs). For example, lysine acetylation in histone H4 is correlated with activation of RNA polymerase I-, II-, and III-driven transcription from chromatin templates, which requires prior chromatin remodeling. However, quantitative understanding of the contribution of particular PTM states to the sequential steps of eukaryotic transcription has been hampered partially because reconstitution of a chromatin template with designed PTMs is difficult. In this study, we reconstituted a di-nucleosome with site-specifically acetylated or unmodified histone H4, which contained two copies of the Xenopus somatic 5S rRNA gene with addition of a unique sequence detectable by hybridization-assisted fluorescence correlation spectroscopy. Using a Xenopus oocyte nuclear extract, we analyzed the time course of accumulation of nascent 5S rRNA-derived transcripts generated on chromatin templates in vitro. Our mathematically described kinetic model and fitting analysis revealed that tetra-acetylation of histone H4 at K5/K8/K12/K16 increases the rate of transcriptionally competent chromatin formation ~3-fold in comparison with the absence of acetylation. We provide a kinetic model for quantitative evaluation of the contribution of epigenetic modifications to chromatin transcription.

biophysics↗

JQ1 affects BRD2-dependent and independent transcription regulation without disrupting H4-hyperacetylated chromatin states

The bromodomain and extra-terminal domain (BET) proteins are promising drug targets for cancer and immune diseases. However, BET inhibition effects have been studied more in the context of bromodomain-containing protein 4 (BRD4) than BRD2, and the BET protein association to histone H4-hyperacetylated chromatin is not understood at the genome-wide level. Here, we report transcription start site (TSS)-resolution integrative analyses of ChIP-seq and transcriptome profiles in human non-small cell lung cancer (NSCLC) cell line H23. We show that di-acetylation at K5 and K8 of histone H4 (H4K5acK8ac) co-localizes with H3K27ac and BRD2 in the majority of active enhancers and promoters, where BRD2 has a stronger association with H4K5acK8ac than H3K27ac. Interestingly, although BET inhibition by JQ1 led to complete reduction of BRD2 binding to chromatin, only local changes of H4K5acK8ac levels were observed. In addition, a remarkable number of BRD2-bound genes, including MYC and its downstream target genes, were transcriptionally upregulated upon JQ1 treatment. Using BRD2-enriched sites and transcriptional activity analysis, we identified candidate transcription factors potentially involved in the JQ1 response in BRD2-dependent and independent manner.

molecular biology↗