Publications by authors named "H Kurumizaka"

The CRISPR-associated endonuclease Cas9 derived from prokaryotes is used as a genome editing, which targets specific genomic loci by single guide RNAs (sgRNAs). The eukaryotes, the target of genome editing, store their genome DNA in chromatin, in which the nucleosome is a basic unit. Despite previous structural analyses focusing on Cas9 cleaving free DNA, structural insights into Cas9 targeting of DNA within nucleosomes are limited, leading to uncertainties in understanding how Cas9 operates in the eukaryotic genome.

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Nucleosome remodelers modify the local structure of chromatin to release the region from nucleosome-mediated transcriptional suppression. Overlapping dinucleosomes (OLDNs) are nucleoprotein complexes formed around transcription start sites as a result of remodeling, and they consist of two nucleosome moieties: a histone octamer wrapped by DNA (octasome) and a histone hexamer wrapped by DNA (hexasome). While OLDN formation alters chromatin accessibility to proteins, the structural mechanism behind this process is poorly understood.

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Article Synopsis
  • The study focuses on H2A.B, a unique variant of the H2A histone, which plays important roles in processes like sperm and embryo development as well as cancer formation, pointing to its distinct transcriptional regulation compared to standard H2A.
  • Researchers used solid-state nanopores to analyze how DNA unwinds from nucleosomes, discovering that H2A.B requires less voltage to completely unwind DNA and does so more rapidly than canonical H2A nucleosomes.
  • The findings highlight that H2A.B facilitates a smoother DNA unwinding process due to quicker disassembly of the histone complex, suggesting a novel method for examining DNA-protein interactions and the dynamics of nucleosomes.
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The chromatin-remodeling enzyme helicase lymphoid-specific (HELLS) interacts with cell division cycle-associated 7 (CDCA7) on nucleosomes and is involved in the regulation of DNA methylation in higher organisms. Mutations in these genes cause immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome, which also results in DNA hypomethylation of satellite repeat regions. We investigated the functional domains of human CDCA7 in HELLS using several mutant CDCA7 proteins.

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