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Hosokawa, H.

Publications and source records attributed to Hosokawa, H..

3 recordsLinked to original sources

LinearCapR: Linear-time computation of per-nucleotide structural-context probabilities of RNA without base-pair span limits

MotivationRNA molecules adopt dynamic ensembles of secondary structures, where the local structural context of each nucleotide-such as whether it resides in a stem or a specific type of loop-strongly shapes molecular interactions and regulatory function. Structural-context probabilities therefore provide a more functionally informative view of RNA folding than the minimum free energy structures or base-pairing probabilities. However, existing tools either require O (N3) time or employ span-restricted approximations that omit long-range base-pairs, limiting their applicability to large and biologically important RNAs. ResultsWe introduce LinearCapR, enabling linear-time, span-unrestricted computation of structural-context marginalized probabilities, using beam-pruned Stochastic Context Free Grammar-based computation. LinearCapR retains global ensemble features lost by span-limited methods and yields superior predictive power on bpRNA-1m(90) dataset, especially for multiloops and exterior regions, as well as long-distance stems. LinearCapR supports analysis of long RNAs, demonstrated on the full genome of SARS-CoV-2. ConclusionsLinearCapR provides the first base-pair-span-unrestricted, linear-time framework for RNA structural-context analysis, retaining key thermodynamic ensemble features essential for functional interpretation. It enables large-scale studies of viral genomes, long non-coding RNAs, and downstream analyses such as RNA-binding protein site prediction. AvailabilityThe source code of LinearCapR is available at https://github.com/hoget157/LinearCapR.

bioinformatics↗

A single microRNA miR-195 rescues the arrested B cell development induced by EBF1 deficiency

Accumulated studies have reported that hematopoietic differentiation was primarily regulated by transcription factors. Early B cell factor 1 (EBF1) is an essential transcription factor for B lymphopoiesis. Contrary to the canonical notion, we found that a single miRNA, miRNA-195 (miR-195) transduction let EBF1 deficient hematopoietic progenitor cells (HPCs) express CD19, carry out V(D)J recombination and class switch recombination, which implied that B cell matured without EBF1. A part of the mechanism was caused by FOXO1 accumulation via inhibition of FOXO1 phosphorylation pathways in which targets of miR-195 are enriched. These results suggested that some miRNA transductions could function as alternatives to transcription factors.

immunology↗

Pioneering, chromatin remodeling, and epigenetic constraint in early T-cell gene regulation by PU.1

PU.1 is a dominant but transient regulator in early T-cell precursors and a potent transcriptional controller of developmentally important pro-T cell genes. Before T-lineage commitment, open chromatin is frequently occupied by PU.1, and many PU.1 sites lose accessibility when PU.1 is later downregulated. Pioneering activity of PU.1 was tested in in this developmentally dynamic context, by quantitating the relationships between PU.1 occupancy and site quality and accessibility as PU.1 levels naturally declined in pro-T cell development, and by using stage-specific gain and loss of function perturbations to relate binding to effects on target genes. PU.1 could bind closed genomic sites, but rapidly opened many of them, despite the absence of its frequent collaborators, C/EBP factors. The dynamic properties of PU.1 engagements implied that PU.1 binding affinity and concentration determine its occupancy choices, but with quantitative tradeoffs for occupancy between site sequence quality and stage-dependent site accessibility in chromatin. At non-promoter sites PU.1 binding criteria were more stringent than at promoters, and PU.1 was also much more effective as a transcriptional regulator at non-promoter sites where local chromatin accessibility depended on the presence of PU.1. Runx motifs and Runx1 binding were often linked to PU.1 at open sites, but highly expressed PU.1 could bind its sites without Runx1. Notably, closed chromatin presented a qualitative barrier to occupancy by the PU.1 DNA binding domain alone. Thus, effective pioneering at closed chromatin sites also depends on requirements beyond site recognition served by non-DNA binding domains of PU.1.

immunology↗