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Biology subjects

Fukai, Y.

Publications and source records attributed to Fukai, Y..

2 recordsLinked to original sources

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↗

Optimal AAV capsid/promoter combinations to target specific cell types in the common marmoset cerebral cortex

To achieve cell type-specific gene expression, using target cell-tropic AAV capsids is advantageous. However, their tropism across brain cell types remains unexplored in non-human primates. We assessed the tropism of nine AAV serotype capsids (AAV1, 2, 5, 6, 7, 8, 9, rh.10 (rh10), and DJ) on marmoset cerebral cortical cell types. Marmoset cerebral cortex was injected with different serotype AAVs expressing enhanced GFP (EGFP) by the ubiquitous chicken {beta}-actin hybrid (CBh) promoter. After 4 weeks, all nine AAV capsid vectors, especially AAV9 and AAVrh10, caused highly neuron-selective EGFP expression. Some AAV capsids, including AAV5, caused EGFP expression in oligodendrocytes to a lesser extent, with minimal or no expression in astrocytes and microglia. Different ubiquitous CMV and CAG promoters showed similar neuron-predominant transduction. Conversely, all nine AAV capsid vectors with the astrocyte-specific hGFA(ABC1D) promoter selectively transduced astrocytes, except AAV5, which transduced oligodendrocytes modestly. Oligodendrocyte-specific mouse myeline basic protein (mMBP) promoter in AAV5 vectors transduced oligodendrocytes specifically and efficiently. Our results suggest optimal combinations of capsids and promoters for cell type-specific expression: AAV9 or AAVrh10 and ubiquitous CBh, CMV, or CAG promoter for neuron-specific transduction; AAV2 or 7 and hGFA(ABC1D) promoter for astrocyte-specific transduction; and AAV5 and mMBP promoter for oligodendrocyte-specific transduction.

neuroscience↗