Chromatin Haiku
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chromatinhaiku.bsky.social
Chromatin Haiku
@chromatinhaiku.bsky.social
1.2K followers 33 following 11 posts
Nuclear events
Narratives in chromatin
By haiku, of course
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chromatinhaiku.bsky.social
Nascent and mature
Ribosomal RNA
Unbalanced in parts

#ChromatinHaiku #RNAsky #28S #Chromatinsky
www.biorxiv.org/content/10.1...
Figure 4E-F from the linked preprint showing the excess of 28S over 18S rRNA across cell types.
August 3, 2025 at 12:52 PM
chromatinhaiku.bsky.social
For mature oocytes
H2A.Z is needed
With MLL2

#ChromatinHaiku @natsmb.nature.com
www.nature.com/articles/s41...
www.nature.com/articles/s41...
Model figure from Mei et al., Figure legend: Small growing oocytes show canonical distributions of H3K4me3 and H2A.Z at active and bivalent gene promoters. In wild-type FGOs, H3K4me3 and H2A.Z form non-canonical broad domains across intergenic regions, whereas H2A.Z is displaced at bivalent gene promoters. In H2A.Z-DKO FGOs, non-canonical H3K4me3 at intergenic regions and H2AK119ub1 at active gene promoters are partially reduced. In Mll2-KO FGOs, ncH2A.Z is partially reduced. The distributions of H3K27me3 and H2AK119ub1 were not investigated in the Mll2-KO FGOs (marked with question marks). H2AK119ub1 at bivalent gene promoters is not shown. Model figure from Xu et al., Figure legend: Maternal depletion of H2A.Z results in aberrant meiosis resumption. Only a few FGOs survived to MII oocytes, with abnormal chromosome alignment. H2A.Z is acetylated (red) at active promoters and enhancers in mouse FGOs. Genes with low CG densities are preferentially downregulated in H2A.ZmKO FGOs. In mESCs, growing oocytes, and early embryos, in addition to active promoters and enhancers, H2A.Z and H2A.Zac are also present at inactive promoters with high CG densities, including Polycomb-target genes.
June 15, 2025 at 12:52 PM
chromatinhaiku.bsky.social
Pol2 stimulates
SETD2 methylation
Of histone H3

#ChromatinHaiku #H3K36
www.science.org/doi/10.1126/...
Fig. 1. Biochemical reconstitution of H3K36me3 deposition by SETD2 during transcription. (A) Schematic of RNA extension-coupled histone mark deposition assay in the presence of all NTPs. (B) Denaturing gel of RNA products and Western blot analysis reveals transcription stimulates H3K36me3 deposition by SETD2. SETD2 concentration is 3.5 μM. (C) Schematic of RNA extension-coupled histone mark deposition assay with pause sites (bp −31, bp −15, and bp +27). (D) Denaturing gel of RNA products and Western blot analysis reveals transcription stimulates H3K36me3 deposition by SETD2 on partially transcribed downstream nucleosome. SETD2 concentration is 3.5 μM. (E) Denaturing gel of RNA products and Western blot analysis reveals transcription stimulates H3K36me3 deposition by SETD2 on transferred upstream nucleosome (bp +115). SETD2 concentration is 700 nM. RNA extension gel and Western blot from (E) is the same as in fig. S13F.
December 13, 2024 at 3:39 PM
chromatinhaiku.bsky.social
STK19
Transcription coupled repair
With TFIIH

#ChromatinHaiku
www.cell.com/cell/fulltex...
www.cell.com/cell/fulltex...
www.cell.com/molecular-ce...
Graphical abstract for one of the papers Graphical abstract for one of the papers Graphical abstract for one of the papers
November 15, 2024 at 2:46 PM
chromatinhaiku.bsky.social
Polycomb restores
H2A ubiquitin
By read-write action

#ChromatinHaiku #ncPRC1-RYBP
www.nature.com/articles/s41...
Figure 2 from the paper: Two distinct acidic patch interactions and ubiquitin binding stabilize the ncPRC1RYBP complex on the nucleosome, suggesting an intra-nucleosome read–write mechanism.
November 13, 2024 at 7:40 PM
chromatinhaiku.bsky.social
Depleting CAF-1
Slows replisome, chromatin
G0 arrest

#ChromatinHaiku @fmattiroli.bsky.social
www.cell.com/molecular-ce...
Graphical abstract for paper. Written abstract is as follows: Long-term perturbation of de novo chromatin assembly during DNA replication has profound effects on epigenome maintenance and cell fate. The early mechanistic origin of these defects is unknown. Here, we combine acute degradation of chromatin assembly factor 1 (CAF-1), a key player in de novo chromatin assembly, with single-cell genomics, quantitative proteomics, and live microscopy to uncover these initiating mechanisms in human cells. CAF-1 loss immediately slows down DNA replication speed and renders nascent DNA hyper-accessible. A rapid cellular response, distinct from canonical DNA damage signaling, is triggered and lowers histone mRNAs. In turn, histone variants’ usage and their modifications are altered, limiting transcriptional fidelity and delaying chromatin maturation within a single S-phase. This multi-level response induces a p53-dependent cell-cycle arrest after mitosis. Our work reveals the immediate consequences of defective de novo chromatin assembly during DNA replication, indicating how at later times the epigenome and cell fate can be altered.
November 12, 2024 at 4:14 PM
chromatinhaiku.bsky.social
Limiting factors
For nuclear receptors
Live cell imaging

#ChromatinHaiku #SingleMoleculeTracking #ProximityAssistedPhotoactivation
www.biorxiv.org/content/10.1...
Figure 4. A model for RARα limited chromatin binding of RARα-RXRα heterodimers. (A) Pool of RXRα (red) and RXR partners (RARα – blue, other T2NRs-yellow) along with some number of chromatin bound RARα-RXRα heterodimers exist under normal conditions. (B) When the pool of free RXRα is increased, the number of chromatin bound RARα-RXRα heterodimers does not change. (C) When the pool of RARα is increased, chromatin binding RARα-RXRα heterodimers increases, until it reaches saturation. Note: For simplicity we have omitted to show heterodimerization of other T2NRs (yellow) with RXRα (red).
November 12, 2024 at 2:23 AM