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Teif lab

@teiflab.bsky.social
3.1K followers 1.1K following 394 posts

Teif lab at the University of Essex. We work on gene regulation in chromatin and applications to liquid biopsies, using approaches of genomics, biophysics, bioinformatics & AI. Our focus is nucleosomics, TF binding, CTCF, cfDNA. generegulation.org

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Teif lab @teiflab.bsky.social · 23/09/2026
Zeng et al, 2026. Transcription factors read a second regulatory code in chromatin www.biorxiv.org/content/10.6... "our findings establish that TFs interpret two complementary layers of genomic information: the primary DNA sequence and a second code written into the nucleosome architecture"
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Teif lab @teiflab.bsky.social · 30/08/2026
AlBawardi et al, 2026. Irregular nucleosome positioning governs a crystalline to liquid-like phase transition and tunes chromatin accessibility www.biorxiv.org/content/10.6... ▶️heterochromatin-like sequences produce compact fibres ▶️positional irregularity (>2-3 bp) triggers a state transition
Abstract: Chromatin must fold tightly enough to protect the genome while being sufficiently accessible for DNA dependent processes such as transcription. The physical rules that balance these competing roles remain unclear, as DNA sequence encodes both biochemical information such as transcription factor binding sites, and biophysical cues that shape chromatin structure. Here, using synthetic chromatin fibres assembled from physiologically relevant DNA sequences, we show that nucleosome positioning dictates the material state of chromatin. Heterochromatin-like sequences produce compact fibres stabilised by nucleosome stacking, whereas euchromatin-like sequences generate irregular nucleosome positioning that yields disrupted, heterogeneous, and mechanically deformable fibres. Quantitative polymer modelling reveals that these irregular arrays are highly dynamic, continually sampling a broad ensemble of conformations as nucleosome stacking breaks down. We identify two previously unrecognised thresholds encoded by nucleosome positioning: minimal positional irregularity (2–3 bp) triggers a transition from an ordered paracrystalline state to a liquid-like phase, whereas an order of magnitude greater irregularity (∼18 bp) is required to generate accessibility and mechanical fragility permissive for transcription factor binding. Euchromatin-like arrays reside at this accessibility threshold. These findings indicate that nucleosome positioning tunes chromatin toward or away from critical structural states that couple genome protection, chromatin dynamics, and transcriptional potential—providing a physical mechanism that helps connect DNA sequence to gene expression.
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Teif lab @teiflab.bsky.social · 18/08/2026
Luo et al, 2026 (review). The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options link.springer.com/article/10.1... 🤯548 references!
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Teif lab @teiflab.bsky.social · 14/08/2026
Our new facility www.essex.ac.uk/news/2026/08...
essex.ac.uk
New lab will train NHS cancer scientists of the future | University of Essex
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Teif lab @teiflab.bsky.social · 26/07/2026
Woolfe et al, 2026. Decoding the mystery of ultra-conservation in developmental enhancers: a role for nucleosome positioning, DNA structure and transcription factor binding www.biorxiv.org/content/10.6... ▶️conserved non-coding elements ... favor nucleosome occupancy at their borders
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Teif lab @teiflab.bsky.social · 17/07/2026
Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity [review by İsa Özdemir and Sarah Hainer] onlinelibrary.wiley.com/doi/10.1002/...
onlinelibrary.wiley.com
Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity
In eukaryotes, DNA is not a naked repository of genetic information but is tightly wound around histone octamers to form nucleosomes. While this packaging solves the spatial problem of fitting 2 mete...
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Teif lab @teiflab.bsky.social · 12/07/2026
Tran et al, 2026. Deconvolving the spatiotemporal chromatin landscape through the cell cycle www.biorxiv.org/content/10.6... ▶️Nucleosome atlas using MNase-seq from synchronized yeast populations at 10-minute intervals through the cell cycle
biorxiv.org
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Teif lab @teiflab.bsky.social · 10/07/2026
Yesterday I gave a webinar for Year 12 students titled “Genomics meets AI: can we detect cancer earlier?” Alongside the science, I found a few useful ways to explain gene regulation to people without a biology background. Sharing in case useful to others. 1/4
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Teif lab @teiflab.bsky.social · 07/07/2026
Chen et al 2026. Genome-wide rotational and translational phasing of nucleosomes with human transcription factors www.cell.com/molecular-ce... ▶️ In vivo nucleosome phasing measured on the same TF-bound DNA molecule ▶️ Phasing around CTCF sites is DNA encoded ▶️ FoxA and NFIA phase adjacent nucleosomes
How transcription factors (TFs) and their binding sites organize and engage nucleosomes at natural genomic locations remains poorly understood. Here, we develop Benzonase-seq to measure the rotational phasing of nucleosomes in human cells and enhance chromatin immunoprecipitation (ChIP)-exo (v6) to measure rotational phasing on the same DNA molecule bound by a TF. Unbound CTCF sites were found to be rotationally accessible on nucleosomes, and this rotational accessibility is encoded by classical dinucleotide periodicities. CTCF binding results in nucleosome displacement to adjacent DNA phasing sequences. Upon examining 40 TF classes, unbound sites were found to be phased either inward or outward or to lack phasing. In all examined cases, TF binding (e.g., NFIA and FoxA) results in adjacent rotational and translational phasing, which is not dinucleotide encoded. Benzonase-seq also more robustly maps nucleosome and subnucleosome positions in hard-to-map CpG islands. These findings provide a clearer view of how TFs engage and position nucleosomes to shape the natural chromatin landscape.
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Teif lab @teiflab.bsky.social · 05/07/2026
Gaspa-Toneu et al, 2026. Single molecule footprinting measures low nucleosome occupancy in mature spermatozoa of mice and men www.biorxiv.org/content/10.6... ▶️ NOMe-seq at 103 and 163 genomic sites in spermatozoa of mice and human ▶️ nucleosome occupancy ∼1.2 to 1.7% in mice; ∼2.3 to 4.5% in human
biorxiv.org
Single molecule footprinting measures low nucleosome occupancy in mature spermatozoa of mice and men
Nucleosomes are fundamental units of DNA packaging and gene regulation in eukaryotes. In mammalian sperm, most nucleosomes are replaced by protamines causing extreme chromatin compaction. Various epig...
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Teif lab @teiflab.bsky.social · 03/07/2026
A good use of AI in text editing is interactive: it highlights issues, you try different approaches, it disagrees, you push back, and the two of you have a dialogue much as you would with a human coauthor. A refined text emerges iteratively, and you learn from the process. The process itself matters
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Teif lab @teiflab.bsky.social · 03/07/2026
Sounds like an excellent idea www.bbc.co.uk/news/article...
bbc.co.uk
NHS to reward people who walk 30 minutes a day
The "marathon a month" scheme, developed with former Olympic medallist Sir Brendan Foster, will launch early next year.
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Teif lab @teiflab.bsky.social · 28/06/2026
1/9 A few thoughts and personal opinions on the use of AI in research evaluation. I suspect many of these changes may be inevitable, so the real question may not be whether this will happen, but how we shape it responsibly 🧵
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Jeffrey Ross-Ibarra @jrossibarra.bsky.social · 26/06/2026
After reading @blekhernia.bsky.social's great blog post on lab AI usage policy (blekhman.substack.com/p/you-need-t...), we made one in lab meeting. Feedback welcome! rilab.ucdavis.edu/ai_expectati...
rilab.ucdavis.edu
Ross-Ibarra Lab Policy on AI Usage
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Teif lab @teiflab.bsky.social · 21/06/2026
Deskilling associated with AI is a real danger for our students as well. How to prevent it? Which tricks do you use to integrate AI in training responsibly?
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Teif lab @teiflab.bsky.social · 12/06/2026
Great preprint by @vram142.bsky.social & Co www.biorxiv.org/content/10.6... "fiber homotypy," where chromatin fibers with similar nucleosome spacing interact more frequently in 3D --> Related to our previous "nucleosome homology recognition" in chromatin royalsocietypublishing.org/rsif/article...
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Teif lab @teiflab.bsky.social · 10/06/2026
Come celebrate Professor Leo Schalkwyk with us! We’re holding a one-day symposium to mark Leo's remarkable career and many contributions to genomics. 📆26 June 2026 📍University of Essex, Colchester Details and registration: schalkwykfest.essex.ac.uk There will be a BBQ as well!
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Teif lab @teiflab.bsky.social · 04/06/2026
Sun et al, 2026. NuRD-enabled CTCF-TET crosstalk orchestrates epigenome reprogramming and genome architecture www.cell.com/molecular-ce...
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Teif lab @teiflab.bsky.social · 15/05/2026
The +1 nucleosome functions in Pol II transcription initiation and the transition to elongation www.biorxiv.org/content/10.6... [Yumeng Zhan, Julio Abril-Garrido, Frauke Grabbe, Paulina Seweryn, Ute Neef, Christian Dienemann, Patrick Cramer]
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Alexis Verger 🧬🧫🧪 @alexis-verger.cpesr.fr · 08/05/2026
Did you know that Pierre Chambon's laboratory was the first to use the term "nucleosome" in 1975 ? www.cell.com/cell/fulltex...
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Teif lab @teiflab.bsky.social · 11/03/2026
Tested LinkedIn for a paper announcement, and it worked perfectly. About 3x more engagements than on Bluesky. Obviously, LinkedIn is a different culture, more formal and less chatty, but for professional things it works just fine. Can't believe it was there all the time, and we just did not use it
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Teif lab @teiflab.bsky.social · 09/03/2026
Adhireksan et al, 2026. Linker histones consolidate heterogenous nucleosome fiber contacts by linking together multiple nucleosomes www.nature.com/articles/s41...
The consensus mode for linker histone (H1) association coincides with ‘on-dyad’ binding to an individual nucleosome, making it challenging to rationalize the chromatin dynamics and compacting activities of H1 in the context of a highly heterogeneous structural scaffold. Here, we investigate the activity of the somatic H1 variants by conducting crystallographic analysis of nucleosomal assemblies and characterization of nucleosome array condensates, which recapitulate long-range nucleosome fiber interactions in chromatin. H1 is observed to associate variant-dependently with nucleosomes through a diversity of binding modes that include linking multiple nucleosomes/fibers together. Binding versatility is facilitated by the proclivity of the H1 globular domain to recognize DNA structural motifs, which are similar between an individual nucleosome and specific niches within clusters of nucleosomes. We propose that linker histones support a structurally and functionally complex repertoire for chromatin regulation by assuming a variety of context-and variant-dependent DNA binding modes.
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Teif lab @teiflab.bsky.social · 05/03/2026
Nucleosome aficionados! Our new review "Nucleosome spacing across cell types, diseases, and ages" is out in NAR: academic.oup.com/nar/article/... A huge effort to pull together what we’ve learned about nucleosome spacing in many systems. Enjoy! @milena-bikova.bsky.social @chrsclrksn.bsky.social
Figure 1.(A) Classical gel electrophoresis experiments showing mono-, di-, tri-, tetra-, and further multinucleosome bands upon chromatin digestion. (B) The nucleosome repeat length (NRL) is defined as the genomic distance between the centres of two neighbouring nucleosomes.Figure 2.Nucleosome mapping using MNase-seq versus ATAC-seq. (A) In MNase-seq, nucleosomes in both open and tightly packed genomic regions are accessible to digestion. MNase preferentially cleaves DNA between nucleosomes and digests DNA until it encounters a histone octamer, which provides a footprint of nucleosome-protected DNA regions. (B) Bulk MNase-seq results in averaged maps across millions of cells, effectively capturing all possible nucleosome positioning configurations. (C) Single-cell MNase-seq (scMNase-seq) results in a noisier and sparser signal. The resulting footprints still represent nucleosome-protected regions, but not all nucleosomes are represented. (D) In ATAC-seq, open regions can be accessed by the enzyme Tn5 transposase, which can insert primers in regions free from the binding of nucleosomes and transcription factors (TFs). (E) For open chromatin regions, nucleosome maps can be obtained from ATAC-seq similar to MNase-seq. (F) Closed, tightly packed chromatin regions may be less represented in ATAC-seq nucleosome maps.
Figure 5.Molecular mechanisms affecting nucleosome spacing. (A) Linker histones H1 and nonhistone chromatin proteins which compete with H1s and modulate nucleosome spacing through structural and electrostatic mechanisms. (B) Chromatin remodellers actively reposition nucleosomes following context-dependent rules. (C) Cell state-dependent chromatin boundaries formed by CTCF and other structural proteins, as well as associated recruitment of chromatin remodellers which space nucleosomes. (D) Gene activity associated with remodeller action and RNA polymerases transcribing through the nucleosomes, leading to smaller distances between nucleosomes in regulatory regions and gene bodies. (E) DNA sequence repeats of different types.Figure 6. Examples of NRL changes in biological systems. (A) Cell differentiation leads to NRL changes between different cell types, e.g. mouse dorsal root ganglia neurons (NRL ∼165 bp) versus cortical astrocytes (NRL ∼183 bp) [175]. Schematic cell shapes are adapted from an image created in BioRender (https://BioRender.com/89trj2t). (B) Paired normal versus tumour breast tissues show NRL shortening in cancer (figure adapted from [36] under the CC BY 4.0 licence (https://creativecommons.org/licenses/by/4.0/)). (C) Nucleosome positioning derived from cfDNA of human volunteers shows NRL increase with age (figure reprinted from [79] under the CC BY 4.0 licence (https://creativecommons.org/licenses/by/4.0/)).
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Eric Topol @erictopol.bsky.social · 20/02/2026
142,000 participants! The largest randomized trial of a multi-cancer early detection (MCED) test failed its primary endpoint genomeweb.com/cancer/grail... Had the enrollment been risk-based instead of age 50, it would likely have been very positive.
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Teif lab @teiflab.bsky.social · 11/02/2026
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Teif lab @teiflab.bsky.social · 08/02/2026
Preparing a lecture about cancer genomics. Looking for a 3D map of human chromatin to show chromosomes 22 and 9 close to each other to demonstrate Philadelphia chromosome translocation. Chromosome territories like the one below don't show them together. Any other visualisations in this style?
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Aaron Quinlan (he/him) @aaronquinlan.bsky.social · 02/12/2025
We are thrilled to announce the first official release (v0.1.8) of #𝗯𝗲𝗱𝗱𝗲𝗿, the successor to one of our flagship tool, #𝗯𝗲𝗱𝘁𝗼𝗼𝗹𝘀! Based on ideas we conceived of long ago (!), this was achieved thanks to the dedication of Brent Pedersen. 1/n
quinlanlab.org
Intro to Bedder – The Quinlan Lab
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Teif lab @teiflab.bsky.social · 23/01/2026
Looks like LinkedIn is becoming more active than bluesky in terms of paper announcements and engagements
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Teif lab @teiflab.bsky.social · 21/01/2026
Today we had very nice interactions in the University of North Dakota (remotely)! Thank you very much @adhasarathy.bsky.social, Motoki Takaku & Co for the invitation to give this talk and hosting the visit!
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Luca Giorgetti lab @FMI @lucagiorgetti.bsky.social · 20/01/2026
Would anyone out there be able to share some Mus Spretus DNA with us? 🐀🧬 Any tissue of origin, for PCR amplification of selected genomic regions. Many thanks in advance!
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Hanneke Vlaming @hannekevlaming.bsky.social · 15/01/2026
The Vlaming lab continues to grow! It's an exciting time in the Vlaming lab: we've just had our 2nd PhD student join, and the 3rd is joining in February. Now, we're looking to recruit a postdoc!
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Teif lab @teiflab.bsky.social · 14/01/2026
Congratulations to Negin Behboodi on successfully passing your PhD viva! We are so proud of you! Keep an eye out for Negin's upcoming big papers! And thank you to the kind examiners @mspivakov.bsky.social and @amarcobio.bsky.social!
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Teif lab @teiflab.bsky.social · 11/01/2026
Schaepe et al, 2026. Thermodynamic principles link in vitro transcription factor affinities to single-molecule chromatin states in cells www.cell.com/cell/fulltex...
The molecular details governing transcription factor (TF) binding and the formation of accessible chromatin are not yet quantitatively understood—including how sequence context modulates affinity, how TFs search DNA, the kinetics of TF occupancy, and how motif grammars coordinate binding. To resolve these questions for a human TF, erythroid Krüppel-like factor (eKLF/KLF1), we quantitatively compare, in high throughput, in vitro TF binding rates and affinities with in vivo single-molecule TF and nucleosome occupancies and in vivo-derived deep learning models. We find that 40-fold flanking sequence effects on affinity are consistent with distal flanks tuning TF search parameters and captured by a linear energy model. Motif recognition probability, rather than time in the bound state, drives affinity changes, and in vitro and in nuclei measurements exhibit consistent, minutes-long TF residence times. Finally, in vitro biophysical parameters predict in vivo sequence preferences and single-molecule chromatin states for unseen motif grammars.
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Teif lab @teiflab.bsky.social · 07/01/2026
Shin et al 2026. CTCF demarcates H3K9me2 or H3K9me3 chromatin domains and restricts the spreading of these modifications faseb.onlinelibrary.wiley.com/doi/abs/10.1... ▶️Related to our previous paper which showed that CTCF forms boundaries of H3K9me2/H3K9me3 nanodomains www.nature.com/articles/s41...
faseb.onlinelibrary.wiley.com
CTCF‐Binding Sites Demarcate Chromatin Domains Enriched With Histone H3K9me2 or H3K9me3 and Restrict the Spreading of These Modifications in Human Cells
To investigate the role of CTCF in chromatin domains enriched with histone H3K9me2 or H3K9me3, we analyzed the distribution of these modifications around CTCF-binding sites in human K562 cells. Genom...
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Jill Moore @moorejille.bsky.social · 07/01/2026
Our paper on the newest version of the Registry of candidate cis-Regulatory Elements (cCREs) is out 🧬 Huge thanks to the many collaborators, experimentalists, analysts and software developers who made this work possible — truly a team effort! A "meme-torial" of the science is coming soon 👀
nature.com
An expanded registry of candidate cis-regulatory elements - Nature
The existing ENCODE registry of candidate human and mouse cis-regulatory elements is expanded with the addition of new ENCODE data, integrating new functional data as well as new cell and tissue types...
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Teif lab @teiflab.bsky.social · 07/01/2026
Structural organization and function of telomeric chromatin [Review by Ruben van der Lugt & Jacqueline Jacobs] www.nature.com/articles/s41...
Fig. 1: Schematic of the human telomeric chromatin architecture. The human telomere is made up of TTAGGG repeats arranged into nucleosomes, bound by a six-subunit shelterin complex (comprising TRF1, TRF2, RAP1, TIN2, TPP1 and POT1). Some complexes are depicted without TPP1 and POT1, which it has been suggested are less abundant than the other subunits. Recent in vitro structural analyses of telomeric chromatin revealed a columnar stacking of histones on TTAGGG repeats, characterized by face-to-face nucleosome arrangements, as well as an alternative open configuration where two histone octamers are oriented at a nearly 90° angle. These in vitro columnar arrays exhibit an NRL of approximately 130 bp. In vivo, however, the telomeric NRL is 157 bp, longer than the NRL of the proposed columnar histone arrangement, but shorter than the ~197-bp NRL of bulk chromatin. To reconcile this, we depict here a model in which shelterin remodels the telomeric chromatin to integrate features of a columnar nucleosome organization with the nucleosome periodicity observed in vivo. At the telomere terminus, a 3′ single-stranded overhang of TTAGGG repeats invades the duplex telomeric DNA to form a lariat structure known as the T-loop. This loop structure serves a protective function by preventing the telomere from being recognized as damaged DNA. The size of the T-loop is variable and may differ between telomeres, contributing to the structural heterogeneity of the telomere. The extent to which nucleosomes are present within the T-loop remains unclear.Fig. 2: Impact of the TPE on the local and distal chromatin environment. Telomere elongation results in the repression of genes in the vicinity of telomeres, a phenomenon known as the TPE. a, Schematic of the repression of telomere-proximal genes via the classical TPE that has been shown at telomere-adjacent artificial reporter genes in human cells. Upon elongation, telomeres accumulate repressive histone modifications (indicated in red) through the activity of a histone methyltransferase (HMT) and HP1. The repressive heterochromatin environment of elongated telomeres spreads to nearby subtelomeric genes (indicated with red and orange DNA strands), resulting in transcriptional repression. The strength of silencing diminishes as the distance from the telomere increases (indicated with fading arrows). Conversely, upon telomere shortening, the human TPE (at telomere-adjacent transgenes) is characterized by loss of the repressive histone modification H3K9me3 and gain of the activating modification H3K9ac. In contrast to telomere-adjacent artificial reporter genes, at natural subtelomeres, spreading of repressive histone modifications from telomeres is not consistently observed, probably due to the presence of boundary elements. b, Schematic of telomere-mediated repression of telomere-distal genes via TPE-OLD. Elongated telomeres acquire the ability to form long-distance loops between telomeres and interstitial telomere sequences (ITSs; that is, sequences of TTAGGG repeats outside of the telomeres). Looping requires binding of shelterin to an ITS and results in transcriptional repression of the affected gene.Fig. 3: Heterogeneity of (sub)telomeric chromatin and its reorganization upon telomere elongation. a, Telomeric and subtelomeric chromatin are organized into distinct domains. The subtelomeric TAR1 site acts as a TSS for the telomeric non-coding RNA TERRA (depicted in red for UUAGGG and in orange for subtelomere-derived RNA). The canonical TERRA promoter contains a high density of CpG dinucleotides, regulated by the DNA methyltransferases DNMT1 and DNMT3B. In contrast, certain subtelomeres (variable across cell lines) contain non-canonical TERRA promoters that lack CpG-rich regions and escape regulation by DNA methylation. Binding of CTCF and cohesin to the centromeric side of TAR1 maintains transcriptionally competent chromatin at the TSS and facilitates the recruitment of RNA polymerase II. The telomeric tract itself displays a bivalent pattern of histone modifications, with both activating (H3K4me3 and H3K27ac) and repressive marks (H3K9me3, H3K27me3 and H4K20me3). TERRA modulates this environment through the formation of RNA:DNA hybrids (R-loops) and G4s. Furthermore, RNA- or G4-binding chromatin remodellers, including Suv39H1, ORC1, NoRC, PRC2 and FUS, are recruited by TERRA and alter the epigenetic landscape. G4-binding proteins, including CTCF and YY1, mediate long-range interactions between distal G4s, contributing to higher-order chromatin organization. The telomeric shelterin complex itself is heterogeneous and probably assembles into subcomplexes (for example, TRF1–TIN2–TPP1–POT1 or TRF2–RAP1). TRF2 is essential for formation of the terminal T-loop, which requires direct interaction between TRF2 and nucleosomes. TRF2-mediated stabilization of nucleosomes may prevent branch migration at the base of the loop, which would result in cleavage of the loop by resolvases. b, TERT-mediated elongation alters the chromatin of telomeres. The length of TERRA molecules is proportional to the telomere length, allowing increased recruitment of chromatin-modifying enzymes…Fig. 4: Schematic of the ALT pathway. ALT is a telomerase-independent, cancer-specific mechanism of telomere maintenance enabled by alterations to the telomeric chromatin. Between 10 and 15% of cancers activate the ALT pathway to maintain telomere length in a telomerase-independent manner. ALT+ cancers frequently display loss of ATRX–DAXX histone chaperone activity, resulting in reduced deposition of the histone variant H3.3 at telomeres and, consequentially, progressive decompaction of the telomeres. This chromatin disruption promotes increased TERRA transcription, leading to accumulation of R-loops and G4s. ALT+ telomeres also display increased levels of the repressive histone mark H3K9me3, partially due to additional mutations such as those encoding the G34R substitution in H3.3 and the R132H substitution in IDH1, which inhibit the histone demethylase KDM4B. The combined effect of R-loops, G4s and decreased nucleosome occupancy cause persistent replication stress, ultimately giving rise to telomeric breaks. Broken telomeres are further enriched in H3K9me3 due to the break-induced recruitment of the CHAMP1–POGZ–HP1 complex. These telomeric breaks are clustered in APBs, membrane-less condensates formed through HP1- and PML-dependent phase separation. Within APBs, broken telomeres invade homologous telomeric templates to initiate HDR-mediated extension. Invasion of the broken strand is stimulated by RAD51AP1, which promotes the switch from TERRA R-loops to stable telomeric D-loops, where telomere elongation takes place.
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Teif lab @teiflab.bsky.social · 04/01/2026
The famous "It takes two to think" by @itaiyanai.bsky.social and martinlercher.bsky.social (www.nature.com/articles/s41...) may have some ramifications in the era of AI :)
Four-panel black-and-white stick-figure cartoon comparing work styles. Panel 1, “Boss”: one person sits on a cart full of books and points forward while three others pull the cart. Panel 2, “Leader”: four people pull the cart together, with the front person pointing the direction while still pulling. Panel 3, “Introvert”: a single person pulls the cart alone. Panel 4, “Introvert with AI”: the same person walks easily while a small robot pulls two book-filled carts behind them.
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Fena Ochs @fenaochs.bsky.social · 02/01/2026
We are looking for a Postdoc at the Center for Gene Expression in Copenhagen. Deadline for applications is the 11th of January. If you are interested in 3D chromatin, SMC complexes, and super-resolution microscopy, join us. www.nature.com/naturecareer...
nature.com
Postdocs at Center for Gene Expression in Department of Cellular and Molecular Medicine - Copenhagen, Hovedstaden (DK) job with University of Copenhagen | 12849488
We are looking for 2 or more highly motivated postdocs interested in ribosome biology, 3D chromatin organisation, or regulation of protein turnove...
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Teif lab @teiflab.bsky.social · 31/12/2025
Wishing you a happy, healthy, successful and science-filled new year!
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Teif lab @teiflab.bsky.social · 29/12/2025
As usual this time of year, started drafting the list of gene regulation conferences for 2026, enjoy! generegulation.org/conferences-... Know of a relevant event that’s missing? Please reply below
generegulation.org
Conferences & Schools – 2026 – Gene Regulation – Teif Lab
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Karsten Rippe @karsten-rippe.bsky.social · 24/12/2025
1/ 🎄 We got our Christmas present today: "Two distinct chromatin modules regulate proinflammatory gene expression" is now published @natcellbio.nature.com doi.org/10.1038/s415.... Our study introduces a scATAC-seq-based framework for genome-wide analysis of gene regulation features.
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Job Dekker @jobdekker.bsky.social · 17/12/2025
A major output of the 4D Nucleome project appeared today. This is the joint effort of many scientists working together and (publicly) sharing data and results for several years. We hope this is of interest to many genome biologists! www.nature.com/articles/s41...
nature.com
An integrated view of the structure and function of the human 4D nucleome - Nature
The 4D Nucleome Project demonstrates the use of genomic assays and computational methods to measure genome folding and then predict genomic structure from DNA sequence, facilitatin...
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Rosana Collepardo @rcollepardo.bsky.social · 05/12/2025
Our Science paper is out! Huge congratulations to @huabin-zhou.bsky.social, Mike Rosen, and the brilliant @janhuemar.bsky.social @juliamaristany.bsky.social and @kieran-russell.bsky.social from our group News: bit.ly/4avnkAr and bit.ly/3XBGVHS Great perspective by @vram142.bsky.social +K Zhang
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Teif lab @teiflab.bsky.social · 04/12/2025
Rudnizky et al., 2025. Ultrafast CTCF dynamics control cohesin barrier function www.biorxiv.org/content/10.1...
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Mikhail Spivakov @mspivakov.bsky.social · 25/11/2025
I'm guest-editing a collection on "Enhancer-promoter interactions" at Genome Biology. Please send us your exciting stories! link.springer.com/collections/...
link.springer.com
Enhancer-promoter interactions
Genome Biology is calling for submissions to our Collection on enhancer-promoter interactions. Enhancer–promoter interactions are central to the regulation ...
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Teif lab @teiflab.bsky.social · 24/11/2025
Maansson et al., 2025. Liquid biopsy epigenetics: establishing a molecular profile based on cell-free DNA [review] febs.onlinelibrary.wiley.com/doi/full/10....
Various analytes of liquid biopsies. Cancer cells shed various analytes into the bloodstream, all of which can be analyzed in liquid biopsies. (A) Extracellular vesicles contain various molecules, including DNA, RNA, and proteins representing the biology of the tumor. (B) Several types of cell-free RNA (cfRNA) molecules can be found in plasma, including noncoding micro-RNA (miRNA), long noncoding RNA (lncRNA), messenger RNA (mRNA), and tumor-derived RNA fusions. (C) Circulating tumor cells (CTCs) from primary tumors or metastatic sites directly represent cancer biology at the site of origin. CTCs can group together with healthy cells, creating CTC clusters. (D) Many features of cell-free DNA (cfDNA) provide great insights into tumor biology. These features include fragmentomics focusing on cfDNA fragment lengths and fragment end motifs (FEMs), 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) patterns and post-translational modifications (PTMs) of circulating histones. In addition, somatic variants, such as single-nucleotide variants (SNVs), insertions and deletions (indels), and copy number alterations (CNAs) are detectable in liquid biopsies.
Origin of cell-free DNA (cfDNA) in healthy individuals and various diseases. (A) In a healthy population, the tissue of origin of cfDNA can be traced to hematopoietic (90%) and nonhematopoietic cells (10%). Of circulating peripheral blood mononuclear cells (PBMCs), monocytes (yellow) and granulocytes (green) are the main contributors to the cfDNA pool. Erythroblasts (pink) and megakaryocytes (blue) are the main contributors from the bone marrow. Nonhematopoietic cfDNA primarily originates from endothelial and liver cells (red). (B, C) Pathological conditions can alter the origin of cfDNA; however, most of the cfDNA still originates from healthy tissues shown in (A) (gray). Patients with acute myocardial infarction (AMI) have increased cfDNA from cardiac (purple) cells (B). Similarly, cancer patients have an increased fraction of cfDNA from the organ of the primary tumor and the metastatic site (C). This is illustrated with an increased fraction of colon (orange) and neuron (brown) cfDNA in a colorectal cancer (CRC) patient with a brain metastasis.
Different cell-free DNA (cfDNA) methylation detection methods. (A) Normal and tumor cells have different methylation profiles, which are detectable in the bloodstream. Several strategies for cfDNA methylation quantification exist, each with their own strengths (+) and limitations (−). (B) Bisulfite conversion is the gold standard of methylation profiling; however, it is limited by high DNA degradation requiring a high input content. (C) As an alternative to bisulfite, enzymatic methyl sequencing (EM-seq) preserves the DNA integrity while providing single base-pair (bp) resolution of 5-methylcytosine (5mC) with higher coverage and less GC bias than bisulfite conversion. (D) Two separate 5mC cfDNA enrichment strategies exist, cell-free methylated DNA immunoprecipitation and high-throughput sequencing (cfMeDIP–seq) and T7-MBD-seq. cfMeDIP utilizes anti-5mC-DNA antibodies to isolate methylated cfDNA fragments, whereas T7-MBD-seq uses methyl-binding domain 2 protein (MBD2) to enrich for 5mC. Precipitated cfDNA is sequenced, generating a coverage profile representing the genomic region's methylation status. (E) 6-letter sequencing with Duet is one of the more recently developed methods and enables quantification of 5mC and 5-hydroxymethylcytosine (5hmC) at single-bp resolution. (F) Native cfDNA is sequenced with long reads using nanopore technology, generating both an epigenetic and genetic profile at single-bp resolution.
Fragmentomics of active and inactive genes. (A) Stable regions in the genome result in cell-free DNA (cfDNA) coverage peaks and valleys corresponding to the underlying chromatin structure. Regions with more dynamic chromatin result in a flatter cfDNA coverage profile. (B) Inactive genes are enriched for 5-methylcytosine (5mC) and do not have a structured cfDNA coverage profile around the transcript start site (TSS). cfDNA fragments from inactive genes have a peak at approximately 165 bp corresponding to caspase-activated DNase (CAD) cleavage in internucleosomal regions, leading to distinct fragment end motifs (FEMs). (C) Active genes are depleted of nucleosomes around the TSS, leading to distinct cfDNA coverage profiles. cfDNA fragments from active genes are shorter, with approximately 10-bp oscillations. Gene activity is also characterized by hypomethylation, causing the DNA to be more loosely bound to the nucleosome, allowing for internucleosomal CAD cleavage and altered FEM frequencies.
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Teif lab @teiflab.bsky.social · 24/11/2025
Some refs on nucleosome-mediated cooperativity in TF binding: ▶️Concept suggested by Polach & Widom, 1996: www.sciencedirect.com/science/arti... ▶️Our first single-bp resolution model, 2010: www.cell.com/biophysj/ful... ▶️Its application to TFs at enhancers, 2011: iopscience.iop.org/article/10.1...
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Reposted by Teif lab
Zeitlinger Lab @zeitlingerlab.bsky.social · 19/11/2025
We are pleased to announce a new preprint by @mlweilert.bsky.social: “Widespread low-affinity motifs enhance chromatin accessibility and regulatory potential in mESCs” (www.biorxiv.org/content/10.1...). See summary and longer recap below: (TLDR; low-affinity motifs matter as pioneers!)
biorxiv.org
Widespread low-affinity motifs enhance chromatin accessibility and regulatory potential in mESCs
Low-affinity transcription factor (TF) motifs are an important element of the cis-regulatory code, yet they are notoriously difficult to map and mechanistically incompletely understood, limiting our a...
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