Teif lab
LightNews LightNews
banner
teiflab.bsky.social
Teif lab
@teiflab.bsky.social
2.9K followers 1K following 340 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. https://generegulation.org
Posts Replies Media Videos
teiflab.bsky.social
February 11, 2026 at 12:18 PM
teiflab.bsky.social
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?
February 8, 2026 at 12:23 PM
Reposted by Teif lab
aaronquinlan.bsky.social
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
Intro to Bedder – The Quinlan Lab
quinlanlab.org
December 2, 2025 at 2:28 AM
teiflab.bsky.social
Looks like LinkedIn is becoming more active than bluesky in terms of paper announcements and engagements
January 23, 2026 at 2:06 PM
teiflab.bsky.social
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!
January 21, 2026 at 11:42 PM
Reposted by Teif lab
lucagiorgetti.bsky.social
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!
January 20, 2026 at 12:59 PM
Reposted by Teif lab
hannekevlaming.bsky.social
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!
January 15, 2026 at 9:33 PM
teiflab.bsky.social
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!
January 14, 2026 at 6:42 PM
teiflab.bsky.social
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.
January 11, 2026 at 11:37 PM
Reposted by Teif lab
annadearman.bsky.social
Do you know of any inclusive online-based journal clubs in psychiatric genetics and/or epigenetics?
January 9, 2026 at 2:00 PM
teiflab.bsky.social
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...
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...
faseb.onlinelibrary.wiley.com
January 7, 2026 at 11:31 PM
Reposted by Teif lab
moorejille.bsky.social
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 👀
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...
www.nature.com
January 7, 2026 at 6:47 PM
teiflab.bsky.social
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.
January 7, 2026 at 8:41 PM
teiflab.bsky.social
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.
January 4, 2026 at 3:27 PM
Reposted by Teif lab
fenaochs.bsky.social
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...
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...
www.nature.com
January 2, 2026 at 8:12 AM
teiflab.bsky.social
Wishing you a happy, healthy, successful and science-filled new year!
December 31, 2025 at 2:04 PM
teiflab.bsky.social
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
Conferences & Schools – 2026 – Gene Regulation – Teif Lab
generegulation.org
December 29, 2025 at 3:29 PM
Reposted by Teif lab
karsten-rippe.bsky.social
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.
December 24, 2025 at 10:44 PM
Reposted by Teif lab
jobdekker.bsky.social
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...
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...
www.nature.com
December 17, 2025 at 8:59 PM
Reposted by Teif lab
nucleosomepolice.bsky.social
Confused by all the histones that are cropping up in organisms that are decidedly NOT eukaryotes? check out our review - fantastic work by team NucEvo in the #Lugerlab
The Expanding Histone Universe: Histone-Based DNA Organization in Noneukaryotic Organisms - www.annualreviews.org/content/jour...
December 9, 2025 at 3:14 PM
Reposted by Teif lab
rcollepardo.bsky.social
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
December 5, 2025 at 9:47 AM
teiflab.bsky.social
Rudnizky et al., 2025. Ultrafast CTCF dynamics control cohesin barrier function www.biorxiv.org/content/10.1...
December 4, 2025 at 6:50 PM
Reposted by Teif lab
mspivakov.bsky.social
I'm guest-editing a collection on "Enhancer-promoter interactions" at Genome Biology. Please send us your exciting stories!

link.springer.com/collections/...
Enhancer-promoter interactions
Genome Biology is calling for submissions to our Collection on enhancer-promoter interactions. Enhancer–promoter interactions are central to the regulation ...
link.springer.com
November 25, 2025 at 10:55 AM
teiflab.bsky.social
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.
November 24, 2025 at 11:24 AM
teiflab.bsky.social
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...
November 24, 2025 at 10:21 AM