Teif lab

Yes, would that be allowed? And removing personal details from it

What about checking with AI the peer-review itself?

This potentially affects many things beyond open source...

Genome Organization: Integrating Mathematics, Physics and Computation for Advances in Biology and Medicine. March 17-20, 2026. Lausanne, Switzerland.
Registration deadline: February 13, 2026. www.cecam.org/workshop-det...

Probably other nearby mutations are not viable or not leading to proliferative advantage. So, the post-mutation selection is more or less understandable. But the mathematics of this translocation probability per se is less clear to me

May be something else as well, because Philadelphia chromosome in Chronic Myeloid Leukemia is said to be from hematopoietic stem or myeloid progenitor cells undergoing non-specific DNA breaks + NHEJ repair. I am thinking in the direction of some bridge connecting these chromosomes in the first place

I randomly became interested in this slide (it's just 1 min of a 2 hour lecture) because the rough estimate of the probability of this event does not quite match the epidemiologically observed incidence rate. Unless there is something in addition to 3D proximity that favours this translocation event

I found another paper where whole-chromosomes have been coloured in lymphocytes journals.plos.org/plosone/arti... Here the positions of chromosomes 9 and 22 are not far but not convincingly close. It would be cool to find a figure with territories of all chromosomes coloured as in the one above

Yes, that's a good point. So far the closest I could find is this one, where only two Philadelphia genes are labeled: bsky.app/profile/teif.... In the lecture (undergraduate) I wanted to make a mathematical argument about this translocation. It is a very rare event, but prevalent in a cancer subtype

Probably this one can work haematologica.org/article/view...

The closest image I found is this relative spatial positioning of chromosomes between GM12878 and K562 cell lines link.springer.com/article/10.1.... But I am looking for a more direct visualisation in the style of chromosome territories, and ideally not in cancer cells

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?

let's hope that it will be complemented by thematic calls that are wide enough to fit those research-led projects anyway (AI, ageing, cancer, etc)

is it known what's the actual reason? Restructuring or lack of funds?

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

Bologna Summer School of Genome Regulation, July 13-17, 2026. www.fondazionegolinelli.it/bologna-summ...

Looks like LinkedIn is becoming more active than bluesky in terms of paper announcements and engagements

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!

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!

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!

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!

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.

Schaepe et al, 2026. Thermodynamic principles link in vitro transcription factor affinities to single-molecule chromatin states in cells www.cell.com/cell/fulltex...

bsky.app/profile/roth...

Do you know of any inclusive online-based journal clubs in psychiatric genetics and/or epigenetics?

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...

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...

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...

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 👀

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.

Structural organization and function of telomeric chromatin [Review by Ruben van der Lugt & Jacqueline Jacobs] www.nature.com/articles/s41...

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