Looks like a major policy shift: Cancer Research UK announces that it is no longer funding open access publishing costs (this includes via block grants, use of core grants at CRUK funded institutes, and any funded projects): news.cancerresearchuk.org/2026/04/01/w...
bsky.app/profile/hell...
I think engagement metrics existed on Twitter before Musk. One thing that happened after he took over is the "confidentiality" of likes so that only the author of the post can view the names of people who liked it. Also, he copied from Bluesky the idea of author control who can engage with each post
Several years ago, we established a "quantitative gene regulation" group on LinkedIn, around 1600 members, but somehow, the community was more active on Twitter, so we did not post in this group for years. May be it's time to revive it? www.linkedin.com/groups/3795224
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
By the way, very nice poster, congratulations to your artist!
bsky.app/profile/maxv...
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.
Adhireksan et al, 2026. Linker histones consolidate heterogenous nucleosome fiber contacts by linking together multiple nucleosomes www.nature.com/articles/s41...
Whatever you like more :)
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/)).](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:7rjg5hcnnloxgwuvwi23aixu/bafkreihl7mkdtxojw23qoqxm7yt57frzc24mjjllszhbohbvb67ffguccy)
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/)).
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
i actually did an attempt at some point to classify short-read sequencing a-la Illumina as Second Generation Sequencing, and Nanopore and Co as Third Generation Sequencing. This leaves space for new generations to be named as they arise
Assuming 15 min per student for oral exam and 15 min per script for marking written exams, the workload is comparable
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.
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.
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