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Jakob Schnabl

@jakobschnabl.bsky.social

Postdoc at the FMI (@fmiscience.bsky.social) in Basel, interested in chromatin, biochemistry and SINE transposons

187 Followers  |  353 Following  |  12 Posts  |  Joined: 13.11.2024  |  1.9439

Latest posts by jakobschnabl.bsky.social on Bluesky

piRNAs are essential for transposon silencing in the animal germline.
But how do hosts trap transposon sequences in genomic loci that help establish a piRNA response?

Looking at a natural transposon invasion, Baptiste Rafanel and Kirsten Senti made some remarkable observations.

03.08.2025 15:39 β€” πŸ‘ 52    πŸ” 19    πŸ’¬ 2    πŸ“Œ 1

Antisense transposon insertions into host genes trigger piRNA mediated immunity https://www.biorxiv.org/content/10.1101/2025.07.28.667215v1

01.08.2025 03:32 β€” πŸ‘ 21    πŸ” 8    πŸ’¬ 0    πŸ“Œ 2

Uncover the hidden power of a tiny protein - the ERVK3-1 microprotein - as it interacts with the HUSH complex, a key player in silencing parasitic genomic elements, shedding light on a po...

🧡 Thread below

Full analysis: https://helixbrief.com/article/aa18903a-395a-48df-be22-64c6cf0fd0be

01.08.2025 14:45 β€” πŸ‘ 4    πŸ” 2    πŸ’¬ 1    πŸ“Œ 0
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Just 2 weeks left!

The Vienna BioCenter PostDoc Program is still accepting applications. We have 16 fully-funded fellowships available for researchers in biology, chemistry, physics, bioinformatics, and more.

Apply now: training.vbc.ac.at/post-docs/vi...

#VBCPostDoc

01.08.2025 07:18 β€” πŸ‘ 6    πŸ” 8    πŸ’¬ 1    πŸ“Œ 1
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How DNA packaging controls the β€œgenome’s guardian” Our cells tightly pack DNA into structures called nucleosomes, which protect DNA but also hide important sites. The key cancer-fighting protein p53 can still access these hidden sites, especially at n...

Our cells pack DNA into tiny bundles that hide important parts. Researchers at the FMI and EPFL found this packing affects how the cancer-fighting protein p53 works, revealing new insights into cancer. www.fmi.ch/news-events/...

31.07.2025 08:58 β€” πŸ‘ 7    πŸ” 4    πŸ’¬ 0    πŸ“Œ 0

last call!
submit your abstract by tonight to be selected for one of the many oral presentations at the leading European Transposon Meeting. We are very much looking forward to your contribution and attendance!

29.07.2025 08:41 β€” πŸ‘ 18    πŸ” 18    πŸ’¬ 0    πŸ“Œ 1
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πŸ“’ Open Call! The Max Perutz Labs invite applications for a Tenure-Track Professorship in Mechanistic Cell and Developmental Biology. More details ➑️ tinyurl.com/3fbkp89c

23.07.2025 13:14 β€” πŸ‘ 35    πŸ” 41    πŸ’¬ 1    πŸ“Œ 2
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A postdoc position in the Torben Heick Jensen lab, Aarhus University, Denmark: Mammalian Nuclear RNA Production and Turnover Systems - Ledig stilling pΓ₯ Aarhus Universitet Ledig stilling ved Institut for MolekylΓ¦rbiologi og Genetik - RNA-biologi og -innovation, Aarhus Universitet

Second call for postdoc positions in the lab. Please follow the link below to apply or get in touch for further information.
mbg.au.dk/aktuelt/ledi...

18.07.2025 09:28 β€” πŸ‘ 2    πŸ” 5    πŸ’¬ 0    πŸ“Œ 0

Pls. share widely

Calling all transposon fans & lovers of genetic innovation

MOBILE GENOME welcomes you in Heidelberg, Nov. 4–7 2025

β†’ Vibrant & friendly community
β†’ Cutting-edge talks from mechanisms to physiology
β†’ Plenty of surprises (TEs never stop innovating)

submit abstract by July 29

16.07.2025 08:43 β€” πŸ‘ 61    πŸ” 47    πŸ’¬ 1    πŸ“Œ 1
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We found a new asymmetry in the large-scale chromosome structure: sister chromatids are systematically shifted by hundreds of kb in the 5β€²β†’3β€² direction of their inherited strands! The work was led by Flavia Corsi, in close collaboration with the Daniel Gerlich lab.
www.biorxiv.org/content/10.1...
1/

15.07.2025 08:11 β€” πŸ‘ 105    πŸ” 57    πŸ’¬ 3    πŸ“Œ 7
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Preprint by the lab of Marc BΓΌhler with first author Josip Ahel "Remodeling Activity of ChAHP Restricts Transcription Factor Access to Chromatin" @biorxivpreprint.bsky.social
buff.ly/mTYarjo
@aheljo.bsky.social
@marcbuhler.bsky.social
@fmiscience.bsky.social

15.07.2025 07:01 β€” πŸ‘ 2    πŸ” 2    πŸ’¬ 0    πŸ“Œ 0
A lovely graphic from The Allied Genetics Conference 2020 depicting the many model organisms that contribute to our understanding of science.

https://genetics-gsa.org/drosophila-2025/professional-development/careers-at-tagc/

A lovely graphic from The Allied Genetics Conference 2020 depicting the many model organisms that contribute to our understanding of science. https://genetics-gsa.org/drosophila-2025/professional-development/careers-at-tagc/

CONCLUSIONS:

To promote the best science being done, we need to look at the incentives of science publishing and funding. Long-term funding produces better science. Short-term and topical agendas encourages irreproducibility.

Funding model organisms generates science we can build on! πŸͺ°πŸͺ±πŸ¦ πŸ πŸπŸΈ

6/6 🧡

10.07.2025 08:21 β€” πŸ‘ 52    πŸ” 20    πŸ’¬ 3    πŸ“Œ 0
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The "reproducibility crisis" in science constantly makes headlines. Repro efforts are often limited. What if you could assess reproducibility of an entire field?

That's what @brunolemaitre.bsky.social et al. have done. Fly immunity is highly replicable & offers lessons for #metascience

A 🧡 1/n

10.07.2025 08:21 β€” πŸ‘ 319    πŸ” 172    πŸ’¬ 10    πŸ“Œ 18
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Enhancer adoption by an LTR retrotransposon generates viral-like particles, causing developmental limb phenotypes - Nature Genetics Activation of an LTR retrotransposon inserted upstream of the Fgf8 gene produces viral-like particles in the mouse developing limb, triggering apoptosis and causing limb malformation. This phenotype c...

Finally out! πŸ₯³ Our paper showing how a transposable element (TE) insertion can cause developmental phenotypes is now published @natgenet.nature.com 🧬🦠🐁
Below is a brief description of the major findings. Check the full version of the paper for more details: www.nature.com/articles/s41588-025-02248-5

09.07.2025 10:04 β€” πŸ‘ 278    πŸ” 124    πŸ’¬ 14    πŸ“Œ 10
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Preprint by the lab of Marc BΓΌhler with first author Jakob Schnabl-Baumgartner "ChAHP Silences SINE Retrotransposons by Inhibiting TFIIIB Recruitment" @biorxivpreprint.bsky.social
buff.ly/hAXKoZ3
@jakobschnabl.bsky.social
@marcbuhler.bsky.social
@fmiscience.bsky.social

08.07.2025 07:01 β€” πŸ‘ 9    πŸ” 4    πŸ’¬ 0    πŸ“Œ 0
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Postdoc Research Group Schur The Schur lab at the Institute of Science and Technology Austria (ISTA) has an open postdoc position for a highly motivated candidate to be part of our ERC-funded project ActinID. Our Group ...

We're hiring a postdoc!
Join our ActinID project to explore an uncharacterized actin-binding protein.

- Background in cell and/or structural biology?
- Eager to bridge both fields?

Get in touch if you're curious or have questions!
#cellbiology #cryoEM #cryoET #actin

ista.ac.at/en/job/postd...

07.07.2025 09:21 β€” πŸ‘ 19    πŸ” 11    πŸ’¬ 0    πŸ“Œ 0
Remodeling Activity of ChAHP Restricts Transcription Factor Access to Chromatin Transcription in eukaryotes is regulated by chromatin-based mechanisms that control nucleosome occupancy, chromatin modifications, and transcription factor binding. We have previously shown that the transcription factor ADNP forms the ChAHP complex with the chromatin remodeler CHD4 and HP1 proteins, acting as a site-specific regulator of transcription and antagonist of CTCF binding. However, the molecular basis of these functions remained unclear. Here, we demonstrate that the CHD4 subunit is essential to antagonize CTCF and silence transcription of transposons, while HP1 proteins are dispensable. Although the remodeling activity of CHD4 is not required for ChAHP chromatin association, it is critical for both transposon repression and CTCF antagonism. Our findings support a model wherein ADNP recruits chromatin remodeling activity in a sequence-specific manner, enabling transcriptional control and local modulation of chromatin architecture. ### Competing Interest Statement The Friedrich Miescher Institute for Biomedical Research (FMI) receives significant financial contributions from the Novartis Research Foundation. Published research reagents from the FMI are shared with the academic community under a Material Transfer Agreement (MTA) having terms and conditions corresponding to those of the UBMTA (Uniform Biological Material Transfer Agreement). Novartis Research Foundation, n.a. Swiss National Science Foundation, grant 310030_188835

🧡 New preprint!
How does a chromatin remodeler know where to act?
In our latest study, we show how the transcription factor ADNP targets CHD4 remodeling activity to silence transposons and block CTCF.
πŸ‘‡ A thread on the ChAHP complex and how it weaves chromatin
πŸ§¬πŸ”¬πŸ§΅
www.biorxiv.org/content/10.1...

06.07.2025 16:25 β€” πŸ‘ 12    πŸ” 5    πŸ’¬ 1    πŸ“Œ 0

More ChAHP within the same week! Check out the work from @aheljo.bsky.social dissecting the molecular activities within the complex

06.07.2025 14:30 β€” πŸ‘ 4    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Remodeling Activity of ChAHP Restricts Transcription Factor Access to Chromatin Transcription in eukaryotes is regulated by chromatin-based mechanisms that control nucleosome occupancy, chromatin modifications, and transcription factor binding. We have previously shown that the transcription factor ADNP forms the ChAHP complex with the chromatin remodeler CHD4 and HP1 proteins, acting as a site-specific regulator of transcription and antagonist of CTCF binding. However, the molecular basis of these functions remained unclear. Here, we demonstrate that the CHD4 subunit is essential to antagonize CTCF and silence transcription of transposons, while HP1 proteins are dispensable. Although the remodeling activity of CHD4 is not required for ChAHP chromatin association, it is critical for both transposon repression and CTCF antagonism. Our findings support a model wherein ADNP recruits chromatin remodeling activity in a sequence-specific manner, enabling transcriptional control and local modulation of chromatin architecture. ### Competing Interest Statement The Friedrich Miescher Institute for Biomedical Research (FMI) receives significant financial contributions from the Novartis Research Foundation. Published research reagents from the FMI are shared with the academic community under a Material Transfer Agreement (MTA) having terms and conditions corresponding to those of the UBMTA (Uniform Biological Material Transfer Agreement). Novartis Research Foundation, n.a. Swiss National Science Foundation, grant 310030_188835

preprint alert: www.biorxiv.org/content/10.1...

06.07.2025 11:55 β€” πŸ‘ 41    πŸ” 10    πŸ’¬ 1    πŸ“Œ 2

For more molecular dissection of ChAHP stay tuned for another preprint from the lab coming soon. Thanks to all the co-authors Especially Fabio, @xxxmichixxx.bsky.social and of course
@marcbuhler.bsky.social

03.07.2025 08:18 β€” πŸ‘ 3    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0

πŸ’‘ Taken together we establish ChAHP as a sequence specific regulator of POL III transcription, which is different from Maf1, a well-established POL III repressor which leads to global POL III repression.

03.07.2025 06:18 β€” πŸ‘ 3    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

🎯 ChAHP’s action is also very precise: We see only SINE transcription affected but other POL III transcripts, like tRNAs are not affected. This precision is fascinating as these elements share the same promoter architecture.

03.07.2025 06:18 β€” πŸ‘ 3    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

βš™οΈ The mechanism: ChAHP doesn't prevent TFIIIC from binding SINEs. Instead, it blocks the next step - TFIIIB recruitment. Think of it as letting someone find the door (TFIIIC) but hiding the key (TFIIIB) needed to open it.

03.07.2025 06:18 β€” πŸ‘ 2    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

πŸ” How do cells silence thousands of SINEs without affecting normal genes? We tested the usual suspects (DNA methylation, heterochromatin) but they had no effect. Then we tested ChAHP and within one hour of ChAHP removal SINEs are up regulated! We use mESCs as a model to study SINE regulation.

03.07.2025 06:18 β€” πŸ‘ 2    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

🧬 Large proportions of genomes come from "jumping genes" - DNA sequences that can copy themselves. SINEs are a special kind of transposons. They are: Short DNA sequences (~200bp) that use POL III for their transcription and still actively transpose!

03.07.2025 06:18 β€” πŸ‘ 2    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0
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ChAHP Silences SINE Retrotransposons by Inhibiting TFIIIB Recruitment Short interspersed nuclear elements (SINEs) are abundant non-autonomous transposable elements derived from RNA polymerase III (POL III)-transcribed short non-coding RNAs. SINEs retain sequence feature...

πŸ“– Happy to share our recent preprint! www.biorxiv.org/content/10.1... We discovered how SINEs are kept silent: the ChAHP protein complex acts as a molecular brake on POL III transcription retrotransposons. A 🧡:

03.07.2025 06:18 β€” πŸ‘ 66    πŸ” 24    πŸ’¬ 1    πŸ“Œ 4
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MORC2 directs transcription-dependent CpG methylation of human LINE-1 transposons in early neurodevelopment Methylation of CpG dinucleotides is essential for silencing genomic repeats such as LINE-1 retrotransposons (L1s) in the germline and soma. Evolutionarily-young L1s are transcribed in human pluripoten...

Very proud of this work where we define how the MORC2 ATPase directs CpG methylation of active human L1 transposons in early development.

Thanks to co-authors, funders & wonderful environment @lundstem.bsky.social

www.biorxiv.org/content/10.1...

Brief thread below (do people still do that?) 1/X

01.07.2025 12:55 β€” πŸ‘ 27    πŸ” 16    πŸ’¬ 1    πŸ“Œ 0
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πŸ†• publication! Cells don’t just fight infection - they fine-tune their immune response. A new study from the Versteeg lab in @narjournal.bsky.social led by Adrian SΓΆderholm uncovers how RNA processing of JAK2 helps regulate immune signals ➑️ tinyurl.com/2py27c8u
@univie.ac.at
@meduniwien.ac.at

01.07.2025 06:28 β€” πŸ‘ 15    πŸ” 5    πŸ’¬ 3    πŸ“Œ 2

@jakobschnabl is following 20 prominent accounts