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Rémi Buisson

@buissonlab.bsky.social
549 followers 313 following 34 posts

Associate Professor at University of California Irvine. APOBEC, innate immunity, DNA damage, RNA viruses, and scuba diving fanatic.

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Rémi Buisson @buissonlab.bsky.social · 21/01/2026
We are seeking a motivated postdoctoral fellow to investigate mechanisms of DNA damage response, APOBEC-mediated mutagenesis, innate immunity, and double-stranded RNA sensing. Located in Southern California, UCI offers an outstanding scientific environment and exceptional quality of life.
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Institut Jacques Monod @ijmonod.bsky.social · 28/10/2025
#JobOffer 💼 Un poste susceptible d’être vacant de Professeur en stabilité des génomes devrait s’ouvrir pour la rentrée 2026 au sein de l’Institut Jacques Monod ➡️ Informations concernant ce poste et la procédure de candidature 🔗 www.ijm.fr/poste-de-pro...
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JStark lab @jstarklab.bsky.social · 17/10/2025
Registration is open for the 2025 SoCal Genome Stability Symposium. Free registration. All talks by trainees. www.cityofhope.org/genome-stabi...
cityofhope.org
SoCal Genome Stability Symposium
The annual Genome Stability Symposium provides a forum for trainees in the Southern California region to present their research on the field of genome stability.
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Rémi Buisson @buissonlab.bsky.social · 20/05/2025
Thanks for the great description of our recent study!
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Rémi Buisson @buissonlab.bsky.social · 18/04/2025
Thanks Debbie!!
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Rémi Buisson @buissonlab.bsky.social · 16/04/2025
Many thanks to @pedroorteg.bsky.social for leading this work, and to @johnmaciejowski.bsky.social and the Abby Green Lab for their contributions to the story.
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Rémi Buisson @buissonlab.bsky.social · 16/04/2025
Today, we report that APOBEC3B targets unprotected single-stranded DNA at replication forks upon ATR inhibition, triggering a reaction cascade involving UNG2 and APE1 that leads to fork collapse and hyperactivation of PARP1, causing replication catastrophe. www.science.org/doi/10.1126/...
science.org
Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe
Upon ATR inhibition, APOBEC3B targets unprotected single-stranded DNA at replication forks, leading to fork breakage.
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Rémi Buisson @buissonlab.bsky.social · 11/04/2025
A beautiful News & Views by @unterholznerlab.bsky.social highlighting our latest paper in @natsmb.nature.com, where we show that transcription stress triggers an inflammatory response through the release of IL-1α. rdcu.be/ehkTV
rdcu.be
Transcription stress causes an inflammatory response via release of IL-1α
Nature Structural & Molecular Biology - DNA damage can be sensed as a danger signal by the innate immune system. Bournique et al. show that the transcription stress caused by DNA lesions can...
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Rémi Buisson @buissonlab.bsky.social · 11/04/2025
Thank you so much for this beautiful review of our paper!!
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Rémi Buisson @buissonlab.bsky.social · 07/04/2025
Thanks!!
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Rémi Buisson @buissonlab.bsky.social · 07/04/2025
Today, we report our new study demonstrating that PACT functions as an inhibitor rather than an activator of PKR, and works together with ADAR1 to suppress aberrant activation of PKR by self-derived double-stranded RNA. www.nature.com/articles/s41...
nature.com
Cooperative role of PACT and ADAR1 in preventing aberrant PKR activation by self-derived double-stranded RNA - Nature Communications
Uncontrolled activation of PKR by endogenous double-stranded RNA (dsRNA) is detrimental to cells, as it leads to global translational shutdown. Here, we show that PACT and ADAR1 establish a threshold ...
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Thomas P200 Burke @findmeinthelab.bsky.social · 07/03/2025
UCI Anteaters standing up for science today!
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Petr Cejka @cejkalab.bsky.social · 28/02/2025
Very sad to read about the science funding situation in the US at the moment. I am waiting for some funding decisions in the coming weeks, but I will likely have opening(s) in my lab in Switzerland in the coming weeks (PhD student/postdoc). As a PhD candidate, you need to have a Master's degree.
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Bret Freudenthal @freudlab.bsky.social · 27/02/2025
Happy to report the 2025/05 NIH Biochemical and Cellular Oncogenesis (BCO) study section meeting has been rescheduled for late April. Just FYI.
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Bret Freudenthal @freudlab.bsky.social · 25/02/2025
The 2025/05 NIH Biochemical and Cellular Oncogenesis (BCO) study section meeting that was supposed to happen tomorrow has been rescheduled to a later date, to be determined. Just FYI for folks wondering. This is so disheartening.
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Rémi Buisson @buissonlab.bsky.social · 25/02/2025
So frustrating! For both reviewers and applicants…. So much work for nothing….
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Rémi Buisson @buissonlab.bsky.social · 06/01/2025
Free access to the paper: rdcu.be/d5pue
rdcu.be
ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage
Nature Structural & Molecular Biology - In this study, the authors show that DNA-damage-mediated transcriptional stress induces NF-κB through IRAK1, allowing damaged cells with impaired...
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Rémi Buisson @buissonlab.bsky.social · 06/01/2025
Our findings provide an alternative mechanism for damaged cells with impaired transcription to initiate an inflammatory response without relying on their own gene expression, a necessary step that injured cells depend on during canonical innate immune responses.
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Rémi Buisson @buissonlab.bsky.social · 06/01/2025
Today @naturesmb.bsky.social 🥳, we report that the activation of NF-κB after DNA damage can occur through two distinct mechanisms. While ATM triggers NF-κB activation after DSBs, we found that IRAK1 specifically induces NF-κB in response to DNA damage causing transcriptional stress.
nature.com
ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage - Nature Structural & Molecular Biology
In this study, the authors show that DNA-damage-mediated transcriptional stress induces NF-κB through IRAK1, allowing damaged cells with impaired transcription to initiate an inflammatory response wit...
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Rémi Buisson @buissonlab.bsky.social · 06/01/2025
Thank you very much! I am glad you liked our story!
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Rémi Buisson @buissonlab.bsky.social · 17/12/2024
Congratulation 🥳
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Rémi Buisson @buissonlab.bsky.social · 09/12/2024
Our detailed protocol revealing our secret to performing perfect in vitro APOBEC deaminase reactions on DNA substrates at near-nucleotide resolution. authors.elsevier.com/a/1kDyIHRzCU...
authors.elsevier.com
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Rémi Buisson @buissonlab.bsky.social · 03/12/2024
Félicitation !!!🥳
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Rémi Buisson @buissonlab.bsky.social · 28/11/2024
We propose that both PACT and ADAR1 act as essential barriers against PKR, creating a threshold of tolerable levels to endogenous dsRNA in cells without activating PKR-mediated translation shutdown and cell death.
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Rémi Buisson @buissonlab.bsky.social · 28/11/2024
Simultaneous deletion of PACT and ADAR1 results in synthetic lethality, which can be fully rescued in PKR-deficient cells. This suggests PACT cooperates with ADAR1 to suppress PKR activation from self-dsRNAs in uninfected cells.
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Rémi Buisson @buissonlab.bsky.social · 28/11/2024
Our Alphafold 3 modeling analysis of PACT reveals the formation of a dimer that surrounds dsRNA, blocking access to both sides of the dsRNA and thereby preventing PKR activation.
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Rémi Buisson @buissonlab.bsky.social · 28/11/2024
We find that cells deficient for PACT hyperactivate PKR in response to several different RNA viruses, raising the question of why cells need to limit PKR activity? We show that it is critical to prevent PKR activation from self-dsRNA.
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Rémi Buisson @buissonlab.bsky.social · 28/11/2024
New Lab Preprint!🥳 Using CRISPR-Translate, a genome-wide CRISPR-Cas9 knockout screening method developed by the lab exploiting translation levels as a readout, we reveal that PACT is an inhibitor of PKR and not an activator during RNA viral infections. www.biorxiv.org/content/10.1...
biorxiv.org
Cooperative Role of PACT and ADAR1 in Preventing Aberrant PKR Activation by Self-Derived Double-Stranded RNA
Double-stranded RNAs (dsRNAs) produced during viral infections are recognized by the innate immune sensor protein kinase R (PKR), triggering a host translation shutoff that inhibits viral replication ...
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Rémi Buisson @buissonlab.bsky.social · 24/11/2024
It was nice seeing you!! And to remember what winter feels like 🥶
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
Thank you very much!!
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
Thanks to @pedroorteg.bsky.social orteg for driving this project
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
Our findings uncover the mechanisms behind replication fork collapse during replication catastrophe and show that APOBEC3B drives cell sensitivity caused by ATR and PARP inhibitors.
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
Additionally, we show that APE1-mediated DNA cleavage is the critical step for PARP1 trapping and hyperactivation in cells, regardless of how abasic sites are formed, likely through the generation of 5'-dRP on DNA.
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
PARP1 activation at the forks mediated by ATR inhibition recruits DNA repair factors such as XRCC1.
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
We find that ATR inhibition depletes RPA, exposing single-stranded DNA at replication forks to APOBEC3B. This triggers a cascade involving UNG2 creating abasic sites and APE1, which subsequently cleaves abasic sites, causing fork collapse and PARP1 activation.
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
New Lab Preprint! We show that ATR inhibition results in hyperactivation of PARP1 at replication forks, driven by APOBEC3B, UNG2, and APE1 reaction cascade targeting unprotected single-stranded DNA at the forks. www.biorxiv.org/content/10.1...
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
Our findings uncover the mechanisms behind replication fork collapse during replication catastrophe and show that APOBEC3B drives cell sensitivity caused by ATR and PARP inhibitors.
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Rémi Buisson @buissonlab.bsky.social · 16/11/2024
Additionally, we show that APE1-mediated DNA cleavage is the critical step for PARP1 trapping and hyperactivation in cells, regardless of how abasic sites are formed, likely through the generation of 5'-dRP on DNA.
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Rémi Buisson @buissonlab.bsky.social · 15/11/2024
Great collaboration with Tim Fonton's team, which uncovered a new role for APOBEC3A during keratinocyte differentiation. @TimFenton10 showed that aberrant activation of GRHL3 in dividing cells could potentially drive mutagenic APOBEC3A activity in cancer. www.embopress.org/doi/full/10....
embopress.org
Differentiation signals induce APOBEC3A expression via GRHL3 in squamous epithelia and squamous cell carcinoma | The EMBO Journal
imageimageAPOBEC3A and APOBEC3B encode DNA editing enzymes with anti-viral roles that generate somatic mutations in cancer. This study provides insight into their expression in healthy and cancerous e...
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Rémi Buisson @buissonlab.bsky.social · 14/11/2024
In our latest paper @pnas, we reported CRISPR-Translate, a genome-wide CRISPR-Cas9 knockout screen-based method designed to identify factors regulating translation. We discovered IRF2 as a novel regulator of OAS3/RNase L-mediated RNA decay during viral infections. www.pnas.org/doi/10.1073/...
pnas.org
A CRISPR-Cas9 knockout screening identifies IRF2 as a key driver of OAS3/RNase L-mediated RNA decay during viral infection | PNAS
OAS-RNase L is a double-stranded RNA-induced antiviral pathway triggered in response to diverse viral infections. Upon activation, OAS-RNase L supp...
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