Rémi Buisson

recruit.ap.uci.eduAssistant Professor of Biomedical Sciences (tenure track)University of California, Irvine is hiring. Apply now!

We're hiring! The Department of Biological Chemistry at UCI is seeking a tenure-track Assistant Professor! This is a broad search across biomedical sciences, including genome stability. Join a dynamic department with excellent research resources, great faculty benefits, and year-round sunshine!

cityofhope.orgSoCal Genome Stability SymposiumThe annual Genome Stability Symposium provides a forum for trainees in the Southern California region to present their research on the field of genome stability.

21 Jan

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.

Rémi Buisson reposted

Institut Jacques Monod

@ijmonod.bsky.social

28 Oct 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...

Rémi Buisson reposted

JStark lab

@jstarklab.bsky.social

17 Oct 2025

Registration is open for the 2025 SoCal Genome Stability Symposium. Free registration. All talks by trainees. www.cityofhope.org/genome-stabi...

science.orgMechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastropheUpon ATR inhibition, APOBEC3B targets unprotected single-stranded DNA at replication forks, leading to fork breakage.

16 Apr 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/...

16 Apr 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.

rdcu.beTranscription stress causes an inflammatory response via release of IL-1αNature 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...

11 Apr 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

nature.comCooperative role of PACT and ADAR1 in preventing aberrant PKR activation by self-derived double-stranded RNA - Nature CommunicationsUncontrolled 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 ...

7 Apr 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...

Rémi Buisson reposted

Thomas P200 Burke

@findmeinthelab.bsky.social

7 Mar 2025

UCI Anteaters standing up for science today!

Rémi Buisson reposted

Petr Cejka

@cejkalab.bsky.social

28 Feb 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.

Rémi Buisson reposted

Bret Freudenthal

@freudlab.bsky.social

27 Feb 2025

Happy to report the 2025/05 NIH Biochemical and Cellular Oncogenesis (BCO) study section meeting has been rescheduled for late April. Just FYI.

Bret Freudenthal@freudlab.bsky.social

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.

Rémi Buisson reposted

Bret Freudenthal

@freudlab.bsky.social

25 Feb 2025

nature.comATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage - Nature Structural & Molecular BiologyIn 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...

6 Jan 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.

6 Jan 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.

rdcu.beATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damageNature 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...

6 Jan 2025

Free access to the paper: rdcu.be/d5pue

authors.elsevier.comauthors.elsevier.com

9 Dec 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...

biorxiv.orgCooperative Role of PACT and ADAR1 in Preventing Aberrant PKR Activation by Self-Derived Double-Stranded RNADouble-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 ...

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...

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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.

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.

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.

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.

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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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.

Thanks to @pedroorteg.bsky.social orteg for driving this project

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PARP1 activation at the forks mediated by ATR inhibition recruits DNA repair factors such as XRCC1.

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.

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.

embopress.orgDifferentiation signals induce APOBEC3A expression via GRHL3 in squamous epithelia and squamous cell carcinoma | The EMBO JournalimageimageAPOBEC3A 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...

15 Nov 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....