Rémi Buisson
@buissonlab.bsky.social
Associate Professor at University of California Irvine. APOBEC, innate immunity, DNA damage, RNA viruses, and scuba diving fanatic.
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.
#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...
Registration is open for the 2025 SoCal Genome Stability Symposium. Free registration. All talks by trainees. www.cityofhope.org/genome-stabi...
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.
cityofhope.org
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/...
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.
science.org
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
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...
rdcu.be
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...
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 ...
nature.com
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.
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 · last yr.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.
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.
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.
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...
nature.com
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
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...
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 ...
biorxiv.org
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...
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....
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...
embopress.org
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/...
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...
pnas.org
