We are looking for a candidate to apply for a postdoc contract in the Juan de la Cierva 2026 call, to join our lab at the @CBM_CSIC_UAM to work on the interplay between the ubiquitin pathway, DNA replication and the replication stress response. aei.gob.es/convocatorias/bus…

Congrats @rodrimartinr on your great thesis defense and thanks to María Villa, AnnaMaria Ruggiano and Jim Sutherland for their work as Thesis Committee. Rodrigo is the first PhD from the lab and we cannot be prouder of his great work. All the best in your future career!

We propose a semi-distributive model for priming in the lagging strand that sets the RSR in a DNA replication control mode (DRC). The DRC modulates the progression of DNA replication through S phase to ensure the maintenance of genomic stability.

Congrats Alicia on the best poster prize in the PhD & Postdoc Annual Meeting @CBM_CSIC_UAM Very proud of you! Many more successes to come!

If you are interested, contact us!

We are looking for a candidate to apply to a #MSCA Postdoctoral Fellowship in our lab in the @CBM_CSIC_UAM, working on the connections between DNA replication dynamics, replication stress and genomic instability in cáncer. Contact us if you are interested and please retweet.

Huge thanks to all people involved, @SMOA_CBM and flow cytometry facilities from @CNIOStopCancer and @CBM_CSIC_UAM.

So, to sum up: VCP/p97 ➡️ POLA/PRIM on chromatin ➡️ priming ➡️ basal RSR activation! This work was led by @Emlecona from @CBM_CSIC_UAM in collaboration with @JMendez_DNA from @CNIOStopCancer. Want to dive a little bit more in our work? Click this link! rdcu.be/eu1yo

And the activation of the RSR induced by VCPi is relevant, as the phosphorylation of CHK1 leads to an arrest in G2/M. More importantly, CHK1 activation is lost when we block the priming action of POLA/PRIM.

What are the consequences of more POLA/PRIM on chromatin? We observed that the inhibition of VCP/p97 also increased priming by POLA/PRIM, as observed in the EdU comet assay.

In fact, we showed that VCP/p97 and POLA/PRIM do interact. Interestingly, VCP/p97 inhibition could not induce the accumulation of POLA/PRIM on chromatin if origin firing is inhibited with CDC7i.

It struck our attention that the increased activation of the RSR induced when VCP/p97 is inhibited is mirrored by the accumulation of POLA/PRIM on chromatin. Could our two guests be working together?

First, we found that VCP/p97 is necessary for DNA replication and its inhibition leads to defects in fork progression and origin firing that result in the activation of the RSR.