SAURINLAB
THE ART OF SCIENCE
is thinking differently
The lab is based at the University of Dundee and we study the process of cell division. Why? Because it is fundamental to all life on earth and it goes wrong in the vast majority of cancers. It is also a beautiful system to understand how signalling networks are regulated in time and space.
We currently have opening for Postdocs, PhD students and Technicians to joining the lab from summer 2026. This is thanks to recent programme funding from Cancer Research UK and The Wellcome Trust. Brief details of each programme (summaries further below):
1) CRUK have funded us for 5 years to examine the role of senescence and senescence evasion in cancer progression and treatment. Find the project summary below and see the publication pages for details of our recent work on this (e.g. Pareri et al, BioRxiv 2025; Crozier et al Mol Cell, 2023, Foy et al Mol Cell, 2023; Foy et al NPJ Breast Cancer 2024; Crozier et al, EMBO J, 2022).
2) The Wellcome Trust have funded an 8-year team award to investigate a fundamental property of all phosphorylation sites that we currently know almost nothing about: how these sites can "flash" on and off individual molecules to drive unique signalling properties and outputs. We discussed this in a previous opinion article (Gelens et al. Dev Cell, 2018) and it builds on our recent work and technologies studying kinases and phosphatases during mitosis (Allan et al, Nat Comms, 2025; Corno EMBO J, 2023; Cordeiro J Cell Biol, 2020). This is an exciting multidisciplinary collaborative project with Tony Ly (Dundee) and Andrea Musacchio (Max Planck, Dortmund) and vacancies are available in all labs. This will provides a unique training environment, with opportunity to work between labs, and to learn a variety of cutting-edge techniques, including AI-based imaging, advance mass spectrometry, and biochemical reconstitutions of kinetochores.
If you are highly motivated and interested in joining one of these projects then take a closer look at the philosophy pages to learn more about the culture in the lab. If you like what you have seen and you want to know more than please contact me for further information (a.saurin - at- dundee.ac.uk).
Find out more about the questions that drive our research on the about page.
And discover more in the philosophy section about what guides our lab and research culture.
You can find out about the different projects in these two areas under the projects tab.
You can find all the people in the lab, past and present.
CRUK Project Summary: Cellular Enlargement as a Drive of Therapy-induced Senescence and Genome Instability.
Most anti-cancer therapies arrest cell cycle progression either directly or indirectly. These include cell cycle inhibitors, cytotoxic chemotherapeutics and radiation. A common outcome of this arrest is permanent exit from the cell cycle into senescence. Although senescence is a desirable outcome of therapy it can also contribute to relapse as cancer cells that escape senescence can drive disease progression and drug-resistance. Understanding what determines these different fates is crucial if we are to improve cancer therapy responses. A large body of recent work from ourselves and others shows that cellular enlargement drives the transition into senescence following cell cycle inhibition. When cancer cells arrest in the cell cycle, they continue to grow in size. This leads to a variety of cellular stresses that feedback to stably reinforce the arrest by inducing p53/p21 to trigger senescence. However, some cancer cells can evade senescence, particularly those lacking p53, and these enlarged cells continue to cycle leading to defects in DNA replication, chromosome segregation and DNA repair. This allows the enlarged non-senescent cells to accumulate genetic and chromosomal instability, potentially driving resistance to therapy. Cellular enlargement is therefore a crucial fate-determinant following a cell cycle arrest that can drive either senescence or genome instability. This proposal aims to mechanistically characterise these size-dependent fates and then use this information to improve cancer therapy responses. Single-cell assays, cell biology, transcriptomics and proteomics will be used to characterise the mechanisms of senescence and genome instability in enlarged cells. Targeted CRISPR screening, live-cell imaging and single-cell sequencing will be used to find strategies to kill enlarged cells or restrict chromosomal instability to prevent drug-resistance.
Wellcome Project Summary: Kinase-phosphatase cooperativity on individual molecules during the cell cycle
Protein phosphorylation regulates protein function to control most aspects of cell biology. Although each phosphorylation site only exists in two states (on/off), the frequency of switching between these states can vary dramatically. Individual molecules that “flash” on and off rapidly can possess unique signalling properties, but these are difficult to study because this dynamic information remains hidden from current analytical methods. This is a major blind-spot in our knowledge because these phosphorylation-dephosphorylation (PdP) dynamics are a fundamental property of all phosphorylation sites, they can produce specific signalling properties and outputs, and they could also be altered to drive disease. This proposal will quantify PdP dynamics for the first time and focus on specific kinase-phosphatase pairs that induce rapid dynamics during mitosis. By combining mathematical modelling, biochemical reconstitution and cell biology, we will uncover how PdP dynamics can produce unique signalling outputs to drive chromosome segregation. During later years, we will examine how PdP dynamics can regulate other cell cycle phases, and we will test our hypothesis that PdP dynamics are deregulated to drive chromosomal instability in cancer. Together, this will reveal a hidden yet fundamental aspect of phospho-regulation that has widespread implications for cell biology and disease.
