School of Molecular Biosciences

24.9.25 

Rankine Building, 108LT 

“Breaks and Crosses - Insights into the molecular mechanisms of meiotic recombination”

What makes us unique? At the cellular level, our genetic diversity is a key element of our individuality, reflecting a unique mix of traits inherited from our parents. To generate viable haploid gametes, the genome must be halved through a specialised form of cell division; meiosis. During meiosis I, homologous chromosomes must be accurately segregated, which first requires their physical linkage. But how do homologous chromosomes pair and become connected? In most organisms, this is achieved through homologous recombination, which repairs programmed DNA double-strand breaks in a biased manner to generate crossovers. How is DNA break formation regulated? And how is the repair machinery directed to favour crossover outcomes? In this talk, I will present our ongoing work using biochemical reconstitution to dissect the molecular mechanisms that underpin meiosis I. In part one, I will discuss the proteins that assemble on meiotic chromatin and how they recruit and activate the break-forming machinery. In part two, I will explore how DNA repair intermediates are stabilised to become mature crossovers. Our findings illuminate not only fundamental aspects of cell biology but also the potential roles of germline-specific factors in the development of somatic cancers.

8.10.25 

42 Bute Gardens 916LT 

“Regulation of plant greoeth by the SNRK1 Signalling"

Plant growth and development are largely influenced by environmental conditions. An increasing body of evidence suggests that environmental information is partly conveyed as sugar signals which have accordingly been linked to stress responses, phase transitions such as germination and flowering, and growth control. A central component of the sugar signalling network is the evolutionarily conserved AMPK/SnRK1 protein kinase. SnRK1 is activated under low carbon conditions often associated with stress, driving a vast metabolic and transcriptional reprogramming that promotes energy-saving and nutrient remobilization strategies.

In this talk, I will show that several aspects of plant growth and development are regulated by the SnRK1 signalling pathway in response to sugar availability but also in response to the phytohormone abscisic acid that signals water scarcity. I will also discuss our progress on the mechanisms by which SnRK1 is regulated by sugar signals, enabling the coordination of metabolism and growth with sucrose supply.

22.10.25

42 Bute Gardens 916LT  

"Targeting extracellular proteases to develop antibiofilm peptides”

Dr Czekster is a Brazilian biochemist and Reader at the University of St Andrews. Her interdisciplinary research focuses on pathogenic bacteria and the development of strategies to combat infectious diseases. Dr. Czekster began her academic training at the Federal University of Rio Grande do Sul (UFRGS), earning a BSc in Molecular Biology and a teaching degree in Biological Sciences, followed by an MSc in Biochemistry, where she investigated enzymes involved in tryptophan biosynthesis. She completed her PhD at the Albert Einstein College of Medicine, specializing in enzymes related to tetrahydrofolate biosynthesis in Mycobacterium tuberculosis. Her postdoctoral work at Yale University expanded her focus to include beta-amino acids, aminoacyl-tRNA synthetases, and their incorporation in nascent proteins by modified ribosomes. In 2015, she joined the University of St Andrews as a postdoctoral researcher in Prof. Jim Naismith’s group, examining the biosynthesis of fungal and plant cyclic peptides including amanitins and segetalins. In 2017, Dr. Czekster became an independent research fellow, and in 2018, she was awarded a prestigious Sir Henry Dale Fellowship from the Wellcome Trust, enabling the establishment of her independent research group in the University of St Andrews. She runs a citizen science project “Antibiotics under our feet” to engage with learning settings and better understand microbes. In 2025 she was one of the winners of the ACS Infectious Diseases Young Investigator Award for her work in chemical biology and infectious diseases.

5.11.25 

Hunterian Art Gallery LT 

"Protein persulfidation enters a new phase" 

To sustain life, nature relies on a limited set of chemical reactions; among them is sulfur-based chemistry, which primarily controls intracellular redox homeostasis and redox signalling. Hydrogen sulfide (H2S), one of the simplest sulfur-containing molecules in cells, has attracted significant attention since its potential physiological roles were first proposed. One of the main mechanisms by which H2S signals is the post-translational modification of cysteine residues, known as persulfidation. Key questions remain about how protein persulfides form in cells and how they affect cellular function, particularly in the context of aging and age-related diseases. This talk will examine structural versus functional effects and controlled versus stochastic formation of persulfides. Specifically, I will introduce liquid–liquid phase separation—a mechanism by which cytoplasmic components (proteins and RNAs) assemble into distinct, membraneless compartments (biomolecular condensates)—as a primary way through which H2S-induced protein persulfidation regulates cellular function and could be used to improve health- and lifespan.

19.11.25 

Rankine 108LT

“Secretion of antibacterial toxins by the Staphylococcus aureus type VII secretion system"

The Type VII protein secretion system (T7SS) is found in mycobacteria and in many Gram-positive bacteria including the human pathogen Staphylococcus aureus. S. aureus encodes a single T7SS that is genetically diverse between strains. The S. aureus T7SS machinery is composed of four membrane proteins, EsaA, EssA, EssB and EssC, and two additional globular proteins EsxA and EsaB. Structural studies and comparison with the mycobacterial T7SS suggest that EssC, a member of the AAA+ ATPase superfamily, protein most likely forms the secretion pore. Some strains of S. aureus secrete a large nuclease toxin, EsaD, through the T7SS that is very potent, and highly active against chromosomal DNA. S. aureus protects itself from the action of the nuclease by producing an anti-toxin that binds tightly to the nuclease, blocking its activity. The nuclease also interacts with a specific chaperone that appears to target the nuclease-anti-toxin complex to the secretion machinery. During secretion by the T7SS, the anti-toxin is probably dissociated from the nuclease and remains inside the cell while the nuclease is secreted. Co-culture experiments indicates that the T7-dependent nuclease mediates competition between closely related S. aureus strains, which is likely to be important during colonization. Recently we have characterised the T7SS-secreted toxin EsxX showing that it is a membrane-depolarising toxin with a glycine zipper motif. EsxX is profoundly toxic to bacteria, displaying toxicity from both cytoplasmic and extracellular compartments. A pair of polytopic membrane proteins, ExiCD, protect cells from intoxication by extracellular EsxX. By contrast, a distinct soluble heterodimer, ExiAB, neutralises cytoplasmic EsxX by sequestration of its glycine zipper motif in a binding groove on ExiB. Our work defines a new class of antibacterial toxin requiring two distinct types of immunity protein which follow different phylogenetic distributions.

3.12.25

Yudowitz LT  

We investigate the precise mechanisms by which dietary nutrients influence cellular and organ function, focusing on the role of metabolites as intracellular signalling molecules. We have recently developed rigorous approaches for subcellular metabolite analysis by liquid chromatography–mass spectrometry (LC–MS), with particular emphasis on acyl-Coenzyme A thioesters (acyl-CoAs).

Our work shows that the nucleus functions as a distinct metabolic compartment, mediating the dynamic relationship between nutrient availability and histone modification. Within the nucleus, metabolites act as substrates, inhibitors, and cofactors for chromatin-modifying enzymes, thereby contributing to the establishment and maintenance of gene expression and cell identity.

Our current research addresses three fundamental questions in nuclear metabolism:

1. What mechanisms support differential metabolism within the nucleus?
2. How does nuclear metabolism influence epigenetic regulation?
3. How do these processes affect physiological responses to dietary nutrients?

In this talk, I will highlight our recent findings on how propionate, a major gut microbiota–derived short-chain fatty acid, shapes hepatocyte function through nuclear propionyl-CoA generation and the emerging chromatin modification, histone lysine propionylation (Kpr). Our results point to a potential role for transient ‘epigenetic’ marks in shaping how the liver responds to nutrient cues.

10.12.25

Rankine 108LT 

“Visualizing Dynamic Regulation of the Ubiquitin-Proteasome System in Response to Signals”

The ubiquitin system is governed by the transient assembly of conformationally dynamic complexes. We are fascinated by how these molecular machines form and function in response to stimuli ranging from endogenous signals to degrader drugs mediating targeted protein degradation. We employ an integrated multidisciplinary approach to investigate crosstalk between cellular perturbations and the ubiquitin system—ranging from the development of chemical biology probes and proteomic profiling techniques, to biochemical reconstitution and high-resolution structures by cryo-EM, to in situ visualization of assemblies using cryo-electron tomography. We then aim to reconstitute these systems to uncover the underlying biochemical and high-resolution structural mechanisms. In this talk, I will present our latest findings on the visualization of dynamic assemblies involved in ubiquitin-mediated regulation.

17.12.25 

Rankine 108LT 

"Nanoscale materials for control of mesenchymal stromal cell phenotype and development of blood cancer models"

After a PhD at Queen Mary University of London on osteoblast response to bioactive composites I moved to Glasgow to study cell-nanoscale interactions. In 2003 I became an independent researcher securing a BBSRC David Phillips Fellowship to explore mesenchymal stem cell response to nanotopography. Appointed to a lectureship in 2008 and a Readership in 2010, I became Professor of Cell Engineering at the University of Glasgow in 2014. I am currently co-Director of the Centre for the Cellular Microenvironment (https://glasgow.thecemi.org). I direct the EPSRC programme grant StemNiche looking at bioengineering stem cell niches for Pharma use and I direct an EPSRC research and partnership hub for health technologies, MAINSTREAM (https://www.mainstream-hub.org), on stem cell manufacturing. I also lead an EPSRC project grant on nanovibrational chondrogenesis, co-I on an EPSRC HT50 programme grant on prediction of blood cancer, am involved in an EPSRC large project led from QMUL looking at on-chip technologies and an EU H2020 grant focussing on GMP manufacture of cells and materials. In terms of translation, we have performed a number of veterinary trials for bone regeneration, most notably Eva the dog, but also 10 other cats and dogs. We are also working towards spin out of nanovibrational bioreactor technology and, against all odds, a human clinical trial of nanovibrated stem cell therapy. Further, I am Director of the EPSRC-SFI lifETIME centre for doctoral training (https://lifetime-cdt.org) that will train more than 80 PhD students in the UK and Ireland with science and leadership skills in non-animal technologies for Phrama drug discovery and regenerative medicine. In 2016 I was elected a Fellow of the Royal Society of Edinburgh and have won a number of awards – most recently the Biochemical Society Industrial-Academic Collaboration Award in 2020. My interest now lies in understanding mesenchymal stem cell ageing in order to allow manufacture of large numbers of high quality stem cells for regenerative therapies, transplant therapies and deign of bioengineered drug screening models. In terms of models, I am interested in models of the bone marrow to study blood cancers. Blood cancer is an area where animal models give poor prediction and so human cell containing models are increasingly important, especially with the new stances of the MHRA and FDA, which are increasingly permissive to non-animal technologies. I will chat about these technologies in the seminar.

18.12.25

Rankine 108LT 

“Single nucleotide resolution mapping of chemicalmodifications to DNA reveals strand biases, accumulation profiles and loss ofgenome integrity that forecast mutational signatures in human cancers”

Full Professor of Toxicology at the ETH Zurich, theSwiss Federal Institute of Technology. Professor Sturla was born in NewYork, USA and studied Chemistry at the University of California at Berkeley andthe Massachusetts Institute of Technology. She carried out a postdoctoralfellowship in Toxicology with Professor Stephen S. Hecht at the University of Minnesota Cancer Center, where her research concerned tobacco carcinogenesisand cancer chemoprevention with dietary compounds. In 2004, Shana became an Assistant Professor at the University ofMinnesota.  Her work there was recognized with an NIH Career DevelopmentAward and, as a Dominican American, she received an American Association forCancer Research Minority Scholar in Cancer Research Award. In 2009, she joinedthe faculty of the ETH Zurich, as Associate Professor with tenure and in 2016was promoted to Full Professor.

She leads the Laboratory of Toxicology at the ETH Zurich.  The goalof her research is to promote chemical, food and drug safety by elucidating thechemical basis of mutagenesis and toxicity, and to promote innovativebioanalysis strategies for predicting chemical hazards on the basis of chemicalstructures and reactivity, molecular responses and in vitro testing. Key areasof research interest include the study of environmental toxicants related tohuman disease, DNA damage and mutagenesis, drug resistance in cancer therapyand biotransformation of xenobiotics by human gut microbiota. She teaches various courses at the ETH including Introduction toToxicology, Biological Chemistry (Nucleic Acids), Molecular Disease Mechanisms(Cancer Section), a Laboratory Course in Toxicology, and the Carcinogenesismodule for the Swiss Masters of Advanced Study in Toxicology.

Shana is the President of the Swiss Society of Toxicology, Member of thePlatform Chemistry of the Swiss Academies of Science, and Editor-In-Chief ofChemical Research in Toxicology.

14.1.26

Hunterian Art Gallery LT 103

“Nucleic acids and ubiquitin in pathogen defence

28.1.26

Rankine 108LT 

"My Journey to Adhesion GPCRs: Seeing What Sticks"

Adhesion G protein-coupled receptors (aGPCRs) are an underexplored class of receptors with growing relevance to neuropsychiatric disorders, where current treatments lack precision and efficacy. My research programme seeks to uncover how these receptors function, spanning molecular mechanisms to behavioural outcomes, with a long-term goal of informing more targeted therapies. In this seminar, I’ll share my career journey into studying aGPCRs and highlight key aspects of my current work in the Centre for Translational Pharmacology. 

11.2.26

Rankine 106LT 

A geneticist studying the immune system, pulling apart how and why different arms of immunity function as they do and what they mean for pathogen defense.

25.2.26

Rankine 108LT 

 "On the multiple roads to cell fate decision: Integrating transcription factors into RNA-regulatory networks"

While the current view states that Transcription Factors (TFs) act on DNA regulatory elements to deploy precise gene programs, an emerging concept proposes that TFs also bind RNA and regulate splicing to promote molecular and cellular diversity. Yet, how the RNA regulatory functions of TFs contribute to their key role in cell fates remains puzzling. From in vitro interactions to tissue development, the seminar will survey some of our latest findings, focusing on the splicing function and RNA-binding ability of the homeodomain TFs, using Drosophila muscle development as a paradigm for cell fate decisions.

11.3.26

Hunterian Art Gallery LT

"The dual specificity MAP kinase phosphatase DUSP2 act as distal regulatory node in T Cell signalling” 

The dual-specificity MAP kinase phosphatases (MKPs) family plays a critical role in the dephosphorylation and inactivation of various MAP kinases in mammalian cells and tissues. MKPs not only provide a mechanism for spatiotemporal feedback control of these essential signalling pathways but also facilitate crosstalk between distinct MAP kinase pathways and other key signalling modules. The ten mammalian MKPs differ in their substrate specificity and subcellular localization. Several MKPs have been implicated in regulating MAPK signalling in T cells. However, studies utilizing genetic mouse models have yielded conflicting results regarding which MKP members contribute to this regulation. This prompted us to re-examine the role of MKPs in controlling MAPK signalling using a human T cell model. Our findings suggest that DUSP2 regulates early MAPK activation in these cells and may function as a part of a distal regulatory node in T cell signalling

Tuesday 17.3.26

Rankine, LT108

"Towards improving organellar acidification and genome stability in the ageing brain”

Ageing is accompanied by a progressive decline in proteostasis, membrane trafficking and genome maintenance, contributing to synaptic dysfunction and neurodegeneration. Two processes particularly vulnerable to ageing are organellar acidification and nuclear envelope integrity, both of which are essential for neuronal function and brain health.

Efficient neurotransmission depends on precise regulation of synaptic vesicle (SV) biogenesis, acidification, neurotransmitter loading, and recycling, steps critically driven by the vacuolar H⁺-ATPase (v-ATPase). Impaired vesicle acidification is increasingly linked to age-related synaptic decline. To investigate mechanisms controlling organellar acidification, we developed an approach to isolate SVs and their recycling intermediates from aged mammalian brains as well as murine models with early lethality, combined with molecular probes to monitor membrane potential and organellar pH. Using this strategy, we studied DMXL2, encoding the synapse-enriched protein Rabconnectin-3a, mutations of which cause neurodevelopmental disorders and intellectual disability. Rabconnectin-3a is recruited to acidifying organelles where it stabilizes v-ATPase expression and activity. Its loss leads to defective vesicle acidification, impaired SV recycling and accumulation of lysosome-like structures, phenotypes consistent with disrupted proteostasis and features reminiscent of accelerated neuronal ageing. In parallel, we identify dynamins, brain-enriched membrane-binding GTPases, as key regulators of nuclear envelope homeostasis. Dynamin deficiency causes nuclear envelope abnormalities, accumulation of DNA damage, impaired autophagic clearance, and reduced DNA repair capacity - hallmarks of cellular ageing. Together, these findings reveal complementary membrane-dependent mechanisms that maintain organellar function and genome stability, and suggest potential targets to counteract synaptic failure and genomic instability in the ageing brain.

25.3.26

42 Bute Gardens, room 916

Lipophilic triphenylphosphonium (TPP) cations are widely used to deliver compounds to the mitochondrial matrix in cells, tissues and whole organisms [1]. The lecture will explore the chemical design, advantages and limitations of strategies using TPP to deliver bioactives. It will distinguish between colocalization and delivery, drawing on examples of bioactives that affect redox signalling and oxidative damage, e.g. MitoCDNB [2] and MitoPerSulf [3]. It will show new ways to deliver activated by endogenous chemicals. Finally, it will explore reporting on endogenous reactive species in the mitochondria of whole organisms, revealing our latest lipid peroxidation sensors, and provide an insight into how to localize sensors to different sites within mitochondria. The lecture will be a mix of published and unpublished work.

8.4.26

Rankine 108LT

22.4.26

Joseph Black B408

"Control of protein synthesis in health and disease”.

The control of mRNA translation plays a crucial role in regulating the synthesis of specific proteins. mRNA translation is regulated in response to a range of prompts including hormones and growth factors. Such control is mediated in the short term largely via the control of translation initiation and elongation factors through phosphorylation, often by dedicated protein kinases.

Two examples of this are the MAP kinase-interacting kinases (MNKs) which phosphorylate eukaryotic initiation factor 4E (eIF4E) and eukaryotic elongation factor 2 kinase (eEF2K). Our recent work has shown that the MNKs play key roles in weight gain and obesity. Mice in which the MNKs have been knocked out fail to gain weight on a high fat (high calorie) diet, HFD. They are also protected from glucose intolerance, fatty liver and other adverse effects of consuming an HFD. Pharmacological inhibition of MNK function has similar effects, suggesting that MNKs may be valuable new targets for tackling obesity and related disorders. eEF2K slows down the speed at which ribosomes translate mRNAs (the elongation rate). The elongation step is prone to errors; these are reduced by the action of eEF2K. Bearing in mind the error/catastrophe theory of ageing, we asked whether eEF2K/eEF2 affect lifespan and showed that reduced eEF2 function (which slows elongation) extends lifespan. Interestingly, eEF2K function is controlled by two major signalling pathways that affect lifespan, the mTORC1 pathway and AMP-activated protein kinase, AMPK.

6.5.26

Joseph Black B408

“Differential Regulation of Phospholipase Cbeta Enzymes”,

Phospholipase C (PLC) enzymes convert phosphatidylinositols into diacylglycerol and inositol polyphosphates, second messengers that activate protein kinase C and increase intracellular calcium. The PLCbeta subfamily, comprised of four isoforms, is activated downstream of G protein-coupled receptors by direct binding of Gaq and Gbg subunits, with maximum activation occurring only at inner leaflets of cell membranes. These isoforms vary in their basal activity, sensitivity to activation by G proteins, and membrane association. However, the molecular basis of these differences is not clear. The proteins vary most in the sequence of their proximal and distal C-terminal regulatory domains (CTDs), which have essential roles in autoinhibition, membrane binding, and regulation by Gaq. Using cryo-electron microscopy and cell-based studies we are revealing the molecular basis for these differences. Our insights could be leveraged to develop new therapeutic strategies for modulating the activity of specific PLCbeta isoforms in disease.

20.5.26

Joseph Black B408

“New approaches to classical optics for multi-scale bioimaging”.

Imaging across length scales remains a central challenge in optical science: high numerical aperture systems offer fine resolution but only within a limited field of view. This talk focuses on recent advances that address this tension using classical optics, with particular emphasis on the Mesolens and the emergence of 3D-printed optical components. The Mesolens provides a unique optical regime, combining high numerical aperture with a multi-millimetre-scale field of view, enabling simultaneous visualisation of sub-cellular detail and large-scale biological structure. I will discuss the optical design principles that underpin mesoscopic imaging with the Mesolens, and I will demonstrate with recent examples of how our approach is enabling volumetric, high-resolution imaging of complex biological and biomedical samples. I will also discuss how additive manufacturing is reshaping optical system design. Advances in high-resolution 3D printing now allow rapid fabrication of custom lenses, hardware, and indeed whole optical microscopes that would be difficult or prohibitively expensive to produce using conventional techniques. I will give an overview of our latest work in 3D printing of optics and hardware for light microscopy, from both simple and bespoke prints to improve the resolution and contrast of existing microscopes to the printing of entire diffraction-limited and super-resolution mesoscale imaging systems.

3.6.26

Rankine 108LT

17.6.26

Bute Gardens, room 916

Dr Constantinos Demetriades

"Spatial Organization of Nutrient Signaling to mTORC1"

Nutrients are the building blocks for cells to grow and proliferate, hence nutrient sensing mechanisms ensure that cells are metabolically active only when all necessary elements are available and all conditions are optimal. Importantly, how information about intra- and extracellular nutrient levels, stresses, and the overall metabolic state of a cell is integrated to form a coordinated response remains enigmatic. Our work aims to elucidate: i) how cells sense the availability of nutrients and the presence of stresses in their environment to adjust their growth, metabolism, and other functions accordingly, ii) how the dysregulation of these cellular mechanisms contributes to the development of human diseases and to ageing, and iii) how we can intervene pharmacologically to efficiently and specifically target such life-threatening conditions. Due to its role as a primary hub in metabolic and nutrient signaling, and a key coordinator of virtually all cellular functions, most of our projects center around the master cellular nutrient sensor, the mTOR kinase. In this talk, I will present highlights of our published and unpublished work on the intricate molecular and cellular mechanisms that reciprocally connect cell growth, metabolism, protein recycling and secretion; and will discuss how this machinery responds to starvation and stress in health and disease.

24.6.26

Adam Smith room 489 

"Inside the Mitochondrion: Live Super-Resolution Imaging of Cristae Membrane Dynamics”

Mitochondria perform multifaceted classical and non-classical roles in the cell, ranging from ATP and ROS production, calcium buffering to regulation of metabolism and immune signaling. Alterations of mitochondrial proteins lead to a plethora of pathologies including neurodegeneration, cancer and diabetes. Among their unique structural features, the inner membrane folds, called cristae membranes have been viewed as static entities for more than six decades. Using technically demanding live-cell STED super-resolution nanoscopy, we recently demonstrated that cristae membranes are highly dynamic and undergo rapid remodelling within seconds. This was also confirmed by others. As cristae membrane dynamics emerge from a previously overlooked view of regulator of mitochondrial function, now is the crucial time to explore their role in physiological and pathological processes. My group investigates fundamental mechanisms regulating and those regulated by cristae membrane dynamics. We employ a diverse set of cell biological, biochemical and genetic tools including but not limited to live-cell STED nanoscopy, APEX2-based proximity proteomics, and metabolic profiling to delineate the relationship between mitochondrial function and cellular homeostasis.

Enabling targeted protein degradation in bacteria

Are aquaporins expressed in stomatal complexes promising targets to enhance stomatal dynamics?

Probing the potential of the plant cell wall to act as a protective barrier against winter temperatures

Making Marvellous Molecules (and finding out what they do)

RETuning the electron transport chain in obesity improves metabolism

The Persulfide and Polysulfide Puzzle: Novel Tools and Methods to Assemble the Pieces

Breaks and Crosses - Insights into the molecular mechanisms of meiotic recombination