To celebrate the tenth anniversary of Dundee’s UNESCO City of Design status, this exhibition showcases a decade of design created by students at Duncan of Jordanstone College of Art & Design, many of whom have already gone on to successful careers as professional designers. The show features stunning and thought-provoking examples of animation, comics, graphic design, illustration, jewellery, metal design and textile design. 

The exhibition is open Mon-Fri 9.30am-7pm, Sat 11am-4pm. Please note that during weekdays in the vacation the Tower Building may close earlier than advertised so we advise arriving no later than 5pm.

Find out more about the University of Dundee Museums.

Main image: Light Above, ear cuff by Lorna Romanenghi, 2019 

Background image: Textile sample by Aimee Coulshed, 2019

Host: Dario Alessi

Venue: MSI Small Lecture Theatre, SLS

Abstract:

Amyotrophic Lateral Sclerosis (ALS) is a neuromuscular disorder characterized by the selective demise of motor neurons (MNs), leading to the paralysis and death of patients within 3-5 years after diagnosis. MNs reside in the spinal cord and possess incredibly long axons, which project to the muscle to control movement. Dysregulation of MN axons (e.g. defects in transport, local translation, cytoskeletal maintenance) is a key contributor to MN death during ALS.

In my talk, I will discuss data on how the neurotrophic factor, brain-derived neurotrophic factor (BDNF), acts as a core regulator of axonal homeostasis in human iPSC-derived MNs. Using bioengineered compartmentalized cultures, we reveal the axonal-specific kinase pathways governed by BDNF that control axonal regeneration and organelle transport. Phosphoproteomics reveal that BDNF governs altered phosphorylation state of cytoskeletal-binding proteins in human motor neurons. Additionally, using metabolic labelling with RNA-sequencing, we reveal that BDNF activates transcription factors and gene-regulatory networks that strikingly overlap with those that promote axonal regeneration of peripheral neurons. These data point towards BDNF as a therapeutic target for counteracting axonal degeneration in ALS.

 I will also briefly touch on my on-going and unpublished work on the crosstalk between the RNA-binding protein, TDP-43, and RNA methylation - specifically how this interaction may contribute to axonal degeneration during ALS. N6-methyladosine (m6A), the most abundant RNA methylation event in the brain, controls the metabolism and localization of mRNAs into axons. Recent work suggests that TDP-43 binds methylated RNA and that m6A levels are perturbed in ALS human spinal cord MNs. Thus, dissecting the interplay between TDP-43 and m6A-ylation on RNA metabolism may reveal how motor neurons perish selectively during ALS.

 Bio:

Dr. Jobert Vargas is a Miriam Mark Research Fellow in Neurodegeneration (Brain Research, UK) and a Target ALS Springboard Postdoctoral Fellow. He is hosted within the Dept. of Neuromuscular Diseases, Queen Square Institute of Neurology UCL, under the mentorship of Prof. Giampietro Schiavo, as well as Prof. Pietro Fratta. His current work broadly explores how axon-specific molecular events in human MNs confer resilience or susceptibility towards ALS pathology. In addition to his independent Fellowships, Jobert has received funding for his work from the UK DRI and Rosetrees Foundation.

 For his PhD, Jobert was a Fellow of the highly selective NIH-UCL Joint Neuroscience Program. His PhD work focused on mitophagy mechanisms, which he performed in the laboratory of Dr. Richard Youle at the NIH (co-mentored by Prof. Schiavo.) His thesis work utilized CRISPR KO lines and chemically-inducible dimerization assays to reveal that the selective autophagy receptor NDP52 associates with FIP200/ULK1 to initiate autophagosome biogenesis on directly damaged mitochondria. This work, along with the work of others, led to development of strategies using multi-specific compounds that mimic receptor proteins to target toxic cellular components for autophagic degradation.

Host: Dario Alessi

Venue: MSI Small Lecture Theatre, SLS

Abstract:

Proteinopathy of the RNA-binding protein TDP-43, defined by cytosolic aggregation and nuclear loss, is a hallmark of the fatal neurodegenerative diseases Amyotrophic Lateral Sclerosis (ALS) and fronto-temporal dementia (FTD), and emerging evidence suggests it may also contribute to Alzheimer's and Lewy body dementias.

 TDP-43 dysfunction causes cryptic splicing, where intronic sequences are aberrantly incorporated into mature RNA. Cryptic splicing signifies TDP-43 dysfunction post-mortem however, how cryptic splicing events affect disease progression is unknown.

 To understand the full extent of TDP-43’s cryptic splicing targets, I comprehensively analyzed cryptic splicing events regulated by TDP-43 in neuronal cell lines and in human post-mortem tissue. I identified hundreds of cryptic splicing targets specifically associated with TDP-43 proteinopathy, providing a strong basis for potential disease biomarkers and therapeutic targets. We discovered that while most cryptic splicing leads to destabilization of the RNA, some cryptic exons are translated and can be detected ante-mortem in ALS biofluids. Through these analyses, I also discovered the mechanism by which intronic ALS/FTLD risk and survival variants in the synaptic gene UNC13A exert their pathogenic effect through altering TDP-43 binding strength and thereby potentiating the inclusion of a destabilizing cryptic exon in UNC13A.

 To further explore how TPD-43 controls RNA stability, we performed the first ever transcriptome wide study of RNA stability after TDP-43 depletion in human neurons using the metabolic labelling technique SLAM-sequencing. Through the development of a novel computational analysis framework, I revealed a profound RNA destabilizing effect of TDP-43 depletion in human neurons.

RNA metabolism dysfunction in ALS is likely an important disease mechanism due to the preponderance of disease-causing mutations found in RNA-binding proteins, therefore is it critical to understand how RNA metabolism is regulated in the cells vulnerable in ALS, namely motor neurons. Therefore, using the techniques I developed to analyze metabolic labelling data, I will briefly touch on my work exploring the effects of the neurotrophic factor, brain-derived neurotrophic factor (BDNF) on the transcription rate of RNA in motor neurons.

 My research aims to explore the regulatory landscape of RNA metabolism in neurons, paving the way for novel therapeutic strategies combating neurodegenerative disease.

 Bio:

Dr. Anna-Leigh Brown received her B.Sc. in Cognitive Psychology and Neuroscience from Jacobs University Bremen in Germany in 2014. Following graduation, she moved to the National Institute of Mental Health in Bethesda, MD, USA where she researched auditory processing and attention. She then transitioned to industry as a data analyst before joining the National Center for Biotechnology Information in Bethesda, MD, USA, where she investigated DNA mutagenesis in cancer. Since 2019, Dr. Brown has been working in Dr. Pietro Fratta's lab at University College London, studying how RNA-binding proteins related to ALS regulate RNA metabolism and stability. In 2023, she received the Jean Corsan Prize for her research on the mechanisms of a genetic risk factor for both ALS and FTD. This work has opened new avenues for exploring the role of genetic variants in neurodegenerative diseases.

Hosts: Nicola Caldwell/ Beatriz Baragana

Venue: MSI Small Lecture Theatre, SLS

Abstract

Infection with blood fluke schistosomes causes schistosomiasis, one of the most devasting and chronically-debilitating neglected tropical diseases (NTD) on the planet. While most human infections still occur in sub-Saharan Africa, recent outbreaks in Europe demonstrate that this NTD is capable of expanding its range and establishing new endemic foci.

Regardless of geographical origin, schistosomiasis is primarily controlled by praziquantel (PZQ), a drug developed in the 1970s and transitioned as the front-line agent for mass drug administration programmes shortly thereafter. Due to the ever-present concern of PZQ-resistant/insensitive schistosomes developing, and in the absence of a deployable vaccine, new (replacement/complementary) drugs are urgently needed to achieve WHO elimination/eradication objectives.

Over the past 10 years, we have utilised phenotypic, whole-organism approaches to identify drug-like small molecules or natural products with anti-schistosomal activities as part of our drug discovery efforts. While the outputs of these ex vivo methods have led to the identification of incredibly-potent anti-schistosomal compounds, we routinely see substantial attrition of chemical matter prior to and during in vivo efficacy experiments in the murine model of schistosomiasis.

Using Schistosoma mansoni lysine demethylase 1 (SmLSD1) as an exemplar, I will demonstrate how both functional genomics- and chemical biology- approaches can be employed to improve selection and prioritisation of new anti-schistosomal targets. Deployment of these intersecting approaches together with orthogonal ones developed by our Dundee collaborators will improve our ability to effectively triage compound/target pairings and increase the pace and streamline the pathway of anti-schistosomal drug discovery.

Scotland's water security faces multifaceted challenges amidst climate change and evolving socio-economic dynamics. This talk explores the resilience of Scotland's water supplies, particularly focusing on Private Water Supplies (PWS). Drawing upon a mixed-methods approach, including surveys and spatial analysis, the impacts of drought events on PWS water quality and availability have been explored.  Historical analysis of meteorological drought using the Standardized Precipitation Evapotranspiration Index (SPEI) is used to understand past drought patterns in Scotland. Investigations were also conducted to analyse the impact of drought on water quality parameters within PWS, to showcase the relationship between meteorological conditions and water safety. Information collected from Local authorities  to explore their perceptions and strategies for managing water scarcity during drought events is investigated. Finally, a forward-looking approach has been taken by utilizing climate model projections to examine future drought scenarios in Scotland. 

The event is available on campus and online.

Please contact [email protected] if you wish to join online.

Attempts to regulate land-use in order to secure the conservation of wetlands and other valuable habitats used to be based wholly on “command-and-control” regulation, with laws telling occupiers what they could and could not do and punishments in the event of non-compliance.  In the same way as efforts to tackle climate change have made use of trading and offset schemes, conservation law has also adopted new methods based on ideas such as Payment for Ecosystem Services, Conservation Burdens and Biodiversity Net Gain.  These use the law of property and contract to create new frameworks of legal obligations for conservation, giving the private sector a much bigger role in determining what is going to happen and engaging new sources of finance.  But they also raise formidable challenges at practical and theoretical levels, such as assessing equivalence and guaranteeing land management over an extended period.  This presentation will give an overview of what has been happening and the challenges to be overcome if the new approach is to deliver real benefits for biodiversity.

This talk will be available on campus and online. 

Please contact [email protected] if you wish to join online.