Professor Shouqing Luo

Professor of Neurobiology

Peninsula Medical School (Faculty of Health), University of Plymouth

Qualifications

Senior Research Fellow
Cambridge Institute for Medical Research
University of Cambridge, UK

Research Fellow
Cambridge Institute for Medical Research
University of Cambridge, UK

Postdoctoral Research Associate
Northwestern University Medical School, USA

Research Fellow
National Institute of Child Health and Human Development
National Institutes of Health (NIH), USA

PhD, Peking Union Medical College & Chinese Academy of Medical Sciences, China 

Professional membership

Roles on external bodies

Associate Editor, Autophagy

Teaching interests

HEA Fellow

Clinical Neurobiology

Current Issues in Neurobiology

Placement and Employability

Academic tutor of Special Study Unit

Director of Postgraduate Studies

Staff serving as external examiners

University of Cambridge

University of Liverpool

University College London

Research interests

Macroautophagy or autophagy is an intracellular bulk degradation system mediated by lysosomes. Autophagy substrates include long-lived cytosolic proteins, intracellular pathogens and damaged organelles. Autophagosomes are then fused to lysosomes and the contents of autophagosomes are degraded by lysosomal hydrolases, and the resulting degraded components are reused for anabolic and catabolic processes. Autophagy is involved in many biological processes of normal physiology, such as mitigating metabolic stress, degradation of aggregate-prone proteins (e.g, mutant huntingtin), tissue homeostasis, and defects in autophagy process are associated with numerous pathophysiologies, including neurodegenerative diseases and tumorigenesis. The research in our lab currently focuses on characterising novel autophagy pathways to tackle neurodegeneration. We are taking on the following research programmes.

1. SQSTM1/p62 phase separation biology - implication in selective autophagy and neurodegeneration

Protein bodies/protein non-membrane structures (e.g. SQSTM1/p62 bodies) represent open macromolecular assemblies at which bio-materials are organised in a dynamic manner. Mounting evidence suggests that these non-membrane compartments are formed as liquid droplets though liquid-liquid phase separation, a process in which bio-macromolecules demix from solution and form a separate liquid phase. Although hundreds of proteins are enriched in protein droplets, only a subset of proteins are believed to promote liquid droplet formation. Protein bodies plays critical roles in ageing and neurodegeneration. It is important to characterise the aetiology of protein body formation. The metazoan autophagy receptor SQSTM1/p62 recognises the cargo via their ubiquitin binding, and it has been best characterised to mediate autophagic clearance of aggregated proteins. p62 body formation is critical for its function as an autophagy receptor. We have recently found that DAXX promotes the phase transition and condensation of p62 to enhance its recruitment of ubiquitinated proteins (Nature Comms, 2019). Based on this work, we are continuing to address p62 phase separation and neurodegeneration.

2. New autophagy approaches to tackle Huntington's disease (HD)

Previously I characterized the BH3-only protein Bim as a dual molecule functioning in both autophagy inhibition and apoptosis induction (Mol Cell, 2012). This has now been widely accepted (follow-up work has been published by other groups numerous journals, e.g. Blood, J Cell Biol, Autophagy, Cell Cycle). Importantly, we found that Bim protein levels are upregulated in the neurons in HD conditions. We hypothesised that Bim may be a driver for HD progression. Recently we characterised that Bim contributes to HD progression (Hum Mol Genet, 2020), and we aim to lower Bim activity to ameliorate HD pathology. 

3. Lipid metabolism in neurodegeneration 

Cholesterol is a lipid essential for mammalian cell membranes. It is known that the brain has a 10-fold higher cholesterol concentration than other tissues. Lipid metabolism is an emerging focus of research into neurodegeneration. We aim to examine if cholesterol esters accumulation contribute to HD neurodegeneration.

Grants & contracts

Recent funding:

2022-2024. Principal applicant, Rosetrees, PGL21/10002, Lowering autophagosomal overload to mitigate synucleinopathies, £91,256

2020-2022, Principal applicant, the Royal Society, IEC\NSFC\191180 - International Exchanges 2019 Cost Share (NSFC), the autophagy role of lncRNAs, £11,700.00

2019-2022. Newton Advanced Fellowship UK Principal Applicant. The Academy of Medical Sciences/the Royal Society (Newton Fund). Selective autophagy regulation in Huntington's Disease and neurodegeneration (NAF\R1\191045), £111,000

2016-2019. Principal applicant, Medical Research Council. Tackling autophagy and apoptosis for the potential therapy of Huntington’s Disease (MR/M023605/1), £528,993

2018-2021. Principal applicant. BRACE Charity. Mechanisms of mitochondrial dysfunction in neurodegeneration (BR18/01), £85,863

2017-2019. Principal applicant. BRACE Charity. New strategies in alleviation of aggregation-prone protein toxicity in dementia diseases (BR17/04), £58,545

2016-2019. Principal applicant. DTS PhD studentship programme. Identification of a Novel Autophagy Pathway, £72,000

2015-2017. Principal applicant. National Natural Science Foundation of China (NSFC). Selective degradation of autophagy (31428014), RMB200,000

2013-2015. Principal applicant. Northcott Medical Foundation. The mechanism of artemisinin derivatives’ modulation in autophagy and cell death (5002), £7250

2013-2016. Principal applicant. PhD studentship in Translational and Stratified Institute. The interaction between autophagy and cell death, £62,000

Conferences organised

• November 2019, 1st Sino-UK neuroscience meeting, Shenzhen, China
• September 2019, The 25th Annual Conference of CLSS, London, UK
• April 2017, The London PhD Network (LPN) 5th Symposium: Neuroscience and CRYO-EM, London, UK
• October 2016, Collaborative strategies to study neurodegeneration, Swindon, UK