Dr Richard Tuxworth MA PhD

Dr Richard Tuxworth

Institute of Cancer and Genomic Sciences
Senior Lecturer in Molecular Genetics

Contact details

Centre for Rare Diseases and Personalised Medicine
Institute of Cancer and Genomic Sciences
College of Medical and Dental Sciences
IBR West Extension Level 2
University of Birmingham
B15 2TT

Richard is a Senior Lecturer in the Institute of Cancer and Genomic Sciences. He is a cell biologist with a particular interest in understanding DNA damage in neurological disease.


  • Associate fellow of the Higher Education Academy 2012
  • PhD (University of London), 1999
  • MA (Cantab), 1998
  • BA (Cantab) in Natural Sciences, 1994


Richard studied for a PhD in cell biology at the MRC Centre for Molecular Cell Biology at University College London with Robert Insall before moving to the University of Minnesota where he was a post-doctoral fellow with Meg Titus. He returned to the UK to work with Bill Chia and Guy Tear at the MRC Centre for Developmental Neurobiology at King's College London. In October 2012 Richard moved to the University of Birmingham as a Lecturer in Molecular Genetics in October 2012 in the School of Clinical and Experimental Medicine.


Postgraduate supervision

Richard currently supervises two PhD students. He is interested in supervising post-graduate students in the following areas: 

  • The molecular and cellular basis of neurodegeneration
  • Drosophila models of disease
  • Lysosomal storage disorders and other inherited metabolic disorders
  • The function of lysosomes in neuronal health and disease
  • Stress signalling in neurons

If you are interested in studying any of these subject areas please contact Richard on the contact details above, or for any general doctoral research enquiries, please email dr@contacts.bham.ac.uk or call +44 (0)121 414 5005.


Richard Tuxworth is a cell biologist interested in disorders of the nervous system. He studies both early-onset inherited forms of neurodegeneration and the more common neurodegenerative disorders associated with old age. His laboratory is particularly interested in understanding how DNA damage impacts on nervous system function in neurological disease and finding out whether manipulating the response of cells to DNA damage could be used therapeutically.

DNA damage in neurological disease

Richard and colleagues in the College of Medical and Dental Sciences are investigating how accumulating DNA damage impacts on central nervous system function in chronic neurological diseases, such as Alzheimer’s diseases, and in acute neurological diseases, such after trauma. Richard’s group uses a combination of cell culture, biochemistry, genetics and genomics to understand the cell biology of neural responses to DNA damage and uses simple models of neurodegenerative disease developed in fruit flies to perform rapid surveys of potential new methods of intervention in neurological disease.

Lysosomal storage disorders and neural development

Lysosomes are low-pH organelles critical for recycling in cells and for coordination of growth and stress signalling. Lysosomes become dysfunctional in a large group of inherited syndromes known as the lysosomal storage disorders. Many result in neuropathology at a young age, including fatal childhood-onset neurodegeneration. The early pathology suggests lysosomal function must be essential for normal neuronal development. To study this, Richard’s group primarily use fruit flies as a simple model system to understand how and why the nervous system is sensitive to changes in lysosomal biology.


Highlight publications

Connolly, K, O'Hare, M, Mohammed, A, Aitchison, K, Anthoney, N, Taylor, M, Stewart, B, Tuxworth, R & Tear, G 2019, 'The neuronal ceroid lipofuscinosis protein Cln7 functions in the postsynaptic cell to regulate synapse development', Scientific Reports, vol. 9, 15592. https://doi.org/10.1038/s41598-019-51588-w

Tuxworth, R, Taylor, M, Anduaga, AM, Hussien-Ali, A, Chatzimatthaiou, S, Longland, J, Thompson, AM, Almutiri, S, Alifragis, P, Kyriacou, CP, Kysela, B & Ahmed, Z 2019, 'Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodegeneration', Brain Communications, vol. 1, no. 1, fcz005. https://doi.org/10.1093/braincomms/fcz005

Recent publications


Tuxworth, R 2019, 'Attenuating the DNA damage response to double strand breaks restores function in models of CNS neurodegeneration', Brain Communications. https://doi.org/10.1093/braincomms/fcz005

Taylor, MJ & Tuxworth, RI 2019, 'Continuous tracking of startled Drosophila as an alternative to the negative geotaxis climbing assay', Journal of Neurogenetics, vol. 33, no. 3, pp. 190-198. https://doi.org/10.1080/01677063.2019.1634065

Tuxworth, R 2019, 'Continuous tracking of startled Drosophila as an alternative to the negative geotaxis climbing assay', Journal of Neurogenetics. https://doi.org/10.1080/01677063.2019.1634065

Mohammed, A, O'Hare, MB, Warley, A, Tear, G & Tuxworth, R 2017, 'in vivo localization of the neuronal ceroid lipofuscinosis proteins, CLN3 and CLN7, at endogenous expression levels', Neurobiology of Disease, vol. 103, pp. 123-132. https://doi.org/10.1016/j.nbd.2017.03.015

Faller, KME, Gutierrez-quintana, R, Mohammed, A, Rahim, AA, Tuxworth, RI, Wager, K & Bond, M 2015, 'The neuronal ceroid lipofuscinoses: Opportunities from model systems', Biochimica et Biophysica Acta. Molecular Basis of Disease. https://doi.org/10.1016/j.bbadis.2015.04.022

Povellato, G, Tuxworth, RI, Hanger, DP & Tear, G 2014, 'Modification of the Drosophila model of in vivo Tau toxicity reveals protective phosphorylation by GSK3β', Biology Open, vol. 3, no. 1, pp. 1-11. https://doi.org/10.1242/bio.20136692

Tuxworth, RI, Chen, H, Vivancos, V, Carvajal, N, Huang, X & Tear, G 2011, 'The Batten disease gene CLN3 is required for the response to oxidative stress', Human Molecular Genetics, vol. 20, no. 10, pp. 2037-2047. https://doi.org/10.1093/hmg/ddr088

Tuxworth, RI, Vivancos, V, O'Hare, MB & Tear, G 2009, 'Interactions between the juvenile Batten disease gene, CLN3, and the Notch and JNK signalling pathways', Human Molecular Genetics, vol. 18, no. 4, pp. 667-78. https://doi.org/10.1093/hmg/ddn396

Slack, C, Overton, PM, Tuxworth, RI & Chia, W 2007, 'Asymmetric localisation of Miranda and its cargo proteins during neuroblast division requires the anaphase-promoting complex/cyclosome', Development (Cambridge), vol. 134, no. 21, pp. 3781-7. https://doi.org/10.1242/dev.010900

Slack, C, Overton, PM, Tuxworth, RI & Chia, W 2007, 'Asymmetric localisation of Miranda and its cargo proteins during neuroblast division requires the anaphase-promoting complex/cyclosome', Development. https://doi.org/10.1242/dev.010900

Tuxworth, RI, Stephens, S, Ryan, ZC & Titus, MA 2005, 'Identification of a myosin VII-talin complex', Journal of Biological Chemistry. https://doi.org/10.1074/jbc.M503699200

Tuxworth, R & Chia, W 2003, 'Asymmetric cell division: Miranda chauffeured by jaguar?', Molecular Cell. https://doi.org/10.1016/S1097-2765(03)00066-2

Tuxworth, RI, Weber, I, Wessels, D, Addicks, GC, Soll, DR, Gerisch, G & Titus, MA 2001, 'A role for myosin VII in dynamic cell adhesion', Current Biology. https://doi.org/10.1016/S0960-9822(01)00097-5

Tuxworth, RI & Titus, MA 2000, 'Unconventional myosins: Anchors in the membrane traffic relay', Traffic.

Review article

Seranova, E, Connolly, KJ, Zatyka, M, Rosenstock, TR, Barrett, T, Tuxworth, RI & Sarkar, S 2017, 'Dysregulation of autophagy as a common mechanism in lysosomal storage diseases', Essays in Biochemistry, vol. 61, no. 6, pp. 733-749. https://doi.org/10.1042/EBC20170055, https://doi.org/10.1042/EBC20170055

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