Dr Martin R. Higgs

Institute of Cancer and Genomic Sciences
Birmingham Fellow for Genomics and Rare Diseases
MRC Career Development Fellow

Contact details

Telephone: +44 (0)121 414 8480
Email: m.r.higgs@bham.ac.uk

Address: Institute of Cancer and Genomic Sciences: IBR West Extension
College of Medical and Dental Sciences
University of Birmingham
Edgbaston
Birmingham
B15 2TT
UK

Martin Higgs is a group leader in the newly formed Institute of Cancer and Genomic Sciences. He is currently the Birmingham Fellow for Genomics and Rare Disease, and leads a research group working on the cellular response to genotoxic stress.

He has published papers in top journals, such as Molecular Cell, Oncogene, Cancer Research and Nature Genetics, and has been invited to speak at both national and international conferences.

Martin’s area of expertise is in the cellular response to DNA damage, and identifying novel regulators of this process. His particular interest is in studying how a single post-translational modification, known as Lysine methylation, regulates this process. In addition, part of his work focuses on the role of the DNA damage response in ensuring human development and preventing rare human diseases.

He also maintains a long-standing interest in the impact of chronic viral infection on this process, and on the consequences of this on the DNA damage response during carcinogenesis.

Qualifications

PhD in Virology, University of Glasgow, 2008
BSc in Molecular & Cellular Biology, University of Stirling, 2004

Biography

Martin graduated with a BSc from the University of Stirling in 2003. He then worked in Leeds with Professor Mark Harris on characterising the hepatitis C virus (HCV) protein p7, before moving to the (former) MRC Virology Unit in Glasgow to study for his PhD with Dr Nigel Stow.

He then undertook post-doctoral research in the laboratory of Professor Jean-Michel Pawlotsky in Paris, France, on the impact of HCV on the cellular response to DNA damage and cellular signalling.

In 2012, he moved to the University of Birmingham to join the group of Professor Grant Stewart, where he studied novel actors in the cellular response to replication stress.

In 2016, he was awarded an MRC Career Development Fellowship and was appointed Birmingham Fellow in Genomics and Rare Disease, and established his research group in 2017.

Teaching

BSc Biomedical Science Advanced Molecular Genetics (Year 2)
BSc Biomedical Science Cancer Pathogenesis and Treatment (Year 3)
BSc Biomedical Science DNA Damage Response (Year 3)
MBChB Cancer: Causes to Cures (Year 2)

Postgraduate supervision

Martin is currently co-supervising doctoral students studying novel actors which regulate the response to genotoxic stress.

Research

Martin’s current research focuses around identifying how cells respond to and resolve DNA damage, particularly that arising during DNA replication.

He is particularly interested in elucidating how protein Lysine methylation contributes to safeguarding genome stability, and in identifying novel factors involved in this response. He is also interested in elucidating how deficiencies in these pathways contribute to human disease.

He also maintains a long-standing interest in the impact of chronic viral infection on this process, and on the consequences of this on the DNA damage response during carcinogenesis.

Other activities

Reviewer for grant funding bodies and journals.

Publications

Higgs MR†, Sato K, Reynolds JR, Begum S, Bayley R, Goula A, Vernet A, Paquin KL, Skalnik DG, Kobayashi W, Takata M, Howlett NG, Kurumizaka H, Kimura H, Stewart GS† (2018). Histone methylation by SETD1A protects nascent DNA through the nucleosome chaperone activity of FANCD2. Mol Cell 71(1):25-41. († co-corresponding author)

Reynolds JJ*, Bicknell LS*, Carroll P*, Higgs MR*, Shaheen R*, et al (2017). Mutations in DONSON disrupt replication fork stability and cause microcephalic dwarfism. Nature Genetics. 49(4):537-549. (* joint first author).

Harley ME, Murina O, Leitch A, Higgs MR, Bicknell LS, Yigit G, Blackford AN, Zlatanou A, Mackenzie K, Reddy K, Halachev M, McGlasson S, Reijns MAM, Fluteau A, Martin C-A, Sabbioneda S, Elcioglu NH, Altmüller J, Thiele H, Greenhalgh L, Chessa L, Maghnie M, Salim M, Bober MB, Nürnberg P, Jackson SP, Hurles ME, Wollnik B, Stewart GS,. Jackson AP (2016). The primordial dwarfism gene TRAIP promotes DNA damage response during genome replication. Nature Genetics. 48(1):36-43.

Higgs MR, Reynolds JJ, Winczura A, Blackford A, Miller ES, Zlatanou N, Borel V, Niemenszyca J, Ryan EL, Davies N, Stankovic S, Boulton SJ, Niedzwiedz W, Stewart GS (2015). BOD1L is required to suppress deleterious resection of stressed replication forks. Mol Cell. 59(3):462-77.

Kotsantis P, Jones RM, Higgs MR, Petermann E (2015). Cancer therapy and replication stress: forks on the road to perdition. Advances in Clinical Chemistry. 69:91-138.

Higgs MR, Chouteau P, Lerat H (2014). Liver let die: oxidative DNA damage and hepatotropic viruses. J. Gen. Virol. 95(5):991-1004

Higgs MR, Lerat H, Pawlotsky JM (2013). Hepatitis C virus-induced activation of beta-catenin promotes c-Myc expression and a cascade of pro-carcinogenetic events. Oncogene. 32:4683-93.

Higgs MR, Lerat H, Pawlotsky JM (2010). Downregulation of Gadd45 Beta expression by hepatitis C virus leads to defective cell cycle arrest. Cancer Res. 70(12):4901-11.

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