Staff Profile

I am a Newcastle University Academic Track (NUAcT) fellow within the Biosciences Institute.

Past Positions:

University of Cambridge - Postdoctoral Research Assistant (2016-2022)

University of Dundee - PhD student (2011-2015)

Qualifications:

PhD in Cell Biology, University of Dundee, 2015

BSc (Hons) Biomedical Sciences, University of Dundee, 2011

Cells in the human body are constantly exposed to fluctuating oxygen levels, making oxygen availability a pivotal factor in regulating cellular function and fate. Hypoxia—defined by a reduction in oxygen supply—drives the progression of diseases such as cancer and inflammation, fuelling critical processes like metastasis and immune response resulting in poor patient outcome. Therefore, understanding how cells adapt to hypoxic conditions is vital for uncovering novel therapeutic targets and improving treatment effectiveness.

The Hypoxia-Inducible Factor (HIF) family of transcription factors play a central role in the body’s response to low oxygen. Under hypoxic conditions, HIF stabilises and activates a transcriptional programme that supports cellular survival and adaptation. However, in tumours, dysregulated HIF activity accelerates disease progression, positioning HIF as both a promising and complex therapeutic target. Despite the availability of several HIF inhibitors, the risk of systemic toxicity from blanket inhibition highlights the need for more refined, targeted approaches.

A key question in the field is how HIF activity is precisely regulated across different cellular contexts. Our research has identified SET1B, a histone methyltransferase, as a crucial HIF coactivator, suggesting that targeting co-regulators could offer a more selective means of modulating HIF. SET1B is part of a larger family of methyltransferases and demethylases—many of which are oxygen-sensitive and HIF-regulated—that modify proteins through methylation, altering their function. This indicates that methylation could play a central role in the broader hypoxia response.

While HIF activation is a critical component of the cellular response to hypoxia, it is inherently slow as a transcriptional programme and cannot account for the rapid changes’ cells need to survive in low-oxygen environments. In contrast, methylation is a fast, reversible post-translational modification capable of swiftly altering protein function. Despite its potential as a key regulator of hypoxia adaptation, the broader role of methylation in both HIF-dependent and independent pathways remains largely unexplored.

My research group uses innovative forward genetic screening and proteomics to interrogate how methylation regulates the cellular response to hypoxia. The ultimate goal of the lab is to identify new therapeutic targets to treat cancer, autoimmunity, and neurodegeneration.

I am always open to inquiries from prospective undergraduate and PhD students as well postdoctoral researchers.

Current lab members:

Dr Nikita Dhillon (Post Doctoral Researcher)

Lukasz Marzec (PhD Student)

Alexander Handyside (PhD Student)

Meagan Farrington (MRes Student)

• Articles

  • Bertlin, JAC, Pauzaite, T, Liang, Q, Wit, N, Williamson, JC, Sia, JJ, Matheson, NJ, Ortmann, BM, Mitchell, TJ, Speak, AO, Zhang, Q, Nathan, JA. VHL synthetic lethality screens uncover CBF-β as a negative regulator of STING. bioRxiv 2024. In Preparation.
  • Ortmann, BM. Hypoxia-inducible factor in cancer: from pathway regulation to therapeutic opportunity. BMJ Oncology 2024. In Preparation.
  • Ortmann, BM, Taylor, CT, Rocha, S. Hypoxia research, where to now?. Trends in Biochemical Sciences 2024. In Preparation.
  • Meng, B, Zhao, N, Mlcochova, P, Ferreira, IA, Ortmann, BM, Davis, T, Wit, N, Rehwinkel, J, Cook, S, Maxwell, PH, Nathan, JA. Hypoxia drives HIF2-dependent reversible macrophage cell cycle entry. Cell Reports 2024. In Preparation.
  • Porter, LM, Guo, W, Crozier, TW, Greenwood, EJ, Ortmann, BM, Kottmann, D, Nathan, JA, Mahadeva, R, Lehner, PJ, McCaughan, F. Cigarette smoke preferentially induces full length ACE2 expression in differentiated primary human airway cultures but does not alter susceptibility to SARS-CoV-2 infection. Heliyon 2023. In Preparation.
  • Kotagiri, P, Mescia, F, Hanson, AL, Turner, L, Bergamaschi, L, Peñalver, A, Richoz, N, Moore, SD, Ortmann, BM, Dunmore, BJ, Morgan, MD, Tuong, ZK, Göttgens, B, Toshner, M, Hess, C, Maxwell, PH, Clatworthy, MR, Nathan, JA, Bradley, JR, Lyons, PA, Burrows, N, Smith, KGC. The impact of hypoxia on B cells in COVID-19. EBioMedicine 2022. In Preparation.
  • Ortmann, BM, Nathan, JA. Genetic approaches to understand cellular responses to oxygen availability. FEBS 2021. In Preparation.
  • Bailey, PSJ, Ortmann, BM, Martinelli, AW, Houghton, JW, Costa, ASH, Burr, SP, Antrobus, R, Frezza, C, Nathan, JA. ABHD11 maintains 2-oxoglutarate metabolism by preserving functional lipoylation of the 2-oxoglutarate dehydrogenase complex. Nature Communications 2020. In Preparation.
  • Ono, M, Yamada, K, Bensaddek, D, Afzal, V, Biddlestone, J, Ortmann, B, Mudie, S, Boivin, V, Scott, MS, Rocha, S, Lamond, AI. Enhanced snoMEN Vectors Facilitate Establishment of GFP-HIF-1α Protein Replacement Human Cell Lines. 2016. In Preparation.
  • Ortmann, B, Bensaddek, D, Carvalhal, S, Moser, SC, Mudie, S, Griffis, E, Swedlow, JR, Lamond, AI, Rocha, S. CDK dependent phosphorylation of PHD1 on Serine 130 determines specificity of substrate targeting. Journal of Cell Science 2016. In Preparation.
  • Ortmann, B, Druker, J, Rocha, S. Cell cycle progression in response to oxygen levels. Cell Mol Life Sci 2014. In Preparation.
  • Moser, SC, Bensaddek, D, Ortmann, B, Mudie, S, Blow, JJ, Lamond, AI, Swedlow, JR, Rocha, S. PHD1 links cell cycle progression to oxygen sensing by hydroxylation of the centrossomal protein Cep192. Developemental Cell 2025. In Preparation.