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Sam obtained her Ph.D. in Genetics from Churchill College and the Department of Genetics, University of Cambridge, UK.  She then moved to the Ludwig Institute of Cancer Research (UCL) to work on cellular signalling.  She joined MRC Toxicology Unit in 2004 to launch genetic screening of molecular markers affecting neuronal outgrowth and degeneration.  This work was performed in the ‘Neuroscience’ group of the former director, Prof. P. Nicotera.  Under the directorship of Prof. A. Willis, Sam joined the ‘Mitochondrial and Cell Death Following Toxic Injury’ group to explore the use of Drosophila melanogaster as an animal model system to study molecular and cellular mechanisms involved in human diseases such as cancer and neurodegeneration.

Research Interests:

Sam’s major research interests are using the fruit fly, Drosophila melanogaster, as an in vivo animal model system to address complex biological questions at the molecular and cellular level.  Based on the skills and expertise she acquired during her Ph.D. training, she has established a research facility employing the fruit fly as an animal model in the MRC Toxicology Unit since 2007.  Her research focuses on molecular signalling pathways associated with cancer biology and neurodegenerative diseases.  Her early contribution has been to establish an in vivo study of the modulators of apoptotic cell death in Drosophila.  Subsequently, she established a genetic model of mitochondrial dysfunction associated with Parkinson’s and Alzheimer’s disease and identified genetic interactions and molecular signalling pathways for several mitochondrial protective genes.  Her research has now expanded to the study of the ultrastructure of cellular organelles, specifically mitochondria and endoplasmic reticulum, by high resolution imaging as well as establishing an expertise in Drosophila optogenetics.  Meanwhile in line with the Unit mission, she has also utilised Drosophila for toxicology studies, as this is an excellent tool to investigate the molecular and genetics mechanisms of toxic substances.

Key Publications:

  1. Yu, Yizhou; Fedele, Giorgio; Celardo, Ivana; Loh, Samantha HY; Martins, L Miguel; "Parp mutations protect from mitochondrial toxicity in Alzheimer’s disease”, Cell Death and Disease (2021)
  2. Popovic, Rebeka; Celardo, Ivana; Yu, Yizhou; Costa, Ana C; Loh, Samantha HY; Martins, L Miguel; "Combined Transcriptomic and Proteomic Analysis of Perk Toxicity Pathways”, International Journal of Molecular Sciences (2021)
  3. Scialò, Filippo; Sriram, Ashwin; Stefanatos, Rhoda; Spriggs, Ruth V; Loh, Samantha HY; Martins, L Miguel; Sanz, Alberto; "Mitochondrial complex I derived ROS regulate stress adaptation in Drosophila melanogaster”, Redox Biology (2020)
  4. Garrido-Maraver, Juan; Loh, Samantha HY; Martins, L Miguel; "Forcing contacts between mitochondria and the endoplasmic reticulum extends lifespan in a Drosophila model of Alzheimer's disease”, Biology Open (2020)
  5. Garrido-Maraver, Juan; Celardo, Ivana; Costa, Ana C; Lehmann, Susann; Loh, Samantha HY; Martins, L Miguel; "Enhancing folic acid metabolism suppresses defects associated with loss of Drosophila mitofusin”, Cell death & disease (2019)
  6. Lynch DS, Loh SHY, Harley J, Noyce AJ, Martins LM, Wood NW, Houlden H, and Plun-Favreau H (2017) Non-syndromic Parkinson's disease in a family with Autosomal Dominant Optic Atrophy due to OPA1 mutation. Neurology Genetics 3 (5), e188
  7. Hall C, Choi M, Yao Z, Tyzac G, Preza E, Arber C, Crisp S, Watson PMD, Kullmann D, Abramov A, Wray S, Sibley C, Lakatos A, Loh SHY, Martins LM, Ule J, Gandhi S, Patani R. (2017) VCP mutations induce motor neuron-specific phenotypes in a human induced pluripotent stem cell model. Cell Reports, 19(9), 1739-1749
  8. Lehmann S, Jardine J, Garrido-Maraver J, Loh SHY, Martins LM (2017) Folinic acid is neuroprotective in a fly model of Parkinson’s disease associated with pink1 mutations. Matters, 3(3), pp1-4
  9. Celardo, I., Lehmann, S., Costa, A. C., Loh, SHY, & Martins, LM (2017). dATF4 regulation of mitochondrial one-carbon metabolism is neuroprotective. Cell Death and Differentiation, 24(4), 638–648
  10. Lehmann S, Loh SHY, Martins LM (2016) Enhancing NAD+ salvage metabolism is neuroprotective in a PINK1 model of Parkinson’s disease. Biology Open, 6(2), bio.022186–7.
  11. Celardo I, Costa AC, Lehmann S, Jones C, Wood N, Mencacci NE, Mallucci GR, Loh SHY and Martins LM (2016) Mitofusin-mediated ER stress triggers neurodegeneration in pink1/parkin models of Parkinson's disease. Cell Death Dis, 7(6): p. e2271.
  12. Lehmann S, Costa AC, Celardo I, Loh SHY, Martins LM (2016) Parp mutations protect against mitochondrial dysfunction and neurodegeneration in a PARKIN model of Parkinson’s disease. Cell Death Dis, 7: p. e2166.


Other publications: 


13. Tufi R, Gandhi S, de Castro IP, Lehmann S, Angelova PR, Dinsdale D, Deas E, Plun-Favreau H, Nicotera P, Abramov AY, Willis AE, Mallucci GR, Loh SHY, Martins LM (2014) Enhancing nucleotide metabolism protects against mitochondrial dysfunction and neurodegeneration in a PINK1 model of Parkinson’s disease. Nat Cell Biol, 2014. 16(2): p. 157-66.

14. de Castro I, Costa A, Celardo I, Tufi R, Dinsdale D, Loh SHY, Martins LM, Drosophila ref (2) P is required for the parkin-mediated suppression of mitochondrial dysfunction in pink1 mutants. Cell Death Dis, 2013. 4: p. e873.

15. Costa A, Loh SHY, Martins LM, Drosophila Trap1 protects against mitochondrial dysfunction in a PINK1/parkin model of Parkinson’s disease. Cell Death Dis, 2013. 4: p. e467

16. de Castro IP, Costa A, Lam D, Tufi R, Fedele V, Moisoi N, Dinsdale D, Deas E, Loh SHY, Martins LM, Genetic analysis of mitochondrial protein misfolding in Drosophila melanogaster. Cell Death Differ, 2012. 19(8): p. 1308-16.

17. Deas E, Plun-Favreau H, Gandhi S, Desmond H, Kjaer S, Loh SHY, Renton AE, Harvey RJ, Whitworth AJ, Martins LM, Abramov, AY, Wood, NW, PINK1 cleavage at position A103 by the mitochondrial protease PARL. Hum Mol Genet, 2011. 20(5): p. 867-79.

18. Lam D, Shah S, de Castro IP, Loh SHY, Martins LM, Drosophila happyhour modulates JNK-dependent apoptosis. Cell Death Dis, 2010. 1: p. e66.

19. Lam, D., Dickens, D., Reid, E.B., Loh, SHY, Moisoi, N., Martins, L.M. MAP4K3 modulates cell death via the post-transcriptional regulation of BH3-only protein. Proc Natl Acad Sci U S A, 2009. 106(29): p. 11978-83.

20. Nanda S, DeFalco TJ, Loh, SH, Phochanukul N, Camara N, Van Doren M, Russell S (2009) Sox100B, a Drosophila group E Sox-domain gene, is required for somatic testis differentiation. Sexual Development, 3(1), pp. 26-37.

21. Loh SH, Francescut L, Lingor P, Bahr M, Nicotera P (2008) Identification of new kinase clusters required for neurite outgrowth and retraction by a loss-of-function RNA interference screen. Cell Death and Differentiation, 15(2), pp. 283-298.

22. Loh SH, Russell S (2000) A drosophila group E Sox gene is dynamically expressed in the embryonic alimentary canal. Mechanism of Development, 93, pp. 185-188.

23. Harden N, Lee J, Loh HY, Ong YM, Tan I, Leung T, Manser E, Lim L (1996) A Drosophila homolog of the Rac- and Cdc42-activated serine/threonine kinase PAK is a potential focal adhesion and focal complex protein that colocalizes with dynamic actin structure. Mol. Cell. Biol., 16, pp.1896-1908.

24. Harden N, Loh HY, Chia W, Lim L (1995) A dominant inhibitory version of the small GTP-binding protein Rac disrupts cytoskeletal structures and inhibits developmental cell shape changes in Drosophila. Development, 121, pp. 903-914.

Review articles

  1. De Castro IP, Martins LM, Loh SHY, Mitochondrial quality control and Parkinson’s disease: a pathway unfolds. Mol Neurobiol, 2011. 43(2): p. 80-6

Book chapters

  1. Costa AC, Martins LM, Loh SHY (2012) Emerging Concepts Linking Mitochondrial Stress Signalling and Parkinson's Disease. INTECH
Senior Investigator Scientist

Contact Details

MRC Toxicology Unit
Gleeson Building
Tennis Court Road


Telephone and Email

+44 (0)1223 3 34390