Dr Yun Fan PhD

Dr Yun Fan

School of Biosciences
Associate Professor in Cell and Developmental Genetics

Contact details

602, School of Biosciences
University of Birmingham
B15 2TT

Dr Fan’s research interest centres on understanding how cell death, cell proliferation and cell differentiation are coordinated to maintain tissue homeostasis.  This has important implications for cancer development and tissue regeneration.  


2005 PhD - Biozentrum, University of Basel, Basel, Switzerland
2001 MS - Sun Yat-sen (Zhongshan) University, Guangzhou, China
1998 BE - Huazhong University of Science and Technology, Wuhan, China


Dr Fan was initially trained as a molecular biologist in China. He then completed his PhD in the field of Neurobiology in Switzerland. He subsequently worked at the University of Texas MD Anderson Cancer Center and the University of Massachusetts Medical School in the United States during which time his research focused on regulation of program cell death (apoptosis) and its related compensatory cell proliferation.  


  • BIO268 - Cell and Developmental Biology (Module organiser)
  • BIO352 - Current Developments and Advances in Eukaryotic Genetics
  • BIOM30 - Metabolism and Mechanisms of Toxicity
Dr Fan is an Associate Fellow recognized by the Higher Education Academy (HEA)

Postgraduate supervision

Please find details of our PhD research projects at FindAPhD:

Competition funded PhD studentships are available.  Applicants are encouraged to contact Dr Fan directly.

Postdoctoral Fellow applications are also welcome. Please contact Dr Fan to explore funding opportunities.


Birmingham Fly Facilityhttps://www.birmingham.ac.uk/research/birmingham-fly-facility/birmingham-fly-facility.aspx


In multicellular organisms, tissue homeostasis requires coordinated cell death, cell proliferation and cell differentiation. Disruption of this balance can lead to many human diseases including degenerative disorders and cancer. Our research is to investigate the molecular control of cell death and how dying cells communicate with their neighbours to maintain tissue homeostasis.

How do cells die?

In response to stresses such as radiation and toxins, cells can get damaged and are removed primarily by apoptosis, a major form of programmed cell death. Regulation of apoptosis is conserved from worms to flies to mammals. Although the core apoptosis pathway has been well studied, it is not yet clear how cells modulate their susceptibilities toward apoptosis. By using the Drosophila eye as a model, we have revealed striking dynamics in the apoptotic susceptibilities of different cell types in a developing organ (Fan and Bergmann, Dev Cell 30: 48). One of our research interests is to dissect the molecular mechanisms controlling cellular responses to apoptotic stresses.

In addition to apoptosis, necrosis is another type of cell death that frequently occurs in response to stresses. Unlike apoptosis, necrosis has long been considered to be passive and uncontrolled. However, recent studies have revealed that necrosis can be genetically regulated therefore potentially manageable. We have developed a Drosophila model to study regulation of necrosis in vivo and its relevance to tumour suppression (Li et al., Cell Death Dis 10: 613). This allows us to further identify and characterise novel regulators of necrosis, with the aim to explore how necrosis can be managed in human diseases including cancer, ischemic injury, neurodegenerative disorders, and inflammatory diseases

How do dying cells communicate?

Work by us and others has revealed that, surprisingly, stress-induced apoptotic cells can actively induce proliferation of their neighbouring cells to compensate for the cell loss. This evolutionarily conserved phenomenon has been termed apoptosis-induced compensatory cell proliferation (apoptosis-induced proliferation or AiP). It is critical for tissue recovery and organismal survival. Under pathological conditions, uncontrolled apoptosis-induced proliferation contributes to tumour development and recurrence.

We have discovered that apoptosis can induce cell proliferation through distinct mechanisms in a context-dependent manner, e.g. in proliferating versus differentiating tissues (Fan and Bergmann, Dev Cell 14: 339). However, our understanding of the molecular mechanisms underlying apoptosis-induced proliferation is far from complete. By taking advantages of Drosophila as a genetically tractable model organism, we have developed several assays to systematically identify and characterize novel regulators of apoptosis-induced proliferation (Fan et al., PLoS Genet 10: e1004131). Deciphering these mechanisms will make substantial contributions to our understanding of the cellular strategies and genetic pathways used to maintain tissue homeostasis in response to apoptosis. Our long-term research goal is to elucidate the relevance of apoptosis-induced proliferation in tissue regeneration and tumorigenesis.

EU FP7 Marie Curie actions BBSRC logo

Dr Fan’s research is supported by the EU FP7 Marie Curie Actions (CIG) and the Biotechnology and Biological Sciences Research Council in the UK.

We are on Facebook and Twitter - Fan Lab (@fanyunfy).

Other activities

Members of the British Society for Developmental Biology and the Genetics Society

2011-2012, Research Assistant Professor, University of Massachusetts Medical School, Worcester, USA

2009-2011, Instructor, University of Texas MD Anderson Cancer Center, Houston, USA

2006-2009, Postdoctoral Fellow, University of Texas MD Anderson Cancer Center, Houston, USA


  • Li M, Sun S, Priest J, Bi X and Fan Y (2019). Characterization of TNF-induced cell death in Drosophila reveals caspase- and JNK-dependent necrosis and its role in tumor suppression. Cell Death Dis 10 (8): 613.
  • Amcheslavsky A, Wang S, Fogarty C, Lindblad JL, Fan Y and Bergmann A (2018). Plasma membrane localization of apoptotic caspases for non-apoptotic functions. Dev Cell 45 (4): 450-464.
  • Li M, Lindblad JL, Perez E, Bergmann A and Fan Y (2016). Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation. BMC Biol 14: 70.
  • Fogarty CE, Diwanji N, Lindblad JL, Tare M, Amcheslavsky A, Makhijani K, Brückner K, Fan Y and Bergmann A (2016). Extracellular Reactive Oxygen Species Drive Apoptosis-Induced Proliferation via Drosophila Macrophages. Curr Biol 26 (5): 575-584.
  • Fan Y* and Bergmann A* (2014). Multiple mechanisms modulate distinct cellular susceptibilities towards apoptosis in the developing Drosophila eye. Dev Cell 30 (1):48-60. (*corresponding authors) 
  • Fan Y*, Wang S, Hernandez J, Yenigun VB, Hertlein G, Fogarty CE, Lindblad JL and Bergmann A* (2014). Genetic models of apoptosis-induced proliferation decipher activation of JNK and identify a requirement of EGFR signaling for tissue regenerative responses in Drosophila. PLoS Genetics 10 (1): e1004131. (*corresponding authors) 
  • Huang Q, Tang X, Wang G, Fan Y, Ray L, Bergmann A, Belenkaya TY, Ling X, Yan D, Lin Y, Ye X, Shi W, Zhou X, Lu F, Qu J and Lin X (2014). Ubr3 E3 ligase regulates apoptosis by controlling the activity of DIAP1 in DrosophilaCell Death Differ 21 (12):1961-70.
  • Christiansen AE, Ding T, Fan Y, Graves HK, Herz HM, Lindblad JL and Bergmann A (2012). Non-cell autonomous control of apoptosis by ligand-dependent Hedgehog signaling in DrosophilaCell Death Differ 20 (2):302-11.
  • Lee TV*, Fan Y*, Wang S, Srivastava M, Broemer M, Meier P and Bergmann A (2011). Drosophila IAP1-mediated ubiquitylation controls processing, but not protein stability, of the initiator caspase DRONC. PLoS Genetics 7 (9): e1002261. (*First authors) 
  • Fan Y, Lee T, Xu D, Chen Z, Lamblin AF, Steller H and Bergmann A (2010). Dual roles of Drosophila p53 in cell death and cell differentiation. Cell Death Differ 17 (6): 912-921.
  • Fan Y and Bergmann A (2010). The cleaved-Caspase-3 antibody is a marker of Caspase-9-like DRONC activity in DrosophilaCell Death Differ 17 (3): 534-539.
  • Xu D, Woodfield SE, Lee TV, Fan Y, Antonio C and Bergmann A (2009). Genetic control of programmed cell death (apoptosis) in Drosophila. Fly (Austin) 3 (1): 78-90.
  • Fan Y and Bergmann A (2008). Apoptosis-induced compensatory proliferation.  The Cell is dead. Long live the Cell!  Trends Cell Biol 18 (10): 467-473.
  • Fan Y and Bergmann A (2008). Distinct mechanisms of apoptosis-induced compensatory proliferation in proliferating and differentiating tissues in the Drosophila eye. Dev Cell 14 (3): 339-410. (evaluated by Faculty of 1000 Biology as “Must Read”)

Book Chapter:

  • Dabrowska C., Li M. and Fan Y. (2016). Apoptotic Caspases in Promoting Cancer: Implications from Their Roles in Development and Tissue Homeostasis. Adv Exp Med Biol 930: 89-112. In: Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy - New Perspectives and Opportunities. Advances in Experimental Medicine and Biology. Springer.

View all publications in research portal