WIMM PI
Curriculum Vitae
Personal Data
Name
Nationality
Email
Tudor Alexandru Fulga
ROMANIAN
tudor.fulga@imm.ox.ac.uk
Present Position
2011-present
Group Leader, MRC Senior research fellow - WIMM, Radcliffe Department
of Medicine, University of Oxford
Previous Positions
2008-2011
Instructor in Cell Biology – Department of Cell Biology, Harvard Medical
School, Boston MA
2004-2007
Postdoctoral Fellow – Department of Pathology, Brigham and Women’s
Hospital, Harvard Medical School, Boston MA. John Douglas French
Alzheimer's Foundation Postdoctoral Fellowship
1998-2003
Ph.D. (PhD title awarded in December 2001) – Structural Biology
Programme/Developmental Biology Programme, EMBL Heidelberg,
Germany. Louis Jeantet PhD Fellowship for East Europe (two fellowships
awarded every year for students throughout East Europe).
1996-1998
Research Assistant (Undergraduate) – Institute of Biochemistry, Bucharest
Romania
1992-1997
B.Sc. Genetics and Molecular Biology – University of Bucharest, Bucharest,
Romania
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Research Achievements
During the first part of my PhD I investigated the process of protein translocation across the
ER and uncovered the first function of the  subunit of the heterodimeric signal recognition
particle receptor (EMBO J 2001; Science, 2002), in the laboratory of Prof. Irmgard Sinning at
EMBL. Because I had completed my PhD studies in less than three years, I shifted my
research towards the field of developmental biology and joined the laboratory of Dr. Pernille
Rørth. My work there was focused on defining the cellular and molecular events controlling
the process of cell migration during development, and led to the discovery of a remarkable
novel mechanism of force generation in invasive migration (Nat Cell Biol., 2002; Nature,
2007). After completing my PhD training, I was drawn to the laboratory of Dr. Mel Feany at
Harvard Medical School, where I studied the mechanisms underlying neurodegeneration in
Alzheimer’s disease. My studies delineated the actin cytoskeleton as a critical mediator of
neurodegeneration in this disorder (Nat Cell Biol., 2006). Apart from potential clinical and
therapeutic relevance, these findings defined a novel mechanism of cytoskeletal cross talk in
neurons. After completing postdoctoral studies, I was offered a junior management position
at Merck & Co. in Boston. Coincidently, at about the same time I became fascinated by the
recent discovery of short non-coding RNAs. While the critical role of microRNAs in
development and disease was undisputed, it was clear at the time that our understanding of
their biological function lagged behind, primarily due to limitations in the technologies
available for in vivo analysis. Declining the Merck offer, I took an Instructor position at
Harvard Medical School working with Prof. David Van Vactor. Together, we developed a
highly versatile in vivo transgenic technology for conditional knock-down of microRNA activity
with precise spatial-temporal resolution (Nat. Methods, 2009). This technology offered the
first opportunity to study the function(s) of every microRNA in the context of intact organisms
during development or adult life and allowed us to discover a novel function of the conserved
miR-8 in controlling synaptic morphogenesis and function. This technique rapidly became
one of the methods of choice for defining tissue-specific microRNA functions in complex
biological systems, and uncovering intricate genetic interactions between microRNAs and
other genes. Additionally, it opened up endless possibilities for dissecting microRNA
regulated pathogenic mechanisms in Drosophila models for human diseases.
Lay Summary of Research
A consistent feature of many human disorders is a pronounced alteration in the levels of
various proteins. Yet, in many cases the upstream regulatory mechanisms controlling the
aberrant production of these proteins, remains unclear. For many years, it was thought that
RNAs only function as structural scaffolds and messengers transferring genetic information
from DNA to proteins. This view was drastically changed over a decade ago, following the
seminal discovery of a class of small non-coding regulatory RNAs called microRNAs. This
discovery revolutionized our view on the regulation of gene expression networks, setting an
important milestone in molecular, developmental and disease biology. MicroRNAs are
fascinating, albeit still rather mysterious, RNA molecules, which are never translated into a
protein sequence and are comprised of only 21 to 24 letters of the genetic alphabet.
Strikingly, these tiny pieces of RNA have the capacity to bind and tune the production of
thousands of different mRNAs functioning as molecular rheostats of gene expression
programs (protein production) in almost every living organism. For example, in mammals it is
estimated that nearly half of the protein-coding genes are targeted by microRNAs and the
vast majority of biological processes are influenced directly or indirectly by microRNAs.
Consequently, microRNAs have been shown to be dysregulated in many complex multifactorial disorders including cancer, viral infections, neurodegeneration, inflammatory
disease, metabolic disorders, and cardiac diseases. The challenge now is to determine
whether these changes in microRNA levels are central to the pathophysiology of human
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diseases or are just epiphenomenal bystanders. Due to the relatively large number of
microRNAs (over 1500 in humans), and their ability to simultaneously target hundreds of
genes for regulation, addressing this question is a daunting task. The goal of our research is
to use genetically tractable model organisms such as Drosophila melanogaster (fruit fly) to
dissect the role of microRNAs during organismal development and their contribution to the
onset and progression of several human disorders for which robust experimental models
have been established in flies. The extensive conservation of molecular and cellular
mechanisms between flies and humans, makes this an ideal system for studying processes
such as neuronal injury, wound injury, cancer and neurodegeneration. Facilitating these
studies, we recently developed highly versatile genome-wide transgenic technologies, which
allow us to silence or hyper-activate microRNAs with precise spatial-temporal resolution in a
living organism. Used in conjunction with cutting-edge techniques for microRNA profiling and
target identification, these offer a unique screening platform to explore in an unbiased fashion
the role of microRNAs in development and disease, and their potential as novel therapeutic
targets.
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All Publications Over the Past 5 Years
Tudor A. Fulga#, Elizabeth M. McNeill, Richard Binari, Julia Yelick, Alexandra Blanche,
Matthew Booker, Michael Schnall-Levin, Yong Zhao, Todd DeLucca, Fernando Bejarano,
Zhe Han, Eric C. Lai, Dennis Wall, Norbert Perrimon#, David Van Vactor# Unbiased screening
by conditional competitive inhibition reveals novel functions of conserved Drosophila miRNAs
during development and adult behaviour. Developmental Cell, Submitted for publication. #
Corresponding author
Katharine J. Marler, Philipp Suetterlin, Asha Dopplapudi, Aine Rubikaite, Jihad Adnan, Nicola
A. Maiorano, Andrew S. Lowe, Ian D. Thompson, Manav Pathania, Angelique Bordey, Tudor
Fulga, David L. Van Vactor, Robert Hindges and Uwe Drescher (2014) BDNF Promotes
Axon Branching of Retinal Ganglion Cells via miRNA-132 and p250GAP. Journal of
Neuroscience, 34(3):969-79.
Wanhe Li, Mike Cressy, Hongtao Qin, Tudor Fulga, David Van Vactor, and Josh Dubnau
(2013) microRNA-276a functions in Ellipsoid Body and Mushroom Body neurons for naive
and conditioned olfactory avoidance in Drosophila. Journal of Neuroscience, 33(13):582133.
Fernando Bejarano, Diane Bortolamiol-Becet, Qi Dai, Kailiang Sun, Abil Saj, Yu-Ting Chou,
David R. Raleigh, Kevin Kim, Jianquan Ni, Joshua W. Hagen, Hong Duan, Jr-Shiuan Yang,
Tudor A. Fulga, David Van Vactor, Norbert Perrimon and Eric C. Lai (2012) A genomewide
transgenic resource for conditional expression of Drosophila microRNAs. Development,
139(15):2821-31.
Manavendra Pathania, Juan Torres-Reveron, Lily Yan, Tomoki Kimura, Tiffany V. Lin,
Valerie Gordon, Zhao-Qian Teng, Xinyu Zhao, Tudor A. Fulga, David Van Vactor, Angélique
Bordey (2012) miR-132 Enhances Dendritic Morphogenesis, Spine Density, Synaptic
Integration, and Survival of Newborn Olfactory Bulb Neurons. PLos One, 7(5):e38174.
Vikram Khurana, Paola Merlo, Brian DuBoff, Tudor A. Fulga, Katherine A. Sharp, Shelag D.
Campbell, Jurgen Gotz and Mel B. Feany (2011) A critical neuroprotective role for an ATMdependent DNA damage checkpoint. Aging Cell, 11(2):360-2.
Vikram Khurana‡, Ilan Elson-Schwab‡, Tudor A. Fulga‡, Erin Mulkearns and Mel B Feany
(2010) Lysosomal proliferation is involved with caspase-cleavage of tau and promotes
neurodegeneration in a Drosophila model of tauopathy. PLoS Genetics, 15;6(7). ‡ Equal
contribution
Carlos M. Loya, David Van Vactor and Tudor A. Fulga (2010) Understanding neuronal
connectivity through the post-transcriptional toolkit. Genes and Development, 24(7):625-35
Carlos M. Loya, Cecilia S. Lu, David Van Vactor# and Tudor A. Fulga# (2009) Transgenic
microRNA inhibition with spatiotemporal specificity in intact organisms Nature Methods,
6(12):897-903. # Corresponding author
Howard Chia-Hao Chang, Douglas N. Dimlich, Takakazu Yokokura, Ashim Mukherjee, Mark
W. Kankel, Anindya Sen, Vasanthi Sridhar, Tudor A. Fulga, Anne C. Hart, David Van Vactor,
Spyros Artavanis-Tsakonas (2008) Modeling Spinal Muscular Atrophy in Drosophila PLoS
ONE 15;3(9):e3209
Tudor A. Fulga# and David Van Vactor# (2008) Synapses and growth cones on two sides of a
highwire Neuron 57(3):339-44. # Corresponding author
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Michelle L. Steinhilb, Dora Dias-Santagata‡, Tudor A. Fulga‡, Daniel L. Felch and Mel B.
Feany (2007) Tau phosphorylation sites work in concert to promote neurotoxicity in vivo Mol.
Biol. Cell 18(12):5060-8 ‡ Equal contribution
Ambra Bianco, Adam Cliffe, Minna Poukkula, Juliette Mathieu, Carlos M. Luque, Tudor A.
Fulga and Pernille Rørth (2007) Two distinct modes of guidance signaling during collective
migration. Nature 448 (7151):362-5.
Magali Periquet, Tudor Fulga, Liisa Myllykangas, Michael G. Schlossmacher and Mel B.
Feany (2007)
-synuclein mediates dopaminergic neurotoxicity in vivo. Journal
of Neuroscience 27 (12):3338-46
Dora Dias-Santagata, Tudor A. Fulga, Atanu Duttaroy and Mel B Feany (2007) Oxidative
stress mediates tau-induced neurodegeneration in Drosophila. J. Clin. Invest. 117 (1):236
Tudor A. Fulga#, Ilan Elson-Schwab, Vikram Khurana, Michelle L. Steinhilb, Tara L. Spires,
Bradley T. Hyman and Mel B. Feany# (2006) Abnormal bundling and accumulation of F-actin
mediates tau-induced neuronal degeneration in vivo. Nature Cell Biology, 9(2):139-48. #
Corresponding author
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Ten Key Publications Throughout your Career
Vikram Khurana‡, Ilan Elson-Schwab‡, Tudor A. Fulga‡, Erin Mulkearns and Mel B Feany
(2010) Lysosomal proliferation is involved with caspase-cleavage of tau and promotes
neurodegeneration in a Drosophila model of tauopathy. PLoS Genetics, 15;6(7). ‡ Equal
contribution
Carlos M. Loya, Cecilia S. Lu, David Van Vactor# and Tudor A. Fulga# (2009) Transgenic
microRNA inhibition with spatiotemporal specificity in intact organisms Nature Methods,
6(12):897-903. # Corresponding author
Michelle L. Steinhilb, Dora Dias-Santagata‡, Tudor A. Fulga‡, Daniel L. Felch and Mel B.
Feany (2007) Tau phosphorylation sites work in concert to promote neurotoxicity in vivo Mol.
Biol. Cell 18(12):5060-8 ‡ Equal contribution
Ambra Bianco, Adam Cliffe, Minna Poukkula, Juliette Mathieu, Carlos M. Luque, Tudor A.
Fulga and Pernille Rørth (2007) Two distinct modes of guidance signaling during collective
migration. Nature 448 (7151):362-5.
Tudor A. Fulga#, Ilan Elson-Schwab, Vikram Khurana, Michelle L. Steinhilb, Tara L. Spires,
Bradley T. Hyman and Mel B. Feany# (2006) Abnormal bundling and accumulation of F-actin
mediates tau-induced neuronal degeneration in vivo. Nature Cell Biology, 9(2):139-48. #
Corresponding author
Tudor A. Fulga and Pernille Rørth. (2002) Invasive cell migration is initiated by guided growth
of long cellular extensions. Nature Cell Biology 4(9):715-719
Martin R. Pool, Joachim Stumm, Tudor A. Fulga, Irmgard Sinning & Bernhard Dobberstein
(2002) Three stages in Signal Recognition Particle interaction with the Ribosome Science
297(5585):1345-8
Tudor A. Fulga, Irmgard Sinning, Bernhard Dobberstein & Martin R. Pool (2001) SR
coordinates Signal Sequence release from SRP with Ribosome binding to the Translocon.
EMBO J. 20(9):2338-47
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Markers of Esteem
2011 MRC Senior Research Fellowship
2010 HMS/HSMD Postdoctoral Fellow Travel Award
2009 Faculty of 1000 associate faculty member
2008 Keystone Symposia Scholarship
2007 BWH & HMS Award for outstanding achievement in clinical, transitional or basic
science research
2006 John Douglas French Alzheimer's Foundation Postdoctoral Fellowship
2005 Harvard University Award of Distinction in Teaching
2002 Best Poster Prize – Santa Cruz Conference on Developmental Biology
1998 Louis Jeantet PhD Fellowship for East Europe (EMBL Heidelberg)
Current Grant Support
MRC Senior Research Fellowship 2011-2016
£ 1,100,688
MRC Confidence in Concept Award 2013-2014
£ 80,640
NDM/WT Research Fund For Proof Of Principle
High Throughput Sequencing Experiments.
£ 9,076
BBSRC Research Project Grant 2014-2016
£ 482,987
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