SDB/ISD Satellite Symposium: Collective Cell Migration (August 4th, 2016)
Preliminary Program (8:00-9:00 a.m. Registration Desk; 9:00-9:05 a.m. Introduction)
Session 1- Early events – Germ Cells and Gastrulation
9:05-9:25 Erez Raz (ICB Munster) – Positioning progenitor cells during organogenesis: lessons
from early gonad development in zebrafish (+10min discussion)
9:35-9:55 Carl-Phillipe Heisenberg (IST Austria) – The physical basis of coordinated tissue
spreading in zebrafish gastrulation (+10min disc)
10:05-10:15 Angela Stathopoulos (Caltech) – The migrations of Drosophila muscle founders
and primordial germ cells are interdependent (+10min disc)
10:25-10:30 Highlight #1 – Rocio Hernandez-Martinez (SKI) – p120-Catenin couples cadherin
switching to (EMT) during mouse gastrulation
10:30-11:00am Break
Session 2 – Early events – 3D Cell Migration and Lateral Line Formation
11:00-11:20 Denis Wirtz (Johns Hopkins) – Engineered models of confined cell migration
(+10min disc)
11:30-11:50 Tatjana Piotrowski (Stowers Institute) – Lateral line migration (+10min disc)
12:00-12:10 Michelle Starz-Gaiano (UMBC) – Novel regulators of STAT signaling influence
border cell specification and migration in Drosophila (+10min disc)
12:20-12:25 Highlight #2 – Thomas Schultheiss (Technion) Bilaterally coordinated ingression
of the splanchnic coelomic epithelium and the formation of ventral body structures
12:25-12:30 Highlight #3 – Lital Attia (Technion) – Collective cell migration of the nephric duct
12:30-1:30pm Lunch on your own – see the back of the program for local food locations
Industry Expert Session- (A series of highlights about cool products/special issues, etc)
1:30-2:00 Seema Grewal (Company of Biologists), Valentina Sasselli (Elsevier),
Kaitie Kramer (Illumina), and Meredith Price & Brian Thompson (Bitplane)
Session 3 – Forces and Collective Migration
2:00-2:20 Celeste Nelson (Princeton) – Choreographing tissue morphogenesis (+10min disc)
2:30-2:50 Jeff Fredberg (Harvard) – Cellular contraction and polarization drive collective
cellular motion (+10min disc)
3:00-3:05 Highlight #4 – Nandan Nerurkar (Harvard) – FGF-mediated tensional gradients drive
collective cell movements to form the avian hindgut
3:05-3:10 Highlight #5 – Melanie White (AStar Singapore) – Imaging how cells first change
their shape and position in the living mouse
3:10-3:30pm: Coffee Break
Session 4 – Case Studies in Collective Cell Migration: The Neural Crest
3:30-3:40 Bec McLennan (Stowers) – Inhibitory signals sculpt collective cell migration of the
neural crest (+5min disc)
3:45-3:55 Kristin Artinger (Colorado) – Cdon promotes neural crest migration by regulating Ncadherin localization downstream of Shh (+5min disc)
4:00-4:10 Dom Alfandari (UMass) – Proteolytic control of neural crest cell migration (+5min)
4:15-4:25 Lisa Taneyhill (UM) – Annexin A6 controls neuronal membrane dynamics throughout
chick cranial sensory gangliogenesis (+5min disc)
4:30pm Close of Symposium
Positioning progenitor cells during organogenesis:
lessons from early gonad development in zebrafish
Erez Raz
University of Münster; Münster, Germany
The positioning of organ progenitor cells constitutes an essential, yet a poorly
understood step during organogenesis. We are studying the arrival and positioning of
the motile population primordial germ cells, the cells that give rise to gametes in the
gonad. Employing high-resolution live-cell microscopy we explore the developmental
mechanisms maintaining this progenitor cell population at the right position. We find that
repulsive cues coupled with physical barriers confine the cells to the location where they
participate in establishing a functional organ and describe their behavior upon
encountering those signals. Using particle-based simulations, we demonstrated the role
of reflecting barriers, and the importance of proper cell–cell adhesion level for
maintaining the tight cell clusters and their correct positioning at the target region. The
combination of these developmental and cellular mechanisms prevents organ fusion,
controls organ positioning and is thus critical for its proper function.
The physical basis of coordinated tissue spreading in zebrafish gastrulation
Hitoshi Morita and Carl-Philipp Heisenberg
Institute of Science and Technology Austria; Klosterneuburg, Austria
Embryo morphogenesis relies on highly coordinated movements of different tissues.
Yet, remarkably little is known about how tissues coordinate their movements to shape
the embryo. In zebrafish embryogenesis, coordinated tissue movements become first
apparent during ‘doming’ when the blastoderm begins to spread over the yolk sac, a
process involving coordinated epithelial surface cell layer expansion and mesenchymal
deep cell intercalations. Here, we find that active surface cell expansion represents the
key process coordinating tissue movements during doming. By using a combination of
theory and experiments, we show that epithelial surface cells not only trigger
blastoderm expansion by reducing tissue surface tension, but also drive blastoderm
thinning by inducing tissue contraction through radial deep cell intercalations. Thus,
coordinated tissue expansion and thinning during doming relies on surface cells
simultaneously controlling tissue surface tension and radial tissue contraction.
The migrations of Drosophila muscle founders
and primordial germ cells are interdependent
Angela Stathopoulos
California Institute of Technology; Pasadena, California, United States
Caudal visceral mesoderm (CVM) cells migrate from posterior to anterior of the
Drosophila embryo as two bilateral streams of cells to support specification of
longitudinal muscles along the gut. To accomplish this long-distance migration, CVM
cells receive input from their environment, but little is known about how this collective
cell migration process is regulated. In a screen, we found that wunen mutants exhibit
CVM cell migration defects. Wunens are lipid phosphate phosphatases shown to
regulate the directional migration of primordial germ cells (PGCs). PGC and CVM cell
types interact during the period when PGCs are en route to the somatic gonadal
mesoderm, and previous studies have shown that CVM cells impact PGC migration. In
turn, we found that CVM cells exhibit an affinity for PGCs, localizing to the position of
PGCs whether mislocalized in the ectoderm or trapped in the endoderm. Furthermore,
CVM cell migration is delayed in mutants lacking PGCs. These data demonstrate PGC
and CVM cell migrations are interdependent and suggest that distinct migrating cell
types can coordinately influence each other to promote effective cell migration during
development.
p120-Catenin couples cadherin switching to
epithelial to mesenchymal transition (EMT) during mouse gastrulation
Rocío Hernández-Martínez and Kathryn V. Anderson
Developmental Biology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering
Cancer Center; New York, United States
p120-catenin regulates cell-cell adhesion through interaction with cytoplasmic tails of
cadherins. Experiments show that p120-catenin promotes cadherin stability on the cell
surface, apparently by inhibiting its endocytosis. It was known that deletion of p120catenin causes embryonic lethality in mice, but the basis of that lethality was unclear.
We generated mouse embryos lacking p120-catenin in all cells, or specifically in the
epiblast. We observed that about half of mutant embryos had a duplication of the
posterior body axis, shown by the ectopic expression of primitive streak markers Wnt3
and T. The remaining mutants developed a cellular bulge at the streak due to defects in
mesoderm migration. In addition to these morphogenetic defects, mesoderm production
is greatly impaired, leading to a paraxial mesoderm deficit and a lack of a complete set
of somites. Accompanying the defects in axis specification, p120-catenin mutant
embryos exhibit apoptosis at the streak. During normal gastrulation Wnt signaling
stimulates an EMT and E-cadherin is down-regulated at the streak. In p120-catenin
mutant embryos, cells at the primitive streak down-regulate E-cadherin, but some of
those cells remain in the epiblast and aberrantly express N-cadherin, indicating that
p120-catenin couples cadherin switching to EMT. Moreover, there is an early expansion
of the Wnt-signaling domain at the streak in p120-catenin mutant embryos,
accompanied by strong nuclear localization of -catenin, suggesting that junctional catenin amplifies Wnt signaling at the site of EMT in the absence of p120-catenin.
Engineered models of confined cell migration
Paul CD, Hung WC, Wirtz D, Konstantopoulos K
John Hopkins University; Baltimore, Maryland, United States
Cells in the body are physically confined by neighboring cells, tissues, and the
extracellular matrix. Although physical confinement modulates intracellular signaling and
the underlying mechanisms of cell migration, it is difficult to study in vivo. Furthermore,
traditional two-dimensional cell migration assays do not recapitulate the complex
topographies found in the body. Therefore, a number of experimental in vitro models
that confine and impose forces on cells in well-defined microenvironments have been
engineered. We describe the design and use of microfluidic microchannel devices,
grooved substrates, micropatterned lines, vertical confinement devices, patterned
hydrogels, and micropipette aspiration assays for studying cell responses to
confinement. Use of these devices has enabled the delineation of changes in
cytoskeletal reorganization, cell-substrate adhesions, intracellular signaling, nuclear
shape, and gene expression that result from physical confinement. These assays and
the physiologically relevant signaling pathways that have been elucidated are beginning
to have a translational and clinical impact.
Signaling interactions that coordinate collective cell migration with organ
morphogenesis in the zebrafish lateral line
Agne Kozlowskaja-Gumbriene, Ren Yi, Richard Alexander, Melania McClain, Tatjana
Piotrowski.
Stowers Institute for Medical Research, Kansas City, Missouri, United States
Organ morphogenesis is driven by cell shape changes and organ size control. Even
though the intracellular mechanisms leading to cell shape changes are fairly well
understood, we are only beginning to understand how signaling pathways coordinate
cell shape changes of select cells with the development of a whole tissue or embryo.
The developing zebrafish lateral line is a powerful model to address this question, as
the lateral line sensory organs form within a collectively migrating group of cells called
the lateral line primordium. As the primordium migrates to the tail tip it periodically
deposits sensory organs, which thereby form a line. The leading region of the
primordium consists of mesenchymal cells, whereas in the trailing region cells apicallybasally polarize and apically constrict to form garlic bulb-shaped sensory organs. We
have previously shown that the two domains are maintained by a feedback mechanism
between the Wnt and Fgf pathways. Here we describe how these signaling pathways
interact with the Notch pathway to coordinate and control cell migration with cell shape
changes and organ size control.
Novel regulators of STAT signaling influence border cell specification
and migration in Drosophila
Afsoon Saadin and Michelle Starz-Gaiano
Department of Biological Sciences, University of Maryland Baltimore County; Baltimore,
Maryland, United States
During animal development, cells are often born in one location but required elsewhere,
necessitating their migration. In some cases, collectives of different cell types
cooperate during morphogenesis, allowing specific cells to take on complementary roles
while moving. We study the polar cell/border cell cluster of the Drosophila ovary to
understand how this occurs. Fruit flies provide a superb context for characterizing
collective cell migration because of the array of genetic tools available and the small
transparent tissues that permit direct imaging. Although both polar cells and border
cells arise in the ovarian epithelium, only border cells become motile, after induction by
the polar cells. Prior work has shown that the well-conserved Signal Transducer and
Activator of Transcription (STAT) signaling pathway is required for this specification and
movement. Through genetic screening, we have identified multiple new regulators of
these events. Specifically, we have uncovered a specific role for a vesicle trafficking
protein that is required in the polar cells for STAT-activator release to the surrounding
epithelial cells. This gene is required for border cell specification. In addition, we found
that the chromatin remodeling factor Brahma modulates STAT signaling, as well as
signaling from other pathways, to promote cell migration. Our work illustrates the
relevance of multiple, overlapping levels of regulation to control STAT activity and
govern collective cell motility generally.
Bilaterally coordinated ingression of the splanchnic coelomic epithelium and
the formation and positioning of ventral body structures
Alaa A. Arraf, Ronit Yelin, Inbar Reshef, and Thomas M. Schultheiss
Department of Genetics and Developmental Biology, Rappaport Faculty of Medicine,
Technion-Israel Institute of Technology; Haifa, Israel
The vertebrate body plan is bilaterally organized around a central axis located in the
body midline. During embryogenesis, the first midline structure to emerge is the
notochord, which is located in the dorsal midline and which secretes multiple factors,
including the BMP antagonists Noggin, Chordin, and Follistatin, as well as Sonic
hedgehog (Shh). Subsequently other midline structure form in more ventral regions,
including the descending aorta, primitive linear heart tube, dorsal and ventral
mesenteries that connect the gut tube and its derivatives to the body wall, sternum,
umbilicus, urinary bladder, uterus, and external genitalia. The mechanisms that ensure
the alignment of these ventral midline structures with the dorsal midline are not well
understood. The current study uses the dorsal mesentery (DM) as a model for
investigating the positioning of ventral midline structures. We document formation of the
DM by way of epithelial-to-mesenchymal transition (EMT) and medial ingression of the
coelomic epithelium (CE) of the lateral plate mesoderm, in which newly generated
mesenchyme cells from the two sides of the CE migrate medially between the aorta and
the endoderm until they meet in the ventral midline, where they generate the DM and
other ventral body structures. Inhibition of BMP signaling in the CE on one side of the
embryo caused a deflection of the DM towards the treated side, attributable at least in
part to reduction in the rate of EMT of the CE on that side. Because BMP antagonists
are expressed in the dorsal midline, this suggests a mechanism in which factors
secreted from the dorsal midline regulate the rate of medial ingression of CE-derived
cells, thereby ensuring alignment of the dorsal and ventral embryonic midlines.
Collective cell migration of the nephric duct
Lital Attia, Ronit Yelin, Tom Schultheiss
Technion- Israel Institute of Technology; Haifa, Israel
During the course of development, the vertebrate nephric duct (ND) extends and
migrates from the place of its initial formation, adjacent to the anterior somites, until it
inserts into the bladder or cloaca in the posterior region of the embryo. The molecular
mechanisms that guide ND migration are still poorly understood. First, a system was
developed for live imaging of ND migration in the chick embryo at the individual cell
level through use of GFP driven by a ND-specific enhancer element of the Gata3 gene.
Use of this system on normal embryos revealed that cells in different regions of the duct
migrate at different rates, with cells at the leading posterior duct tip migrating 4-fold
faster than more anterior duct cells. This system and other approaches were then used
to examine the role of FGF signaling during ND migration. It was found that FGF
receptor inhibition blocks nephric duct migration. In combination with data showing
expression of FGF Receptors and FGF response genes in the ND, and FGF ligands in
surrounding tissues, these results indicate that FGF signaling is required for nephric
duct migration. Placement of a localized source of FGF signal adjacent to the nephric
duct did not affect the duct migration path, indicating that FGF signaling is not sufficient
to determine the migration pathway of the nephric duct. Taken together, these studies
indicate that FGF signaling acts as a “motor” that is required for duct migration, but that
other signals are likely needed to determine the directionality of the duct migration
pathway. We have also used this experimental system to investigate the role of
canonical Wnt signaling in ND migration. We find that Wnt signaling is required for
cohesiveness of migrating ND cells, and that when Wnt signaling is inhibited, individual
cells wander away from the ND structure. We are currently investigating the cellular
and molecular basis of the loss of ND cell cohesiveness upon the lowering of Wnt
signaling.
Choreographing tissue morphogenesis
Celeste Nelson
Princeton University; New Jersey, United States
During development, simple populations of cells are transformed into the complex forms
of the mature organism, giving rise to polarized body plans, surface appendages, and
internal organs. These dynamic changes in tissue morphology that arise during
morphogenesis are known as tissue morphodynamics. For several decades, much of
our understanding of tissue development was static, limited to patterns of gene
expression and cell differentiation as inferred from still images taken of specimens that
were fixed at different developmental stages. Recent advances in cell labeling and
three-dimensional timelapse imaging, however, have enabled an explosion of studies
examining the dynamic movements and cell shape changes that accompany tissue
morphogenesis. These technological breakthroughs, coupled with sophisticated
manipulations of gene expression and signaling, have revealed some fundamental
biochemical and mechanical factors that regulate tissue morphodynamics across
species.
Collective migration and cell jamming in asthma, cancer, and development
Jeff Fredberg
Harvard Medical School; Boston, Massachusetts, United States
Collective cellular migration within the epithelial layer impacts development, wound
healing, and cancer invasion, but remains poorly understood. Prevailing conceptual
frameworks tend to focus on the isolated role of each particular underlying factor –
taken one at a time or at most a few at a time – and thus may not be tailored to describe
a cellular collective that embodies a wide palette of physical and molecular interactions
that are both strong and complex. To bridge this gap, we shift the spotlight to the
emerging concept of cell jamming, which points to only a small set of parameters that
govern when a cellular collective might jam and rigidify like a solid, or instead unjam and
flow like a fluid. This talk highlights cell jamming, its established role in human epithelial
cell layers derived from the airways of non-asthmatic and asthmatic donors, and its
speculative but emerging roles in development and cancer cell invasion.
FGF-mediated tensional gradients drive collective cell movements
to form the avian hindgut
Nandan L. Nerurkar, L. Mahadevan, and Cliff J. Tabin
Harvard Medical School; Boston, Massachusetts, United States
The recent resurgent interest in physical aspects of morphogenesis has advanced our
understanding of the types of forces involved, and the subcellular machinery that enact
them. Ultimately, embryonic forces are under genetic control, but upstream signals that
spatiotemporally regulate them remain largely unknown. Here we aim to address this in
the context of gut tube formation in the chick embryo. The internalization of the
endoderm to form the gut tube is a fundamental, yet poorly understood process in
establishing the vertebrate body plan. We identified a collective polarized movement of
endoderm cells that drives hindgut formation, and using a combination of biophysical
and molecular approaches, determined that these movements arise through an FGFmediated contractile gradient. FGF8 generates tension in the endoderm through RhoAdependent contraction, and as a result, the posterior-to-anterior gradient in FGF8
generates a parallel gradient in tension. This force imbalance drives movement of cells
from anterior (low tension/FGF8) to posterior (high tension/FGF8). A key feature of this
mechanism, revealed by mathematical modeling, is the positive feedback that results,
whereby passive anterior cells are pulled posteriorly by active contracting cells, and in
doing so are exposed to increasing FGF8 concentrations, contract themselves, and pull
more cells posteriorly. This is analogous to a tug of war game, where as one team
begins to win, they recruit players from the opposing team. This is why posterior
movement of the endoderm outpaces axis elongation despite the fact that both
processes are coordinated by the same FGF8 gradient. This work represents some of
the first mechanistic insight into how the regulation of tissue-scale physical forces in
vertebrate development can be traced to signaling pathways. Specifically we show that
modulation of tissue-level forces by diffusible signals represents a fundamental
mechanism by which morphogenesis is carried out.
Imaging how cells first change their shape and position
in the living mouse embryo
Melanie White
Institute of Molecular and Cell Biology, Agency for Science, Technology and Research;
Singapore
Every cell in the mammalian body originates from the pluripotent inner mass of the
embryo, yet the mechanical forces forming this structure are unknown. We developed
new quantitative imaging technologies to track changes in cell shape and position in
living mouse embryos. These enabled us to characterize the main morphogenetic
mechanisms forming the pluripotent inner mass and show how mechanical forces acting
within the embryo control cell shape and positioning events. We revealed that during
embryo compaction, cells extend long filopodia that cause cells to elongate and draw
their neighbors closer. Combining membrane segmentation and actomyosin laser
ablation we show how anisotropies in tensile forces drive some cells inside the embryo
to establish the first spatial segregation of cells during mammalian development.
Inhibitory signals sculpt collective cell migration of the neural crest
Rebecca McLennan, Caleb M. Bailey, Jessica M. Teddy, Linus J. Schumacher,
Jason A. Morrison, Hua Li, Madelaine M. Gogol, Jennifer C. Kasemeier-Kulesa,
Ruth E. Baker, Philip K. Maini, Paul M. Kulesa
Stowers Institute for Medical Research; Kansas City, Missouri, United States
The neural crest are an excellent model to study collective cell migration since they are
highly invasive and sculpted into discrete streams that reach precise targets. Although
some intrinsic signals from the neural tube have been identified to regulate neural crest
delamination, it is largely unknown what signals inhibit neural crest migration so as to
maintain collective cell migration along stereotypical pathways away from the neural
tube. In this study, we used differential expression screening to compare the neural
crest microenvironment with migrating neural crest cells and discovered a number of
novel secreted and membrane-bound factors whose expression was confirmed to be in
between neural crest streams. By using in vitro stripe assays combined with time-lapse
microscopy, we identified factors that inhibited neural crest cell behaviors. Here, we will
discuss the identification of one of these candidates, DAN, a BMP antagonist and its
potential role to both maintain cohesion within the neural crest stream and influence the
timing of neural crest migration through inhibition.
Cdon promotes neural crest migration by regulating N-cadherin
localization downstream of Shh
Davalyn R. Powell, Jason S. Williams, and Kristin Bruk Artinger
Department of Craniofacial Biology, University of Colorado School of Dental Medicine;
Aurora, Colorado, United States
A fundamental question in developmental biology is how migratory neural crest cells
(NCCs) initiate migration, how cells migrate in a directed fashion along a specific
pathway, how cells know where and when to stop migrating and subsequently
differentiate. We have identified Cdon, Cell adhesion down regulated by oncogenes, a
key component of the Sonic Hedgehog (Shh) signaling pathway as a critical factor in
regulating NCC migratory behaviors. We hypothesize that Cdon functions as an
integrator of cell polarity/adhesion and Shh signaling during NCC migration and
regulates N-Cad targeting to the NCC plasma membrane in response to Shh cues
required for persistent migration. Crispr mutants of cdon results in aberrant migration of
trunk NCCs with reduced directedness of migration and increased velocity. cdon is
required cell-autonomously for directed NCC migration and functions downstream of
canonical Shh signaling. Interestingly, we have determined that Shh acts as a
chemoattractant for truck NCC migration and that the likely mediated by cdon. In
addition, in the absence of cdon, N-cadherin is not localized to the plasma membrane
suggesting that Cdon regulates N-cadherin localization. New live cell imaging data will
be presented suggesting cdon is expressed in leader neural crest cells of the migratory
front but not in the subsequent migrating cells. These results reveal a novel role for the
cdon-N-cadherin-Shh axis in zebrafish neural crest migration.
Proteolytic control of neural crest cell migration
Dominique Alfandari, Ketan Mathavan, Vikram Khedgikar
Dept. of Veterinary and Animal Sciences and the Molecular and Cellular Biology
program, University of Massachusetts Amherst; Amherst, Massachusetts, United States
Cranial Neural Crest (CNC) cells are a transient population of pluripotent stem cells that
are induced at the border of the neural and non-neural ectoderm during early
embryogenesis. They must migrate through precise route to invade the ventral tissues
and contribute to the formation of the face. We have previously shown that CNC migrate
first collectively prior to segregating into single cells. To achieve this process a fine
control of cell-cell and cell matrix adhesion must be achieved. ADAM cell surface
metalloproteases are enzymes that are involved in this process. We have shown
previously that ADAM9 and 13 cleave the extracellular domain of Cadherin-11 to
produce a fragment that can inhibit contact inhibition of locomotion and promote cell
migration. In addition we have shown that the ADAM13 cytoplasmic domain is cleaved
by gamma-secretase translocates into the nucleus where it regulates multiple gene
expression. Using Proteomics, we have identified new substrates that are cleaved from
the neural crest cell surface during migration. In particular the protocadherin PCNS
(pcdh8l) expression is controlled at both transcriptional and post transcriptional levels by
the ADAM13 metalloprotease. Previous work has shown that PCNS is absolutely critical
for CNC migration. Here we show that the proteolytic activity and the cytoplasmic
domain of ADAM13 regulate PCNS gene expression and protein level to support CNC
migration in vivo. To better understand ADAM13’s ability to regulate gene expression
we used Mass Spectrometry to identify proteins that interact with the cytoplasmic
domain and regulate nuclear translocation and nuclear function. We also investigated
the role of the extracellular fragment of the cleaved cell adhesion molecules in
regulating signaling pathways that mediate cellular migration.
Annexin A6 controls neuronal membrane dynamics
throughout chick cranial sensory gangliogenesis
Lisa A. Taneyhill
University of Maryland; College Park, Maryland, United States
Cranial sensory ganglia are components of the peripheral nervous system that possess
a significant somatosensory role and include neurons within the trigeminal and
epibranchial nerve bundles. Although it is well established that these ganglia arise from
interactions between neural crest and neurogenic placode cells, the molecular basis of
ganglia assembly is still poorly understood. Members of the Annexin protein superfamily
play key roles in sensory nervous system development throughout metazoans. Annexin
A6 is expressed in chick trigeminal and epibranchial placode cell-derived neuroblasts
and neurons, but its function in cranial ganglia formation has not been elucidated. To
this end, we interrogated the role of Annexin A6 using gene perturbation studies in the
chick embryo. Our data reveal that placode cell-derived neuroblasts lacking Annexin A6
ingress, differentiate, and migrate normally to the ganglionic anlage, where neural crest
cell corridors correctly form around them. Strikingly, while Annexin A6-depleted placodal
neurons still express mature neuronal markers, they fail to form bipolar projections,
which are considered morphological features of mature neurons, and no longer
innervate their designated targets. Moreover, ectopic expression of Annexin A6 causes
some placodal neurons to form extra protrusions alongside their bipolar projections.
These data suggest that the molecular program associated with neuronal maturation
can be uncoupled from the required morphology change and, importantly, reveal
Annexin A6 to be a key membrane scaffolding protein during sensory neuron
membrane biogenesis for placodal neurons to adopt their final cell shape. Collectively,
our results provide novel insight into mechanisms underscoring morphological changes
within placodal neurons during cranial gangliogenesis and lend support for a new model
of neuronal maturation involving independent, yet required, molecular programs that
control neuronal gene expression and orchestrate changes in cell shape.
Industry Experts
The Company of Biologists
Dr. Seema Grewal
Email: seema.grewal@biologists.com
Web: www.biologists.com
Bitplane
Meredith H. Price and Brian Thompson
Email: meredith.price@bitplane.com
Web: www.bitplane.com
Illumina
Kaitie Kramer
Email: kkramer@illumina.com
Web: http://www.illumina.com/
Elsevier
Valentina Sasselli
Email: v.sasselli@elsevier.com
Web: https://www.elsevier.com/
Advanced Cell Diagnostics
Arthur Haynes, Senior Account Executive, US Midwest
Email: ahaynes@acdbio.com
Web: http://www.acdbio.com
Chroma
Paul Millman
Email: pmillman@chroma.com
Web: www.chroma.com
Developmental Dynamics
Parker Antin
Email: pba@email.arizona.edu
Web: http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-0177
North Central Instruments
Mike Hehr
Email: mikeh@ncimicro.com
Web: https://www.ncimicro.com/
Gene Tools
Alexandra Vincent
Email: alexandra.vincent@gene-tools.com
Web: http://www.gene-tools.com/
SDB Satellite Imaging Symposium Travel Awards
Angela Stathopoulos
Dominique Alfandari
Lital Attia
Kristin Artinger
Melanie Denise White
Nandan Nerurkar
Tom Schultheiss
Michelle Starz-Gaiano
Rocío Hernandez
Lisa Anne Taneyhill
Rebecca McLennan
Acknowledgements
The Co-Organizers of the Satellite Imaging Symposium (Roberto and Paul) would very
much like to thank the Society for Developmental Biology (SDB) for their generous
financial support and organizational help, in particular, Dr. Ida Chow and Ms. Sophia
Stellabotte. We very much appreciate the financial contributions from our industry
experts, including The Company of Biologists, Bitplane, Illumina, Advanced Cell
Diagnostics, Chroma, Developmental Dynamics, Elsevier, North Central Instruments,
and Gene Tools.
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Boke
Bouffard
Bruce
Burkard
Bush
Cabrera Quio
Cai
Institution
Harvard School of Dental Medicine
Stowers Institute for Medical Research
Tufts University
Northeastern University
Stowers Institute for Medical Research
St. Peter's University
University of Chicago
UMass
Developmental Biology Program
University of Pittsburgh
Centre de recherche sur le cancer, l'Hotel dieu de Québec
University of California San Francisco
University of Colorado Anschutz Medical Campus
University of Southern California
Thomas Jefferson University
Harvard Medical School
Technion-Israel Institute of Technology
Bar -Ilan university
Icahn School of Medicine at Mount Sinai
University of Miami
Smith College
University of Toronto
Boston College
Augsburg College
University of Chicago
New York University
Institute of Molecular Genetics of the AS CR
UCSD
Harvard Medical School
Northeastern University
University of Toronto
University of Maryland
UCSF
Research Institute of Molecular Pathology
Pennsylvania State University
Email Address
apengnaruto@163.com
aai@stowers.org
Dany.Adams@Tufts.edu
adesina.a@husky.neu.edu
zaf@stowers.org
agapitoma@gmail.com
kamilahsan@uchicago.edu
alfandar@vasci.umass.edu
k-anderson@ski.mskcc.org
angilerk@pitt.edu
rifdat.aoidi.1@ulaval.ca
ripla.arora@ucsf.edu
kristin.artinger@ucdenver.edu
askary@usc.edu
sophie.astrof@gmail.com
yatsuta@genetics.med.harvard.edu
litalat@tx.technion.ac.il
efratavigad@gmail.com
neeta.bala@mssm.edu
saptaparni@bio.miami.edu
mbarresi@smith.edu
dj_barua487@hotmail.com
bearcee@bc.edu
beckmanm@augsburg.edu
beiriger@uchicago.edu
yb372@nyu.edu
shohag@img.cas.cz
jbloomekatz@ucsd.edu
elvan_boke@hms.harvard.edu
bouffard.j@husky.neu.edu
ashley.bruce@utoronto.ca
burkarda@vcu.edu
jeffrey.bush@ucsf.edu
luis.cabrera.quio@imp.ac.at
huc163@psu.edu
Andrea
Ying
Katia
Adam
Jerome
Joanne
Guiqian
Ajay
Seok-Yong
Christie
Jessica
Jennifer
Martin
Charlotte
Miguel
Philip
Helene
Erin
Susana
Chitra
Damian
Suresh
Dillon
Agnik
Mary
Dennis
Seth
Elizabeth
Fayzeh
Megan
Jelena
Albert
Jaime
Cameron
Kerstin
Kelli
Lydie
Cantu
Cao
Carneiro
Carte
Chal
Chan
Chen
Chitnis
Choi
Ciarlo
Clark
Cloutier
Cohn
Colle
Concha
Copenhaver
Cousin
Cram
da Silva
Dahia
Dalle Nogare
Damodaran
Damuth
Dasgupta
Dickinson
Discher
Donoughe
Driver
El Banna
Eldred
Erceg
Erives
Espina
Exner
Feistel
Fenelon
Flasse
University of California, San Francisco
Tongji Univ
Federal University of Rio de Janeiro
Harvard University
Brigham and Women's Hospital
Hampton University
The University of Georgia
NICHD
Chonnam National University Medical School
Harvard University
Dalhousie University
Whitehead Institute / MIT
University of Florida
University College London
Universidad de Chile
Oregon Health & Science University
UMass-Amherst
Northeastern University
Harvard Medical School
Hospital for Special Surgery
NIH
South Dakota State University
Georgetown University
SUNY Upstate Medical University
Baylor College of Medicine
U Penn
Harvard University
NIDCD, NIH
Carleton College
University of Cambridge
Harvard Medical School
University of Iowa
Universidad Andres Bello
University of California, Berkeley
University of Hohenheim
University of Toronto
Danstem
Andrea.Cantu@ucsf.edu
yingcao@tongji.edu.cn
kcarneiro@histo.ufrj.br
ancarte@g.harvard.edu
dr.jchal@gmail.com
joanne.chan@hamptonu.edu
gqchen@uga.edu
abchitnis@gmail.com
zebrafish@chonnam.ac.kr
cciarlo@fas.harvard.edu
Jessica.Clark@dal.ca
jenniferkcloutier@gmail.com
mjcohn@ufl.edu
colle.charlotte@gmail.com
miguelconcha@gmail.com
copenhav@ohsu.edu
hcousin@vasci.umass.edu
erincram@gmail.com
sdasilva@genetics.med.harvard.edu
dahiac@hss.edu
damiandn@gmail.com
suresh.d.gen@gmail.com
dld66@georgetown.edu
dasgupta@upstate.edu
mdickins@bcm.edu
discher@seas.upenn.edu
seth.donoughe@gmail.com
drivere@nidcd.nih.gov
elbannaf@carleton.edu
me360@cam.ac.uk
jerceg@genetics.med.harvard.edu
albert-erives@uiowa.edu
jaime.espina2501@gmail.com
cexner@berkeley.edu
k.feistel@uni-hohenheim.de
kelli.fenelon@sickkids.ca
lydieflasse@gmail.com
Laina
Kristin
Jenna
Héctor
Laura
Ming
Sushant
Svetlana
Erin
Raghav
Seema
Sumant
Jennifer
Olivier
Lu
Nicholas
Richard
Hannah
Kieran
Tiffany
Maxwell
Rocio
Christopher
Tyl
Sevan
Bau-Lin
Tyler
Anneliis
Tatsuro
Vahan
Philip
Adam
Harini
Andrew
Bridget
Ruth
Karyn
Freyer
Gallik
Galloway
Gálvez García
Gammill
Gao
Gavhale
Gavrilov
Golden
Goyal
Grewal
Grover
Gutzman
Hamant
Han
Hanovice
Harland
Harris
Harvey
Heanue
Heiman
Hernandez-Martinez
Hess
Hewitt
Hopyan
Huang
Huycke
Ihermann-Hella
Ikeda
Indjeian
Ingham
Isabella
Iyer
Jacob
Jacques-Fricke
Johnson
Jourdeuil
Memorial Sloan-Kettering Cancer Center
University of Illinois at Chicago
Massachusestts General Hospital/Harvard Medical School
UPF
University of Minnesota
Indiana University Northwest
University of Prince Edward Island
Memorial Sloan Kettering Cancer Center
University of Colorado Anschutz Medical Campus
Johns Hopkins University
Development
University of Dayton
University of Wisconsin-Milwaukee
ENS Lyon
Cincinnati Children's Hospital
University of Pittsburgh School of Medicine
UC Berkeley
Tufts University
Peter MacCallum Cancer Centre
The Francis Crick Institute
Harvard Medical School, Boston Children's Hospital
Sloan-Kettering Institute
Institute of Molecular Life Sciences, University of Zurich
NIH
Program in Developmental and Stem Cell Biology, Hospital for Sick Children, Toronto
NCI-Frederick/NIH
Harvard Medical School
Institute of Biotechnology, University of Helsinki
Kyoto University
MRC Clinical Sciences Centre
Lee Kong Chian School of Medicine
University of Chicago
University of Illinois at Urbana-Champaign
SUNY Upstate Medical University
Carleton College
Wesleyan University
University of Maryland
lainaleefreyer@gmail.com
kgalli3@uic.edu
jenna_galloway@hms.harvard.edu
hector.galvez@upf.edu
gammi001@umn.edu
minggao@iun.edu
sgavhale@upei.ca
gavrilos@mskcc.org
erin.golden@ucdenver.edu
rgoyal7@jhu.edu
s.grewal@biologists.com
sumantgrover@gmail.com
gutzman@uwm.edu
olivier.hamant@ens-lyon.fr
lu.han@cchmc.org
nhanovic@pitt.edu
harland@berkeley.edu
Hannah.Harris@tufts.edu
kieran.harvey@petermac.org
tiffany.heanue@crick.ac.uk
heiman@genetics.med.harvard.edu
hernandr@mskcc.org
christopher.hess@uzh.ch
hewittt@mail.nih.gov
sevan.hopyan@sickkids.ca
huangbl@mail.nih.gov
thuycke@fas.harvard.edu
anneliis.ihermann@helsinki.fi
i.tatsuro@ascidian.zool.kyoto-u.ac.jp
vahan.indjeian@imperial.ac.uk
pingham@imcb.a-star.edu.sg
aisabella@uchicago.edu
hiyer4@illinois.edu
jacoba@upstate.edu
jacquebt@umn.edu
rijohnson@wesleyan.edu
kjourdeu@umd.edu
Pekka
Yasuhiko
Tomas
Andrew
Aisha
Yung Hae
Min Jung
Takae
Yoshihiko
Emily
Naden
Robb
Erina
Jochen
Elizabeth
Rusty
Christine
Stephanie
Tae
ChangHee
Vicki
Feixue
Jianying
Ang
Ke
Yingcui
Yi-Tzu
Lara
Hongxiang
Maria
Deirdre
John
Harsha
Abdullah Al
Tamrat
Sumanth
Cristian
Katajisto
Kawakami
Kazmar
Kelleher
Khalid
Kim
Kim
Kiyama
Kobayashi
Kolenbrander
Krogan
Krumlauf
Kuranaga
Kursawe
Lamkin
Lansford
Larkins
Lau
Lee
Lee
Leung
Li
Li
Li
Li
Li
Lin
Linden
Liu
Loscertales
Lyons
Mably
Mahabaleshwar
Mahmud
Mamo
Manohar
Marchant
University of Helsinki and Karolinska Institutet
University of Minnesota
IMP Vienna
University of Missouri
UMASS Lowell
University of Copenhagen
Sookmyung Women's University
The University of Texas Health Science Center at Houston
Okayama University
Stanford University
American University
Stowers Institute
Tohoku University
University of Oxford
Harvard University/Boston Children's Hospital
USC-CHLA
University of Florida
New York University School of Medicine
Brigham and Women's Hospital / Harvard Medical School
Harvard Medical School
McGill University
Institute of Developmental and Regenerative Biology, Hangzhou Normal University
Institute of Life Sciences, Hangzhou Normal University
University of Southern California
Albert Einstein College of Medicine
University of Hartford
Duke University
Duke University
University of Georgia
Massachusetts General Hospital/Harvard Medical School
U.C. San Diego/SIO
Hampton University
NICHD - NIH
CHU Ste Justine, University of Montreal
Hannover medical school
University of Virginia
Universidad Andres Bello
pekka.katajisto@helsinki.fi
kawak005@umn.edu
tomas.kazmar@imp.ac.at
amkmv4@mail.missouri.edu
aisha_khalid@student.uml.edu
yung.kim@sund.ku.dk
minkim@sookmyung.ac.kr
Takae.Kiyama@uth.tmc.edu
ag19051@s.okayama-u.ac.jp
emkolen@gmail.com
nkrogan@american.edu
rek@stowers.org
kuranaga@cdb.riken.jp
kursawe@maths.ox.ac.uk
elizabeth.lamkin@gmail.com
lansford@usc.edu
christinelarkins@ufl.edu
stephanie.lau2@nyumc.org
tjlee@partners.org
chlee@genetics.med.harvard.edu
vicki.leung@mail.mcgill.ca
lifx@hznu.edu.cn
ljy241@126.com
angli@usc.edu
ke.li@phd.einstein.yu.edu
yinli@hartford.edu
yl181@duke.edu
lara.linden@duke.edu
LHX@UGA.EDU
mloscertales@mgh.harvard.edu
dclyons1@gmail.com
john.mably@hamptonu.edu
harsha.mahabaleshwar@nih.gov
mahmudszn@gmail.com
Mamo.Tamrat@mh-hannover.de
sm9ne@virginia.edu
foo.marchant@gmail.com
John
Megan
Alexandra
David
Hillary
Sean
Reginald
Eric
Cecilia
Christian
Kusumika
Mahua
Rachel
Nathan
Akankshi
William
Senthil
Nandor
Ferez
Caroline
Nandan
Neil
Christof
M. Angela
Lee
Megan
Maria Cecília
Tomoko
Oscar
Karen
Morihiro
Tatiana
Kouhei
Andrea
Karin
Serge
JUNGEUN
Marken
Martik
Mascaro
Matus
McGraw
McKinney
McNulty
Miska
Moens
Mosimann
Mukherjee
Mukhopadhyay
Mullen
Mundell
Munjal
Munoz
Muthuswamy
Nagy
Nallaseth
Nazaire
Nerurkar
Neumann
Niehrs
Nieto
Niswander
Norris
Nunes
Obara
Ocaña
Oegema
Okada
Omelchenko
Oonuma
Page-McCaw
Panser
Parent
PARK
College of William and Mary
California Institute of Technology
Brown University
Stony Brook University
Oregon Health & Science University
Stowers Institute for Medical Research
TSRI
The Gurdon Institute
Fred Hutchinson Cancer Research Center
Institute of Molecular Life Sciences, University of Zurich
Harvard University
NIH
MD Anderson Cancer Center
Harvard Medical School
Harvard Medical School
Stowers Institute for Medical Research
BIDMC, Harvard Medical School
Harvard Medical School, MGH, Department of Pediatric Surgery
Life Sciences Institute NJ/Complex Biological Systems Alliance, Boston, MA
UMASS Lowell
Harvard Medical School
Johns Hopkins University
Institue of Molecular Biology (IMB)
instituto de Neurociencias CSIC-UMH
Univ of Colorado Anschutz Medical Campus
Harvard University
Federal University of Rio de Janeiro
OUHSC
Instituto de Neurociencias de Alicante CSIC-UMH
Ludwig Institute for Cancer Research/UCSD
National Institutes of Health
MSKCC
Konan university
Vanderbilt University
I.M.P.
University of Toronto
Stowers Institute for Medical Research
jpmarken@gmail.com
mmartik@caltech.edu
alexandra_mascaro@brown.edu
david.matus@stonybrook.edu
mcgraw@ohsu.edu
samckinn@outlook.com
rmcnulty@scripps.edu
mjl76@cam.ac.uk
cmoens@fhcrc.org
christian.mosimann@imls.uzh.ch
kmukherjee@mgh.harvard.edu
mukhopam@mail.nih.gov
rdmullen@MDanderson.org
nmundell@genetics.med.harvard.edu
akankshimunjal@gmail.com
wim@stowers.org
smuthusw@bidmc.harvard.edu
nnagy@mgh.harvard.edu
ferez.nallaseth@gmail.com
caroline_nazaire@student.uml.edu
nlnerurkar@genetics.med.harvard.edu
neumann@jhmi.edu
niehrs@imb.de
anieto@umh.es
Lee.Niswander@ucdenver.edu
megannorris@fas.harvard.edu
mcof.nunes@gmail.com
tomoko-obara@ouhsc.edu
oocana@umh.es
koegema@ucsd.edu
morihiro.okada@nih.gov
omelchet@mskcc.org
koonuma861116@gmail.com
andrea.page-mccaw@vanderbilt.edu
karin.panser@imp.ac.at
serge.parent@mail.utoronto.ca
jup@stowers.org
Travis
Clarissa
Maria
Nishal
Suyapa
Michael
Alice
Olivier
Victoria
Chen
Laurel
Maria
Erez
Michal
Ariel
Daniela
Victor
Marine
Erin
Miguel
Ankur
Andrew
Elizabeth
Thomas
Nikki
Vrutant
Natalia
Itzik
Pragya
Pratik
Sarah
Lilianna
Ruth
Jia
James
Riley
Michael
Parsons
Pasiliao
Pasten
Patel
Penalva-Lopez
Piacentino
Pieplow
Pourquie
Prince
Qian
Raftery
Ramirez
Raz
Reichman-Fried
Reyes
Roellig
Roman-Rivera
Roux
Rutherford
Salinas-Saavedra
Saxena
Schiffmacher
Schoell
Schultheiss
Seagraves
Shah
Shylo
sibony
Sidhwani
Singh
Smith
Solnica-Krezel
Solomon
Song
Spurlin
St. Clair
Stark
University of Nevada Las Vegas
University of Toronto
UNIVERSITY OF ANDES, CHILE
Stowers Institute for Medical Research
St. Peter's University
California Institute of Technology
California State University, Long Beach
Harvard University
The University of Chicago
THE UNIVERSITY OF HK
Univ. Nevada Las Vegas
Boston University School of Medicine
University of Münster
University of Münster
Universidad Andres Bello
Caltech
University of Puerto Rico-Bayamon
Institut de recherches cliniques de Montréal
EMBL
University of Florida
University of Illinois at Chicago
University of Maryland
Eastern Connecticut State University
Technion-Israel Institute of Technology
University of Central Oklahoma
University of Houston
Yale University
Technion
University of California-San Diego
Indian Institute of Technology Kanpur
University of Pittsburgh
Washington University in St. Louis
Amherst College
University of Delaware
Princeton University
University of Vermont
Brigham Young University
travis.parsons@unlv.edu
clarissa.pasiliao@mail.utoronto.ca
mpasten@uandes.cl
nip@stowers.org
spenalvalopez14@mail.saintpeters.edu
mpiacent@caltech.edu
pieplowalice@gmail.com
pourquie@genetics.med.harvard.edu
vprince@uchicago.edu
qianchen@hku.hk
laurel.raftery@unlv.edu
mramirez@bu.edu
erezraz@uni-muenster.de
mreichm@uni-muenster.de
ariel.reyes@unab.cl
daniroel@hotmail.com
victor.roman4@upr.edu
marine.roux@ircm.qc.ca
bearcee@bc.edu
mssaavedra@whitney.ufl.edu
saxenaa@uic.edu
aschiffm@umd.edu
schoelle@my.easternct.edu
tschulth@tx.technion.ac.il
nseagraves@uco.edu
yypulido@uh.edu
Natalia.Shylo@yale.edu
itziksibo@gmail.com
psidhwani@ucsd.edu
sprtk@iitk.ac.in
sjs152@pitt.edu
solnical@wustl.edu
rsolomon15@amherst.edu
jsong@udel.edu
jspurlin@princeton.edu
riley.st-clair@med.uvm.edu
mstark@byu.edu
Michelle
Angela
Colin
Haley
Kuo-Hui
Jessica
Abhinav
Jacqui
Yuta
Patrick
Lisa
You Chi
Hirotaka
Stefania
Shifaan
Gerald
Sophia
Fan
Rosa
Michael
Marina
Zer
Sha
Yiqun
Vijay
Songjia
Jason
Melanie
Tanya
Jason
Alison
Chyong-Yi
Shu-Yu (Simon)
Daixi
Tianchi
FENGZHU
Jiing-Wei
Starz-Gaiano
Stathopoulos
Stewart
Stinnett
Su
Sullivan-Brown
Sur
Tabler
Takase
Tam
Taneyhill
Tang
Tao
Tavano
Thowfeequ
Tiu
Touri
Tu
Uribe
Veeman
Venero Galanternik
Vue
Wang
Wang
Warrier
Wen
Wen
White
Whitfield
Williams
Wirshing
Wu
Wu
Xin
Xin
XIONG
Xiong
University of Maryland Baltimore County
Caltech
Institute of Medical Biology
The University of Chicago
The Jackson Laboratory
West Chester University of Pennsylvania
Clark University
University of Texas
Kyoto University
Children's Medical Research Institute
University of Maryland
McGill University
The Hospital for Sick Children
MPI-CBG
Columbia University
Stanford University
St. Peter's University
University of Texas at Austin
Caltech
Kansas State University
NICHD, NIH
MD Anderson Cancer Center
University of Michigan
Harvard University
University of Illinois, Chicago
The University of Hong Kong
University of Toronto
A*STAR
University of Sheffield
University of Colorado Denver
Northeastern University
University of Maryland
Vanderbilt University
Yale University
Yale University
Harvard Medical School
Peking University
starz@umbc.edu
angelike@caltech.edu
colin.stewart@imb.a-star.edu.sg
hkstinnett@uchicago.edu
bluewaysu@gmail.com
jsullivan@wcupa.edu
surabhinav@rocketmail.com
jacquitabler1@gmail.com
yu-takase@develop.zool.kyoto-u.ac.jp
ptam@cmri.org.au
ltaney@umd.edu
you.tang@mail.mcgill.ca
hirotaka.tao@sickkids.ca
tavano.stefania@gmail.com
at2656@cumc.columbia.edu
geraldctiu@stanford.edu
sophia.touri9@gmail.com
fantu@utexas.edu
ruribe2@caltech.edu
veeman@ksu.edu
marina.venerogalanternik@nih.gov
zervue@gmail.com
shawang86t@gmail.com
yiqunwang@g.harvard.edu
vijay.govind.warrier@gmail.com
james.wenton@hotmail.com
j.wen@utoronto.ca
whitemd@imcb.a-star.edu.sg
t.whitfield@sheffield.ac.uk
Jason.s.williams@ucdenver.edu
wirshing.a@husky.neu.edu
chyongwu@gmail.com
simon.wu@vanderbilt.edu
daixi.xin@gmail.com
tianchi.xin@yale.edu
xiongfzwmq@gmail.com
jingwei_xiong@pku.edu.cn
Cindy
Mamiko
Gen
Kunyan
Ronit
Shuo-Ting
Wenjing
Shiaulou
Magdalena
Yiqun
Kongju
Michael
Aaron
Daniel
Xu
Yajima
Yamada
Yang
Yelin
Yen
Yi
Yuan
Zernicka-Goetz
Zhang
Zhu
Zimber
Zorn
Zuch
Arizona State University
Brown University
Wakayama Med Univ
Harvard School of Dental Medicine
Thechnion
Baylor College of Medicine
Institut Biology of Leiden
Yale University School of Medicine
University of Cambridge
Harvard School of Dental Medicine
Leiden University
Histogen Inc.
Cincinnati Children's Hospital
Boston University
Graduate School of Biostudies, Kyoto University
cindyxu@asu.edu
Mamiko_Yajima@brown.edu
gensan7@wakayama-med.ac.jp
yingzi_yang@hsdm.harvard.edu
ryelin@tx.technion.ac.il
yenshuoting@gmail.com
76601733@qq.com
shiaulou.yuan@yale.edu
mz205@cam.ac.uk
Yiqun_Zhang@hsdm.harvard.edu
k.zhu.2@biology.leidenuniv.nl
mzimber@histogeninc.com
aaron.zorn@cchmc.org
dtzuch@gmail.com
mikeda@virus.kyoto-u.ac.jp