Kai Johnsson, Institute of Chemical Sciences and

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Cellular Motility Versus Tissue Motion in Early Amniote
Embryos — Which Cells Are Really Moving?
Charles Little, Brenda Rongish, András Czirók, Cheng Cui, Evan
Zamir and Rusty Lansford1
Department of Anatomy and Cell Biology, University of Kansas
Medical Center, Kansas City, KS; California Institute of
Technology, Beckman Institute, Pasadena, CA1
Provocative new ideas regarding morphological complexity have
emerged from comparative genomic studies. It is now clear that
the genomes of primitive animals, which do not form
organs, “…include many of the genes responsible for guiding
development
of
other
animals’ complex
shapes
and
organs” (Pennisi, 2008). Thus, developmentally simple animals
possess the same number of genes that vertebrates use to make
complex body parts. This unexpected realization prompts the
obvious
question — If
genomic
complexity
is
not
the
underpinning
of
vertebrate
organogenesis — What
is?
We
hypothesize that tissues and organs arise from emergent
biophysical and biomechanical processes that comprise a
biomechanical morphogenetic code. To study morphogenetic
forces we use computational time-lapse imaging to capture
cellular
displacements
and
tissue
motion
during
avian
gastrulation and the formation of the primary vascular
network. Engineering approaches and statistical physics allow
calculation of tissue displacements using the motion of ECM
fibrils as in situ markers for passive motion, while
simultaneously
tracking,
individual,
total
cellular
displacement(s). This approach allows computation of active
cellular autonomous motility (locomotion) versus passive
convective tissue motion. The data demonstrate that passive
tissue motion is responsible for much of what has heretofore
been termed “migration”. Our work has important implications
for understanding cellular guidance mechanisms and chemotactic
gradients purported to drive morphogenesis at early stages of
amniote embryogenesis.
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