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Molecular mechanism of protrusion formation during cell-to-cell spread of Listeria.
[wiskott-aldrich syndrome]
The
bacterial
pathogen
Listeria
monocytogenes
spreads
within
human
tissues
using
a
motility
process
dependent
on
the
host
actin
cytoskeleton
.
Cell-
to
-cell
spread
involves
the
ability
of
motile
bacteria
to
remodel
the
host
plasma
membrane
into
protrusions
,
which
are
internalized
by
neighboring
cells
.
Recent
results
indicate
that
formation
of
Listeria
protrusions
in
polarized
human
cells
involves
bacterial
antagonism
of
a
host
signaling
pathway
comprised
of
the
scaffolding
protein
Tuba
and
its
effectors
N-WASP
and
Cdc
42
.
These
three
human
proteins
form
a
complex
that
generates
tension
at
apical
cell
junctions
.
Listeria
relieves
this
tension
and
facilitates
protrusion
formation
by
secreting
a
protein
called
InlC
.
InlC
interacts
with
a
Src
Homology
3
(
SH
3
)
domain
in
Tuba
,
thereby
displacing
N-WASP
from
this
domain
.
Interaction
of
InlC
with
Tuba
is
needed
for
efficient
Listeria
spread
in
cultured
human
cells
and
infected
animals
.
Recent
structural
data
has
elucidated
the
mechanistic
details
of
InlC
/
Tuba
interaction
,
revealing
that
InlC
and
N-WASP
compete
for
partly
overlapping
binding
surfaces
in
the
Tuba
SH
3
domain
.
InlC
binds
this
domain
with
higher
affinity
than
N-WASP
,
explaining
how
InlC
is
able
to
disrupt
Tuba
/
N-WASP
complexes
.