Axon
regeneration
is
abortive
in
the
central
nervous
system
following
injury.
Orchestrating
microtubule
dynamics
has
emerged
as
a
promising
approach
to
improve
axonal
regeneration.
The
severing
enzyme
spastin
essential
for
development
and
through
remodeling
of
arrangement.
To
date,
however,
little
known
regarding
mechanisms
underlying
action
neural
after
spinal
cord
Here,
we
use
glutathione
transferase
pulldown
immunoprecipitation
assays
demonstrate
that
14-3-3
interacts
with
spastin,
both
vivo
vitro,
via
Ser233
phosphorylation.
Moreover,
show
protects
from
degradation
by
inhibiting
ubiquitination
pathway
upregulates
spastin-dependent
ability.
Furthermore,
improving
interaction
between
Fusicoccin
(FC-A)
promotes
neurite
outgrowth
vitro
.
Western
blot
immunofluorescence
results
revealed
protein
upregulated
neuronal
compartment
injury
In
addition,
administration
FC-A
not
only
locomotor
recovery,
but
also
nerve
contusion
lateral
hemisection
models.
However,
application
inhibitor
spastazoline
successfully
reverses
these
phenomena.
Taken
together,
indicate
molecular
switch
regulates
levels,
14-3-3/spastin
an
important
target
regulation
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: Jan. 11, 2023
Abstract
Choroid
plexus
(ChP)
epithelium
is
composed
of
specialized
multiciliated
cells.
By
using
multiple
microscopic
techniques,
biochemical
approaches
in
various
mutant
mice
and
longitudinal
analysis
from
mouse
embryogenesis
to
aging,
we
show
that
ChP
cilia
are
built
on
a
gradient
events
which
spatio-temporally
regulated.
We
uncover
develop
prenatally
since
early
tissue
morphogenesis,
proceeds
as
multi-step
process
characterized
by
basal
body
multiplication
axoneme
formation
directly
at
the
apical
cellular
compartment.
Our
data
also
choroid
contain
both
primary
motile
features.
Remarkably,
demonstrate
undergo
resorption,
starting
youth,
through
tubulin
destabilization
process,
primarily
controlled
polyglutamylation
levels
could
be
mitigated
removal
microtubule-severing
enzyme
spastin.
Notably,
this
phenotype
preserved
human
samples.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: July 27, 2023
Abstract
Axon
regeneration
is
abortive
in
the
central
nervous
system
following
injury.
Orchestrating
microtubule
dynamics
has
emerged
as
a
promising
approach
to
improve
axonal
regeneration.
The
severing
enzyme
spastin
essential
for
development
and
through
remodeling
of
arrangement.
To
date,
however,
little
known
regarding
mechanisms
underlying
action
neural
after
spinal
cord
Here,
we
use
glutathione
transferase
pulldown
immunoprecipitation
assays
demonstrate
that
14-3-3
interacts
with
spastin,
both
vivo
vitro,
via
Ser233
phosphorylation.
Moreover,
show
protects
from
degradation
by
inhibiting
ubiquitination
pathway
upregulates
spastin-dependent
ability.
Furthermore,
agonist
Fusicoccin
(FC-A)
promotes
neurite
outgrowth
vitro
which
needs
activation.
Western
blot
immunofluorescence
results
revealed
protein
upregulated
neuronal
compartment
injury
.
In
addition,
administration
FC-A
not
only
locomotor
recovery,
but
also
nerve
contusion
lateral
hemisection
models;
application
inhibitor
spastazoline
successfully
reverses
these
phenomena.
Taken
together,
indicate
molecular
switch
regulates
levels,
small
molecule
effectively
mediates
recovery
mice
requires
participation.
Highlights
formation
complex
phosphorylation
at
S233
site.
involved
phosphorylation-ubiquitination
crosstalk
thus
impacting
stability.
agonists
Fusicoccin-A
can
facilitate
repair
mice.
Activation
function
prerequisite
Graphical
Axon
regeneration
is
abortive
in
the
central
nervous
system
following
injury.
Orchestrating
microtubule
dynamics
has
emerged
as
a
promising
approach
to
improve
axonal
regeneration.
The
severing
enzyme
spastin
essential
for
development
and
through
remodeling
of
arrangement.
To
date,
however,
little
known
regarding
mechanisms
underlying
action
neural
after
spinal
cord
Here,
we
use
glutathione
transferase
pulldown
immunoprecipitation
assays
demonstrate
that
14-3-3
interacts
with
spastin,
both
vivo
vitro,
via
Ser233
phosphorylation.
Moreover,
show
protects
from
degradation
by
inhibiting
ubiquitination
pathway
upregulates
spastin-dependent
ability.
Furthermore,
improving
interaction
between
Fusicoccin
(FC-A)
promotes
neurite
outgrowth
vitro
.
Western
blot
immunofluorescence
results
revealed
protein
upregulated
neuronal
compartment
injury
In
addition,
administration
FC-A
not
only
locomotor
recovery,
but
also
nerve
contusion
lateral
hemisection
models.
However,
application
inhibitor
spastazoline
successfully
reverses
these
phenomena.
Taken
together,
indicate
molecular
switch
regulates
levels,
14-3-3/spastin
an
important
target
regulation
Axon
regeneration
is
abortive
in
the
central
nervous
system
following
injury.
Orchestrating
microtubule
dynamics
has
emerged
as
a
promising
approach
to
improve
axonal
regeneration.
The
severing
enzyme
spastin
essential
for
development
and
through
remodeling
of
arrangement.
To
date,
however,
little
known
regarding
mechanisms
underlying
action
neural
after
spinal
cord
Here,
we
use
glutathione
transferase
pulldown
immunoprecipitation
assays
demonstrate
that
14-3-3
interacts
with
spastin,
both
vivo
vitro,
via
Ser233
phosphorylation.
Moreover,
show
protects
from
degradation
by
inhibiting
ubiquitination
pathway
upregulates
spastin-dependent
ability.
Furthermore,
improving
interaction
between
Fusicoccin
(FC-A)
promotes
neurite
outgrowth
vitro
.
Western
blot
immunofluorescence
results
revealed
protein
upregulated
neuronal
compartment
injury
In
addition,
administration
FC-A
not
only
locomotor
recovery,
but
also
nerve
contusion
lateral
hemisection
models.
However,
application
inhibitor
spastazoline
successfully
reverses
these
phenomena.
Taken
together,
indicate
molecular
switch
regulates
levels,
14-3-3/spastin
an
important
target
regulation
