Biomolecules,
Год журнала:
2025,
Номер
15(5), С. 672 - 672
Опубликована: Май 6, 2025
Neural
stem
cells
(NSC)
are
multipotent,
self-renewing
that
give
rise
to
all
neural
cell
types
within
the
central
nervous
system.
During
adulthood,
most
NSCs
exist
in
a
quiescent
state
which
can
be
reactivated
response
metabolic
and
signalling
changes,
allowing
for
long-term
continuous
neurogenesis
injury.
Ensuring
critical
balance
between
quiescence
reactivation
is
required
maintain
limited
NSC
reservoir
replenishment
throughout
lifetime.
The
precise
mechanisms
pathways
behind
this
at
focus
of
current
research.
In
review,
we
highlight
discuss
recent
studies
using
Drosophila,
mammalian
zebrafish
models
contributing
understanding
molecular
underlying
NSCs.
Proceedings of the National Academy of Sciences,
Год журнала:
2018,
Номер
115(38)
Опубликована: Сен. 5, 2018
Seizures
induced
by
visual
stimulation
(photosensitive
epilepsy;
PSE)
represent
a
common
type
of
epilepsy
in
humans,
but
the
molecular
mechanisms
and
genetic
drivers
underlying
PSE
remain
unknown,
no
good
animal
models
have
been
identified
as
yet.
Here,
we
show
an
model
PSE,
Drosophila,
owing
to
defective
cortex
glia.
The
glial
membranes
are
severely
compromised
ceramide
phosphoethanolamine
synthase
(cpes)-null
mutants
fail
encapsulate
neuronal
cell
bodies
Drosophila
cortex.
Expression
human
sphingomyelin
1,
which
synthesizes
closely
related
phosphocholine
(sphingomyelin),
rescues
abnormalities
underscoring
evolutionarily
conserved
role
these
lipids
membranes.
Further,
compromise
plasma
membrane
structure
that
underlies
collapse
cpes
leads
phenotype.
Stem
cells
reside
in
specialized
microenvironments,
called
niches,
that
regulate
their
development
and
the
of
progeny.
However,
maintenance
niches
are
poorly
understood.
In
Drosophila
brain,
cortex
glial
provide
a
niche
promotes
self-renewal
proliferation
neural
stem
cell-like
(neuroblasts).
central
neuroblasts
progeny
control
post-embryonic
morphogenesis
glia
through
PDGF-like
ligands,
this
PDGFR
receptor
tyrosine
kinase
(RTK)
signaling
is
required
for
expression
DE-cadherin,
which
sustains
neuroblasts.
Thus,
an
RTK-dependent
feed-forward
loop,
actively
maintain
each
other.
When
EGFR
RTK
constitutively
activated
glia,
they
overexpress
PDGF
orthologs
to
stimulate
autocrine
signaling,
uncouples
growth
survival
from
neuroblasts,
drives
neoplastic
transformation
elimination
These
results
fundamental
insights
into
regulation,
show
niche-neural
cell
becomes
hijacked
drive
tumorigenesis.
Neuronal
processing
is
energy
demanding
and
relies
on
sugar
metabolism.
To
nurture
the
Drosophila
nervous
system,
blood-brain
barrier
forming
glial
cells
take
up
trehalose
from
hemolymph
then
distribute
metabolic
products
further
to
all
neurons.
This
function
provided
by
glucose
lactate
transporters
of
solute
carrier
(SLC)
5A
family.
Here
we
identified
three
SLC5A
genes
that
are
specifically
expressed
in
overlapping
sets
CNS
cells,
rumpel,
bumpel
kumpel.
We
generated
mutants
viable
fertile,
lacking
discernible
phenotypes.
Loss
rumpel
causes
subtle
locomotor
phenotypes
flies
display
increased
daytime
sleep.
In
addition,
kumpel
double
mutants,
an
even
greater
extent
triple
oogenesis
disrupted
at
onset
vitollegenic
phase.
indicates
a
partially
redundant
between
these
genes.
Rescue
experiments
exploring
this
effect
indicate
can
be
affected
cells.
Moreover,
expression
heterologous
mammalian
transporters,
with
known
transport
properties,
suggest
Bumpel
and/or
Kumpel
or
lactate.
Overall,
our
results
imply
redundancy
nutrient
sensing
functions
affecting
ovarian
development
behavior.
Nature Communications,
Год журнала:
2022,
Номер
13(1)
Опубликована: Авг. 25, 2022
Abstract
Neural
stem
cells
(NSCs)
live
in
an
intricate
cellular
microenvironment
supporting
their
activity,
the
niche.
Whilst
shape
and
function
are
inseparable,
morphogenetic
aspects
of
niche
development
poorly
understood.
Here,
we
use
formation
a
glial
to
investigate
acquisition
architectural
complexity.
Cortex
glia
(CG)
Drosophila
regulate
neurogenesis
build
reticular
structure
around
NSCs.
We
first
show
that
individual
CG
grow
tremendously
ensheath
several
NSC
lineages,
employing
elaborate
proliferative
mechanisms
which
convert
these
into
syncytia
rich
cytoplasmic
bridges.
further
undergo
homotypic
cell–cell
fusion,
using
defined
cell
surface
receptors
actin
regulators.
Cellular
exchange
is
however
dynamic
space
time.
This
atypical
fusion
remodels
borders,
restructuring
syncytia.
Ultimately,
combined
growth
builds
multi-level
architecture
niche,
creates
modular,
spatial
partition
population.
Our
findings
provide
insights
how
forms
organises
while
developing
intimate
contacts
with
ABSTRACT
Nutrient
intake
is
obligatory
for
animal
growth
and
development,
but
nutrients
alone
are
not
sufficient.
Indeed,
insulin
homologous
hormones
required
normal
even
in
the
presence
of
nutrients.
These
communicate
nutrient
status
between
organs,
allowing
animals
to
coordinate
metabolism
with
supply.
Insulin
related
hormones,
such
as
insulin-like
factors
peptides,
play
important
roles
development
metabolism,
defects
production
signaling
leading
hyperglycemia
diabetes.
Here,
we
describe
hormone
family
signal
transduction
pathways
activated
by
these
hormones.
We
highlight
coordinating
maternal
fetal
during
pregnancy,
how
secretion
regulated
at
different
life
stages.
Additionally,
discuss
cell
growth,
stem
proliferation
differentiation.
provide
examples
role
across
multiple
model
organisms:
Caenorhabditis
elegans,
Drosophila,
zebrafish,
mouse
human.
Stem Cell Reports,
Год журнала:
2018,
Номер
11(4), С. 883 - 896
Опубликована: Сен. 20, 2018
Neural
stem
cells
(NSCs)
have
the
ability
to
exit
quiescence
and
reactivate
in
response
physiological
stimuli.
In
Drosophila
brain,
insulin
receptor
(InR)/phosphatidylinositol
3-kinase
(PI3K)/Akt
pathway
triggers
NSC
reactivation.
However,
intrinsic
mechanisms
that
control
InR/PI3K/Akt
during
reactivation
remain
unknown.
Here,
we
identified
heat
shock
protein
83
(Hsp83/Hsp90),
a
molecular
chaperone,
as
an
regulator
of
Hsp83
is
both
necessary
sufficient
for
by
promoting
activation
InR
larval
brains
presence
dietary
amino
acids.
Both
its
co-chaperone
Cdc37
physically
associate
with
InR.
Finally,
defects
observed
depleted
hsp83
were
rescued
over-activation
pathway,
suggesting
functions
upstream
Given
conservation
our
finding
may
provide
insights
into
underlying
mammalian
Molecular Biology of the Cell,
Год журнала:
2019,
Номер
30(14), С. 1757 - 1769
Опубликована: Май 8, 2019
Stem
cell
maintenance
by
niche
signaling
is
a
common
theme
across
phylogeny.
In
the
Caenorhabditis
elegans
gonad,
broad
outlines
of
germline
stem
(GSC)
regulation
are
same
for
both
sexes:
GLP-1/Notch
from
mesenchymal
distal
tip
maintains
GSCs
in
gonad
sexes
and
does
so
via
two
key
regulators,
SYGL-1
LST-1.
Yet
most
recent
analyses
GSC
have
focused
on
XX
hermaphrodites,
an
essentially
female
sex
making
sperm
larvae
oocytes
adults.
Here
we
focus
XO
males.
Sexual
dimorphism
architecture,
reported
previously,
suggested
that
molecular
responses
to
or
numbers
might
also
be
sexually
distinct.
Remarkably,
this
not
case.
This
work
extends
our
understanding
dimorphic
but
demonstrates
niches
drive
similar
response
maintain
number
their
pools.
PLoS Biology,
Год журнала:
2019,
Номер
17(6), С. e3000276 - e3000276
Опубликована: Июнь 6, 2019
The
ability
of
neural
stem
cells
(NSCs)
to
transit
between
quiescence
and
proliferation
is
crucial
for
brain
development
homeostasis.
Drosophila
Hippo
pathway
maintains
NSC
quiescence,
but
its
regulation
during
remains
unknown.
Here,
we
show
that
CRL4Mahj,
an
evolutionarily
conserved
E3
ubiquitin
ligase,
essential
reactivation
(exit
from
quiescence).
We
demonstrate
damaged
DNA-binding
protein
1
(DDB1)
Cullin4,
two
core
components
Cullin4-RING
ligase
(CRL4),
are
intrinsically
required
reactivation.
have
identified
a
substrate
receptor
CRL4,
Mahjong
(Mahj),
which
necessary
sufficient
Moreover,
CRL4Mahj
forms
complex
with
Warts
(Wts/large
tumor
suppressor
[Lats]),
kinase
the
signaling
pathway,
Mahj
promotes
ubiquitination
Wts.
Our
genetic
analyses
further
support
conclusion
triggers
by
inhibition
Given
Cullin4B
mutations
cause
mental
retardation
cerebral
malformation,
similar
regulatory
mechanisms
may
be
applied
human
brain.