Neuronal autophagy in the control of synapse function
Neuron,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 1, 2025
Neurons
are
long-lived
postmitotic
cells
that
capitalize
on
autophagy
to
remove
toxic
or
defective
proteins
and
organelles
maintain
neurotransmission
the
integrity
of
their
functional
proteome.
Mutations
in
genes
cause
congenital
diseases,
sharing
prominent
brain
dysfunctions
including
epilepsy,
intellectual
disability,
neurodegeneration.
Ablation
core
neurons
glia
disrupts
normal
behavior,
leading
motor
deficits,
memory
impairment,
altered
sociability,
which
associated
with
defects
synapse
maturation,
plasticity,
neurotransmitter
release.
In
spite
importance
for
physiology,
substrates
neuronal
mechanisms
by
affect
synaptic
function
health
disease
remain
controversial.
Here,
we
summarize
current
state
knowledge
autophagy,
address
existing
controversies
inconsistencies
field,
provide
a
roadmap
future
research
role
control
function.
Language: Английский
TGFB signaling induces mitophagy via PLSCR3-mediated cardiolipin externalization in conjunction with a BNIP3L/NIX-, BNIP3-, and FUNDC1-dependent mechanism
Jiong Yan,
No information about this author
Xin Chen,
No information about this author
Swati Choksi
No information about this author
et al.
Autophagy,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 22, 2025
Selective
clearance
of
damaged
mitochondria
through
mitophagy
is
crucial
for
the
maintenance
mitochondrial
homeostasis.
While
can
be
activated
by
various
toxins,
physiologically
relevant
signal
that
triggers
less
studied.
TGFB/TGFβ
signaling
has
been
linked
to
autophagic
induction,
but
its
specific
role
in
not
well
understood.
Here,
we
discovered
a
novel
induction
paradigm
stimulated
TGFB1.
The
mitophagic
response
exclusively
mediated
SMAD2,
SMAD3,
and
SMAD4
underlying
TGFB
receptor
signaling.
transcriptional
regulation
activates
genes
involved
canonical
pathway
which
required
TGFB1-induced
mitophagy.
Moreover,
TGFB1
promotes
flux
upregulating
PLSCR3
externalizes
cardiolipin
conjunction
with
MAP1LC3/LC3/GABARAPs-interacting
proteins
(BNIP3L/NIX,
BNIP3,
FUNDC1)-dependent
mechanism.
Overall,
our
study
characterized
essential
components
engaged
demonstrated
an
important
induces
Language: Английский
Molecular and epigenetic responses to crowding stress in rainbow trout (Oncorhynchus mykiss) skeletal muscle
Frontiers in Endocrinology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 16, 2025
Chronic
stress
is
a
critical
challenge
in
fish
aquaculture,
adversely
affecting
growth,
health,
and
overall
productivity.
Among
the
most
significant
chronic
stressors
intensive
farming
crowding,
which
triggers
release
of
cortisol,
primary
hormone
fish.
Cortisol
re-allocates
energy
away
from
growth-related
processes
toward
response
mechanisms.
Consequently,
overcrowded
often
exhibit
slower
growth
rates,
impaired
skeletal
muscle
development.
Understanding
mechanisms
underlying
crowding
their
long-term
effects,
including
epigenetic
changes,
essential
for
optimizing
conditions,
enhancing
welfare.
This
study
aims
to
characterize
physiological,
transcriptomic,
epigenomic
responses
juvenile
rainbow
trout
(Oncorhynchus
mykiss)
exposed
30
days
high
stocking
densities.
Crowding
led
decreased
weight
high-density
(HD)
group.
It
also
resulted
elevated
cortisol
levels,
oxidative
DNA
damage,
protein
carbonylation
muscle.
Using
RNA-seq,
we
identified
4,050
differentially
expressed
genes
(DEGs),
through
whole-genome
bisulfite
sequencing
(WGBS),
detected
11,672
methylated
(DMGs).
Integrative
analyses
revealed
263
with
negative
correlation
between
upregulated
expression
downregulated
methylation,
primarily
associated
autophagy,
mitophagy,
insulin
signaling
pathway.
Conversely,
299
exhibited
reverse
trend,
mainly
linked
ATP-dependent
chromatin
remodeling.
offers
first
detailed
exploration
molecular
stress,
integrating
RNA-seq
WGBS
analysis
trout,
offering
valuable
information
improving
aquaculture
practices.
Language: Английский
VPS13 and bridge-like lipid transporters, mechanisms, and mysteries
Frontiers in Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: April 28, 2025
Bridge-like
lipid
transporters
(BLTPs)
have
recently
been
revealed
as
key
regulators
of
intraorganellar
trafficking,
with
their
loss
being
associated
defective
synaptic
signalling
and
congenital
neurological
diseases.
This
group
consists
five
protein
subfamilies
[BLTP1-3,
autophagy-related
2
(ATG2),
vacuolar
sorting
13
(VPS13)],
which
mediate
minimally
selective
transfer
between
cellular
membranes.
Deceptively
simple
in
both
structure
presumed
function,
this
review
addresses
open
questions
to
how
bridge-like
work,
the
functional
consequences
bulk
on
signalling,
summarises
some
recent
studies
that
shed
light
surprising
level
regulation
specificity
found
family
transporters.
Language: Английский