Maternal PRDM10 activates essential genes for oocyte-to-embryo transition
Nature Communications,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Feb. 24, 2025
PR/SET
domain-containing
(PRDM)
proteins
are
metazoan-specific
transcriptional
regulators
that
play
diverse
roles
in
mammalian
development
and
disease.
Several
members
such
as
PRDM1,
PRDM14
PRDM9,
have
been
implicated
germ
cell
specification
homoeostasis
essential
to
fertility-related
processes.
Others,
PRDM14,
PRDM15
PRDM10
a
role
early
embryogenesis
embryonic
stem
maintenance.
Here,
we
describe
the
first
PRDM
family
member
with
maternal
effect.
Absence
of
Prdm10
results
catastrophic
failure
oocyte-to-embryo
transition
complete
arrest
at
2-cell
stage.
We
multiple
defects
oocytes,
zygotes
stage
embryos
relating
accumulate
target
gene
transcripts
egg.
Transcriptomic
analysis
integration
genome-wide
chromatin-binding
data
reveals
new
targets,
including
cytoskeletal
protein
encoding
Septin11.
demonstrate
express
Septin11,
absence
PRDM10,
disrupts
Septin-complex
assembly
polar
body
extrusion
site
MII
oocytes.
Our
study
sheds
light
into
essentiality
requirement
likely
evolutionary
conservation
this
regulatory
axis
human
female
cells.
The
marks
beginning
but
mechanisms
underlying
process
incompletely
described.
Here
they
show
activates
Septin11
is
required
for
progression
through
transition.
Language: Английский
Quantitative proteomic landscape of the pathophysiology of adhesive arachnoiditis and its clinical significance: Structure and mechanism of TNC and RANBP1 proteins
International Journal of Biological Macromolecules,
Journal Year:
2024,
Volume and Issue:
unknown, P. 138444 - 138444
Published: Dec. 1, 2024
Language: Английский
Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease
The Journal of Physiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 20, 2024
Abstract
Alzheimer's
disease
(AD),
the
most
common
form
of
dementia
among
elderly,
affects
numerous
individuals
worldwide.
Despite
advances
in
understanding
molecular
underpinnings
AD
pathology,
effective
treatments
to
prevent
or
cure
remain
elusive.
is
characterized
not
only
by
pathological
hallmarks
such
as
amyloid
plaques
and
neurofibrillary
tangles
but
also
impairments
synaptic
physiology,
circuit
activity
cognitive
function.
Synaptic
homeostatic
plasticity
plays
a
vital
role
maintaining
stability
neural
functions
amid
genetic
environmental
disturbances.
A
key
component
this
regulation
presynaptic
potentiation,
where
increased
neurotransmitter
release
compensates
for
reduced
postsynaptic
glutamate
receptor
functionality,
thereby
stabilizing
neuronal
excitability.
The
synapse
stabilization
AD,
however,
remains
unclear.
Moreover,
recent
transcriptomics
have
illuminated
complex
roles
glial
cells
regulating
function
ageing
brains
progression
neurodegenerative
diseases.
Yet,
impact
AD‐related
abnormalities
signalling
on
has
been
fully
delineated.
This
review
discusses
findings
how
dysregulation
plasticity.
There
increasing
evidence
that
disrupted
signalling,
particularly
through
aberrant
histone
acetylation
transcriptomic
changes
glia,
compromises
AD.
Notably,
sphingosine
pathway
identified
being
protective
physiology
epigenetic
mechanisms,
presenting
potential
therapeutic
targets
treating
disorders.
image
Language: Английский