Journal of Developmental Biology,
Год журнала:
2023,
Номер
11(2), С. 26 - 26
Опубликована: Июнь 6, 2023
Whole
genome
duplication
(WGD)
or
polyploidization
can
occur
at
the
cellular,
tissue,
and
organismal
levels.
At
cellular
level,
tetraploidization
has
been
proposed
as
a
driver
of
aneuploidy
instability
correlates
strongly
with
cancer
progression,
metastasis,
development
drug
resistance.
WGD
is
also
key
developmental
strategy
for
regulating
cell
size,
metabolism,
function.
In
specific
tissues,
involved
in
normal
(e.g.,
organogenesis),
tissue
homeostasis,
wound
healing,
regeneration.
propels
evolutionary
processes
such
adaptation,
speciation,
crop
domestication.
An
essential
to
further
our
understanding
mechanisms
promoting
its
effects
compare
isogenic
strains
that
differ
only
their
ploidy.
Caenorhabditis
elegans
(C.
elegans)
emerging
an
animal
model
these
comparisons,
part
because
relatively
stable
fertile
tetraploid
be
produced
rapidly
from
nearly
any
diploid
strain.
Here,
we
review
use
polyploids
tools
understand
important
sex
determination,
dosage
compensation,
allometric
relationships)
cycle
regulation
chromosome
dynamics
during
meiosis).
We
discuss
how
unique
characteristics
C.
will
enable
significant
advances
role
disease.
PLoS Biology,
Год журнала:
2024,
Номер
22(1), С. e3002453 - e3002453
Опубликована: Янв. 5, 2024
To
achieve
a
stable
size
distribution
over
multiple
generations,
proliferating
cells
require
means
of
counteracting
stochastic
noise
in
the
rate
growth,
time
spent
various
phases
cell
cycle,
and
imprecision
placement
plane
division.
In
most
widely
accepted
model,
is
thought
to
be
regulated
at
G1/S
transition,
such
that
smaller
than
critical
pause
end
G1
phase
until
they
have
accumulated
mass
predetermined
threshold,
which
point
proceed
through
rest
cycle.
However,
based
solely
on
specific
checkpoint
G1/S,
cannot
readily
explain
why
with
deficient
control
mechanisms
are
still
able
maintain
very
distribution.
Furthermore,
model
would
not
easily
account
for
variation
during
subsequent
anticipated
G1/S.
address
questions,
we
applied
computationally
enhanced
quantitative
microscopy
(ceQPM)
populations
cultured
human
lines,
enables
highly
accurate
measurement
dry
individual
throughout
From
these
measurements,
evaluated
factors
contribute
maintaining
homeostasis
any
Our
findings
reveal
accurately
maintained,
despite
disruptions
normal
machinery
or
perturbations
growth.
Control
generally
confined
regulation
length.
Instead
imposed
lines
examined,
find
coefficient
(CV)
population
begins
decline
well
before
transition
continues
S
G2
phases.
Among
different
types
tested,
detailed
response
growth
differs.
general,
when
it
falls
below
exponential
natural
increase
CV
effectively
constrained.
We
both
mass-dependent
cycle
modulation
reducing
within
population.
Through
interplay
coordination
2
processes,
emerges.
Such
previously
unappreciated
general
principles
cells.
These
same
regulatory
processes
might
also
operative
terminally
differentiated
Further
dynamical
studies
should
lead
better
understanding
underlying
molecular
control.
Current Biology,
Год журнала:
2023,
Номер
33(9), С. 1744 - 1752.e7
Опубликована: Апрель 19, 2023
Although
polyploidization
is
frequent
in
development,
cancer,
and
evolution,
impacts
on
animal
metabolism
are
poorly
understood.
In
Xenopus
frogs,
the
number
of
genome
copies
(ploidy)
varies
across
species
can
be
manipulated
within
a
species.
Here,
we
show
that
triploid
tadpoles
contain
fewer,
larger
cells
than
diploids
consume
oxygen
at
lower
rate.
Drug
treatments
revealed
major
processes
accounting
for
tadpole
energy
expenditure
include
cell
proliferation,
biosynthesis,
maintenance
plasma
membrane
potential.
While
inhibiting
proliferation
did
not
abolish
consumption
difference
between
triploids,
altered
cellular
biosynthesis
or
electrical
potential
did.
Combining
these
results
with
simple
mathematical
framework,
propose
decrease
total
surface
area
lowered
production
activity
components
including
Na
Physiological Reviews,
Год журнала:
2024,
Номер
104(4), С. 1679 - 1717
Опубликована: Июнь 20, 2024
Depending
on
cell
type,
environmental
inputs,
and
disease,
the
cells
in
human
body
can
have
widely
different
sizes.
In
recent
years,
it
has
become
clear
that
size
is
a
major
regulator
of
function.
However,
we
are
only
beginning
to
understand
how
optimization
function
determines
given
cell’s
optimal
size.
Here,
review
currently
known
control
strategies
eukaryotic
intricate
link
intracellular
biomolecular
scaling,
organelle
homeostasis,
cycle
progression.
We
detail
size-dependent
regulation
early
development
impact
differentiation.
Given
importance
for
normal
cellular
physiology,
must
account
changing
conditions.
describe
sense
stimuli,
such
as
nutrient
availability,
accordingly
adapt
their
by
regulating
growth
Moreover,
discuss
correlation
pathological
states
with
misregulation
long
time
this
was
considered
downstream
consequence
dysfunction.
newer
studies
reveal
reversed
causality,
misregulated
leading
pathophysiological
phenotypes
senescence
aging.
summary,
highlight
important
roles
dysfunction,
which
could
implications
both
diagnostics
treatment
clinic.
PLoS Genetics,
Год журнала:
2024,
Номер
20(9), С. e1011387 - e1011387
Опубликована: Сен. 3, 2024
A
programmed
developmental
switch
to
G
/
S
endocycles
results
in
tissue
growth
through
an
increase
cell
size.
Unscheduled,
induced
endocycling
cells
(iECs)
promote
wound
healing
but
also
contribute
cancer.
Much
remains
unknown,
however,
about
how
these
iECs
affect
growth.
Using
the
D
.
melanogaster
wing
disc
as
model,
we
find
that
populations
of
initially
size
then
subsequently
undergo
a
heterogenous
arrest
causes
severe
undergrowth.
acquired
DNA
damage
and
activated
Jun
N-terminal
kinase
(JNK)
pathway,
but,
unlike
other
stressed
cells,
were
apoptosis-resistant
not
eliminated
from
epithelium.
Instead,
entered
JNK-dependent
reversible
senescent-like
arrest.
Senescent
promoted
division
diploid
neighbors,
this
compensatory
proliferation
did
rescue
Our
study
has
uncovered
unique
attributes
their
effects
on
have
important
implications
for
understanding
roles
Mitochondria,
classically
known
as
the
powerhouse
of
cells,
are
unique
double
membrane-bound
multifaceted
organelles
carrying
a
genome.
Mitochondrial
content
varies
between
cell
types
and
precisely
doubles
within
cells
during
each
proliferating
cycle.
also
increases
to
variable
degree
differentiation
triggered
after
exit
from
The
mitochondrial
is
primarily
maintained
by
regulation
biogenesis,
while
damaged
mitochondria
eliminated
mitophagy.
In
any
with
given
content,
steady-state
number
shape
determined
balance
fission
fusion
processes.
increase
in
alteration
causatively
linked
process
differentiation.
Here,
we
critically
review
quantitative
aspects
detection
methods
shape.
Thereafter,
quantitatively
link
these
properties
differentiating
highlight
implications
such
on
stem
functionality.
Finally,
discuss
an
example
size
predicted
analysis
content.
To
significance
analyses
properties,
propose
three
independent
rationale
based
hypotheses
relevant
experimental
designs
test
them.
Abstract
Endocycling
cells
grow
and
repeatedly
duplicate
their
genome
without
dividing.
Cells
switch
from
mitotic
cycles
to
endocycles
in
response
developmental
signals
during
the
growth
of
specific
tissues
a
wide
range
organisms.
The
purpose
switching
endocycles,
however,
remains
unclear
many
tissues.
Additionally,
can
conditional
signals,
which
have
beneficial
or
pathological
effects
on
However,
impact
these
unscheduled
development
is
underexplored.
Here,
we
use
Drosophila
ovarian
somatic
follicle
as
model
examine
tissue
function.
Follicle
normally
at
mid-oogenesis.
Inducing
prematurely
resulted
lethality
resulting
embryos.
Analysis
ovaries
with
premature
cell
revealed
aberrant
follicular
epithelial
structure
pleiotropic
defects
oocyte
growth,
gene
amplification,
migration
special
set
known
border
cells.
Overall,
findings
reveal
how
disrupt
function
cause
development.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Март 14, 2024
Summary
A
programmed
developmental
switch
to
G
/
S
endocycles
results
in
tissue
growth
through
an
increase
cell
size.
Unscheduled,
induced
endocycling
cells
(iECs)
promote
wound
healing
but
also
contribute
cancer.
Much
remains
unknown,
however,
about
how
these
iECs
affect
growth.
Using
the
D.
melanogaster
wing
disc
as
model,
we
find
that
populations
of
initially
size
then
subsequently
undergo
a
heterogenous
arrest
causes
severe
undergrowth.
acquired
DNA
damage
and
activated
Jun
N-terminal
kinase
(JNK)
pathway,
but,
unlike
other
stressed
cells,
were
apoptosis-resistant
not
eliminated
from
epithelium.
Instead,
entered
JNK-dependent
reversible
senescent-like
arrest.
Senescent
promoted
division
diploid
neighbors,
this
compensatory
proliferation
did
rescue
Our
study
has
uncovered
unique
attributes
their
effects
on
have
important
implications
for
understanding
roles
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 9, 2025
ABSTRACT
Understanding
how
final
organ
size
is
established
during
development
raises
two
key
questions:
organs
increase
their
mass
and
they
stop
growing
upon
reaching
an
appropriate
size.
While
growth
driven
by
conserved
signaling
pathways,
the
mechanisms
underlying
arrest
remain
elusive.
Studies
on
Drosophila
imaginal
wing
discs
have
provided
a
model
whereby
coincides
with
of
cell
proliferation
at
end
larval
phase.
Here,
through
3D
reconstruction
volume
measurements,
we
show
that
grow
continuously
throughout
larva-to-pupa
(L/P)
transition
proceed
to
later
pupal
period.
This
supplemental
phase
involves
switch
L/P
uncouples
from
tissue
growth,
important
contribution
Insulin/IGF
signaling.
These
findings
challenge
existing
open
new
avenues
for
our
understanding
determination.
Abstract
Tetraploidisation
plays
a
crucial
role
in
evolution,
development,
stress
adaptation,
and
disease,
but
its
beneficial
or
pathological
effects
different
tissues
remain
unclear.
This
study
aims
to
compare
physiological
unphysiological
tetraploidy
eight
steps:
1)
mechanisms
of
diploidy-to-tetraploidy
transition,
2)
induction
elimination
tetraploidy,
3)
tetraploid
cell
characteristics,
4)
stress-induced
5)
comparison
vs.
6)
consequences
7)
nutritional
pharmacological
prevention
strategies
tetraploidisation,
8)
knowledge
gaps
future
perspectives.
Unphysiological
is
an
adaptive
response
at
given
threshold,
often
involving
mitotic
slippage.
If
cells
evade
through
apoptosis
immune
surveillance,
they
may
re-enter
the
cycle,
causing
genetic
instability,
micronuclei
formation,
aneuploidy,
modification
epigenome
development
diseases.
The
potential
contributions
neurodegenerative,
cardiovascular
diabetes
related
diseases
are
summarized
schematic
figures
contrasted
with
cancer
development.
responsible
for
transition
from
tolerance
tetraploidisation
not
fully
understood.
Understanding
these
critical
importance
allow
targeted
therapies.