bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: May 26, 2023
SUMMARY
How
the
body
interacts
with
brain
to
perform
vital
life
functions
such
as
feeding
is
one
of
fundamental
questions
in
physiology
and
neuroscience.
Here,
we
use
a
whole-animal
scanning
transmission
electron
microscopy
dataset
Drosophila
map
out
neuronal
circuits
that
connect
entire
enteric
nervous
system
via
insect
vagus
nerve
at
synaptic
resolution.
This
revealed
periphery-brain
feedback
loop
which
Piezo-expressing
mechanosensory
neurons
sense
food
intake
convey
information
onto
serotonergic
within
brain.
These
integrate
interoceptive
external
central
inputs,
turn
stabilize
rhythmic
activity
serotonin
receptor
7
expressing
peripheral
motor
drive
swallowing.
Strikingly,
very
same
also
share
an
efference
copy
their
aforementioned
neurons,
thereby
closing
motor-sensory-modulatory
loop.
Our
analysis
elucidates
elemental,
albeit
surprisingly
complex
reinforcement
circuit
patterns
are
stabilized
through
afferent
signaling
upon
completion
rewarding
action.
The
motif
constructed
allow
distinction
between
self-generated
action
those
response
environment.
ABSTRACT
Whole-body
health
relies
on
complex
inter-organ
signalling
networks
that
enable
organisms
to
adapt
environmental
perturbations
and
changes
in
tissue
homeostasis.
The
intestine
plays
a
major
role
as
centre
by
producing
local
systemic
signals
are
relayed
the
body
maintain
intestinal
organismal
Consequently,
disruption
of
homeostasis
associated
with
diseases
multi-organ
dysfunction.
In
recent
years,
fruit
fly
Drosophila
melanogaster
has
emerged
prime
model
organism
study
tissue-intrinsic
adult
due
its
genetic
tractability
functional
conservation
mammals.
this
Review,
we
highlight
research
contributed
our
understanding
how
interacts
microenvironment
distant
organs.
We
discuss
implications
these
findings
for
whole-body
pathophysiology,
future
studies
might
advance
knowledge
interplay
between
rest
disease.
Abstract
Conditional
gene
regulation
in
Drosophila
through
binary
expression
systems
like
the
LexA-LexAop
system
provides
a
superb
tool
for
investigating
and
tissue
function.
To
increase
availability
of
defined
LexA
enhancer
trap
insertions,
we
present
molecular,
genetic,
studies
301
novel
Stan-X
traps
derived
from
mobilization
index
SX4
line.
This
includes
insertions
into
distinct
loci
on
X,
II,
III
chromosomes
that
were
not
previously
associated
with
or
targeted
constructs,
an
insertion
ptc,
seventeen
natural
transposons.
A
subset
was
expressed
CNS
neurons
known
to
produce
secrete
insulin,
essential
regulator
growth,
development,
metabolism.
Fly
lines
described
here
generated
characterized
by
students
teachers
international
network
genetics
classes
at
public,
independent
high
schools,
universities
serving
diversity
students,
including
those
underrepresented
science.
Thus,
unique
partnership
between
secondary
schools
university-based
programs
has
produced
resources
Drosophila,
establishing
instructional
paradigms
devoted
unscripted
experimental
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
166, P. 115298 - 115298
Published: Aug. 17, 2023
The
natural
compound
plumbagin
has
a
wide
range
of
pharmacological
and
potential
therapeutic
activities,
although
its
role
in
neuroretina
degeneration
is
unknown.
Here
we
evaluated
the
effects
on
retina
homeostasis
fruit
fly
Drosophila
melanogaster
fed
with
high
glucose
diet,
model
hyperglycemia-induced
eye
impairment
to
study
pathophysiology
diabetic
retinopathy
at
early
stages.
To
this
aim,
visual
system
flies
orally
administered
been
analyzed
structural,
functional,
molecular/cellular
level
as
for
instance
neuronal
apoptosis/autophagy
dysregulation
oxidative
stress-related
signals.
Our
results
demonstrated
that
ameliorates
performance
hyperglycemic
flies.
eye-structure,
clearly
altered
by
hyperglycemia,
i.e.
defects
pattern
ommatidia,
irregular
rhabdomeres,
vacuoles,
damaged
mitochondria,
abnormal
phototransduction
units
were
rescued,
least
part,
plumbagin.
In
addition,
it
reactivated
autophagy,
decreased
presence
cell
death/apoptotic
features,
exerted
antioxidant
retina.
terms
mechanisms
favoring
death/survival
ratio,
Nrf2
signaling
activation
may
be
one
strategies
which
reduced
redox
unbalance
mainly
increasing
levels
glutathione-S-transferase.
Likewise,
act
additively
and/or
synergistically
inhibiting
mitochondrial-endoplasmic
reticulum
stress
unfolded
protein
response
pathways,
prevented
damage
induced
reactive
oxygen
species.
These
provide
an
avenue
further
studies,
helpful
develop
novel
candidates
drug
targets
against
neurotoxicity
glucose,
key
aspect
retinal
complications
diabetes.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: May 23, 2024
Abstract
Pancreatic
β
cells
secrete
insulin
in
response
to
glucose
elevation
maintain
homeostasis.
A
complex
network
of
inter-organ
communication
operates
modulate
secretion
and
regulate
levels
after
a
meal.
Lipids
obtained
from
diet
or
generated
intracellularly
are
known
amplify
glucose-stimulated
secretion,
however,
the
underlying
mechanisms
not
completely
understood.
Here,
we
show
that
Drosophila
secretory
lipase,
Vaha
(CG8093),
is
synthesized
midgut
moves
brain
where
it
concentrates
insulin-producing
process
requiring
Lipid
Transfer
Particle,
lipoprotein
originating
fat
body.
In
dietary
fat,
stimulates
insulin-like
peptide
release
(ILP),
deficiency
results
reduced
circulatory
ILP
diabetic
features
including
hyperglycemia
hyperlipidemia.
Our
findings
suggest
functions
as
diacylglycerol
lipase
physiologically,
by
being
molecular
link
between
lipid
amplified
gut-brain
axis.
Wellcome Open Research,
Journal Year:
2025,
Volume and Issue:
10, P. 112 - 112
Published: Feb. 28, 2025
We
developed
a
cost-effective
enzyme-based
rRNA-depletion
method
tailored
for
Drosophila
melanogaster,
addressing
the
limitations
of
existing
commercial
kits
and
lack
peer-reviewed
alternatives.
Our
employs
single-stranded
DNA
probes
complementary
to
Drosophila
rRNA,
forming
DNA-RNA
hybrids.
These
hybrids
are
then
degraded
using
RNase
H
enzyme,
effectively
removing
rRNA
enriching
all
non-ribosomal
RNAs,
including
mRNA,
lncRNA
small
RNA.
When
compared
removal
kit,
our
approach
demonstrated
superior
efficiency
mapping
percentage,
confirming
its
effectiveness.
Additionally,
successfully
enriched
non-coding
transcriptome,
making
it
valuable
tool
studying
ncRNA
in
Drosophila.
The
probe
sequences
protocol
made
freely
available,
offering
reliable
alternative
experiments.
Cells,
Journal Year:
2025,
Volume and Issue:
14(6), P. 415 - 415
Published: March 12, 2025
Metabolic
syndrome
(MetS)
is
a
subclinical
disease,
resulting
in
increased
risk
of
type
2
diabetes
(T2D),
cardiovascular
diseases,
cancer,
and
mortality.
Dynamical
network
biomarkers
(DNB)
theory
has
been
developed
to
provide
early-warning
signals
the
disease
state
during
preclinical
stage.
To
improve
efficiency
DNB
analysis
for
target
genes
discovery,
intervention
based
on
control
proposed.
However,
its
biological
validation
specific
such
as
MetS
remains
unexplored.
Herein,
we
identified
eight
candidate
from
adipose
tissue
model
mice
at
stage
by
analysis.
Using
Drosophila,
conducted
RNAi-mediated
knockdown
screening
these
vasa
(also
known
DDX4),
encoding
DEAD-box
RNA
helicase,
fat
metabolism-associated
gene.
Fat
body-specific
abrogated
high-fat
diet
(HFD)-induced
enhancement
starvation
resistance
through
up-regulation
triglyceride
lipase.
We
also
confirmed
that
DDX4
expressing
adipocytes
are
HFD-fed
high
BMI
patients
using
public
datasets.
These
results
prove
potential
search
therapeutic
targets
diseases
PLoS Genetics,
Journal Year:
2025,
Volume and Issue:
21(5), P. e1011690 - e1011690
Published: May 2, 2025
Drosophila
larval
growth
requires
efficient
conversion
of
dietary
nutrients
into
biomass.
Lactate
dehydrogenase
(Ldh)
and
glycerol-3-phosphate
(Gpdh1)
support
this
metabolic
program
by
cooperatively
promoting
glycolytic
flux.
Consistent
with
their
cooperative
functions,
the
loss
both
enzymes,
but
not
either
single
enzyme
alone,
induces
a
developmental
arrest.
However,
Ldh
Gpdh1
exhibit
complex
often
mutually
exclusive
expression
patterns,
suggesting
that
lethal
phenotypes
exhibited
Gpdh1;
double
mutants
could
be
mediated
non-autonomously.
Supporting
possibility,
we
find
arrest
displayed
extends
beyond
simple
disruption
instead
stems,
in
part,
from
changes
systemic
factor
signaling.
Specifically,
demonstrate
simultaneous
results
elevated
Upd3,
cytokine
involved
Jak/Stat
Furthermore,
show
upd3
loss-of-function
mutations
suppress
phenotype,
indicating
Upd3
signaling
restricts
development
response
to
decreased
Together,
our
findings
reveal
mechanism
which
disruptions
can
modulate