Inflammatory
gut
disorders,
including
inflammatory
bowel
disease
(IBD),
can
be
impacted
by
dietary,
environmental,
and
genetic
factors.
While
the
incidence
of
IBD
is
increasing
worldwide,
we
still
lack
a
complete
understanding
gene-by-environment
interactions
underlying
inflammation
IBD.
Here,
profiled
colon
transcriptome
52
BXD
mouse
strains
fed
with
chow
or
high-fat
diet
(HFD)
identified
subset
that
exhibit
an
IBD-like
signature
on
HFD,
indicating
interplay
genetics
significantly
affect
intestinal
inflammation.
Using
gene
co-expression
analyses,
modules
are
enriched
for
IBD-dysregulated
genes
found
these
IBD-related
share
cis
-regulatory
elements
responsive
to
STAT2,
SMAD3
,
REL
transcription
We
used
module
quantitative
trait
locus
analyses
identify
loci
associated
expression
modules.
Through
prioritization
scheme
involving
systems
in
integration
external
human
datasets,
Muc4
Epha6
as
top
candidates
mediating
differences
HFD-driven
This
work
provides
insights
into
contribution
risk
identifies
two
candidate
genes,
MUC4
EPHA6
may
mediate
susceptibility
humans.
Inflammatory
gut
disorders,
including
inflammatory
bowel
disease
(IBD),
can
be
impacted
by
dietary,
environmental
and
genetic
factors.
While
the
incidence
of
IBD
is
increasing
worldwide,
we
still
lack
a
complete
understanding
gene-by-environment
interactions
underlying
inflammation
IBD.
Here,
profiled
colon
transcriptome
52
BXD
mouse
strains
fed
with
chow
or
high-fat
diet
(HFD)
identified
subset
that
exhibit
an
IBD-like
signature
on
HFD,
indicating
interplay
genetics
significantly
affect
intestinal
inflammation.
Using
gene
co-expression
analyses,
modules
are
enriched
for
IBD-dysregulated
genes
found
these
IBD-related
share
cis-regulatory
elements
responsive
to
STAT2,
SMAD3,
REL
transcription
We
used
module
quantitative
trait
locus
(ModQTL)
analyses
identify
loci
associated
expression
modules.
Through
prioritization
scheme
involving
systems
in
integration
external
human
datasets,
Muc4
Epha6
as
top
candidates
mediating
differences
HFD-driven
This
work
provides
insights
into
contribution
risk
identifies
two
candidate
genes,
MUC4
EPHA6,
may
mediate
susceptibility
humans.
Inflammatory
gut
disorders,
including
inflammatory
bowel
disease
(IBD),
can
be
impacted
by
dietary,
environmental
and
genetic
factors.
While
the
incidence
of
IBD
is
increasing
worldwide,
we
still
lack
a
complete
understanding
gene-by-environment
interactions
underlying
inflammation
IBD.
Here,
profiled
colon
transcriptome
52
BXD
mouse
strains
fed
with
chow
or
high-fat
diet
(HFD)
identified
subset
that
exhibit
an
IBD-like
signature
on
HFD,
indicating
interplay
genetics
significantly
affect
intestinal
inflammation.
Using
gene
co-expression
analyses,
modules
are
enriched
for
IBD-dysregulated
genes
found
these
IBD-related
share
cis-regulatory
elements
responsive
to
STAT2,
SMAD3,
REL
transcription
We
used
module
quantitative
trait
locus
(ModQTL)
analyses
identify
loci
associated
expression
modules.
Through
prioritization
scheme
involving
systems
in
integration
external
human
datasets,
Muc4
Epha6
as
top
candidates
mediating
differences
HFD-driven
This
work
provides
insights
into
contribution
risk
identifies
two
candidate
genes,
MUC4
EPHA6,
may
mediate
susceptibility
humans.
Abstract
Inflammatory
gut
disorders,
including
inflammatory
bowel
disease
(IBD),
can
be
impacted
by
dietary,
environmental
and
genetic
factors.
While
the
incidence
of
IBD
is
increasing
worldwide,
we
still
lack
a
complete
understanding
gene-by-environment
interactions
underlying
inflammation
IBD.
Here,
profiled
colon
transcriptome
52
BXD
mouse
strains
fed
with
chow
or
high-fat
diet
(HFD)
identified
subset
that
exhibit
an
IBD-like
signature
on
HFD,
indicating
interplay
genetics
significantly
affect
intestinal
inflammation.
Using
gene
co-expression
analyses,
modules
are
enriched
for
IBD-dysregulated
genes
found
these
IBD-related
share
cis-regulatory
elements
responsive
to
STAT2,
SMAD3,
REL
transcription
We
used
module
quantitative
trait
locus
(ModQTL)
analyses
identify
loci
associated
expression
modules.
Through
prioritization
scheme
involving
systems
in
integration
external
human
datasets,
Muc4
Epha6
as
top
candidates
mediating
differences
HFD-driven
This
work
provides
insights
into
contribution
risk
identifies
two
candidate
genes,
MUC4
EPHA6,
may
mediate
susceptibility
humans.
Inflammatory
gut
disorders,
including
inflammatory
bowel
disease
(IBD),
can
be
impacted
by
dietary,
environmental,
and
genetic
factors.
While
the
incidence
of
IBD
is
increasing
worldwide,
we
still
lack
a
complete
understanding
gene-by-environment
interactions
underlying
inflammation
IBD.
Here,
profiled
colon
transcriptome
52
BXD
mouse
strains
fed
with
chow
or
high-fat
diet
(HFD)
identified
subset
that
exhibit
an
IBD-like
signature
on
HFD,
indicating
interplay
genetics
significantly
affect
intestinal
inflammation.
Using
gene
co-expression
analyses,
modules
are
enriched
for
IBD-dysregulated
genes
found
these
IBD-related
share
cis
-regulatory
elements
responsive
to
STAT2,
SMAD3
,
REL
transcription
We
used
module
quantitative
trait
locus
analyses
identify
loci
associated
expression
modules.
Through
prioritization
scheme
involving
systems
in
integration
external
human
datasets,
Muc4
Epha6
as
top
candidates
mediating
differences
HFD-driven
This
work
provides
insights
into
contribution
risk
identifies
two
candidate
genes,
MUC4
EPHA6
may
mediate
susceptibility
humans.