Genome biology,
Journal Year:
2024,
Volume and Issue:
25(1)
Published: Jan. 31, 2024
Abstract
Background
Pervasive
usage
of
alternative
promoters
leads
to
the
deregulation
gene
expression
in
carcinogenesis
and
may
drive
emergence
new
genes
spermatogenesis.
However,
little
is
known
regarding
mechanisms
underpinning
activation
promoters.
Results
Here
we
describe
how
cancer-testis-specific
transcription
activated.
We
show
that
intergenic
intronic
CTCF
binding
sites,
which
are
transcriptionally
inert
normal
somatic
cells,
could
be
epigenetically
reprogrammed
into
active
de
novo
germ
cancer
cells.
BORIS/CTCFL,
testis-specific
paralog
ubiquitously
expressed
CTCF,
triggers
epigenetic
reprogramming
sites
units
transcription.
BORIS
initiates
recruitment
chromatin
remodeling
factor,
SRCAP,
followed
by
replacement
H2A
histone
with
H2A.Z,
resulting
a
more
relaxed
state
nucleosomes
flanking
sites.
The
relaxation
around
facilitates
multiple
additional
factors,
thereby
activating
from
given
site.
demonstrate
can
cancer-testis
genes,
long
noncoding
RNAs,
retro-pseudogenes,
dormant
transposable
elements.
Conclusions
Thus,
functions
as
factor
reprograms
clustered
transcriptional
start
promoting
both
cells
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 12, 2024
Here
we
used
a
series
of
CTCF
mutations
to
explore
CTCF's
relationship
with
chromatin
and
its
contribution
gene
regulation.
impact
depends
on
the
genomic
context
bound
sites
unique
binding
properties
WT
mutant
proteins.
Specifically,
signal
strength
is
linked
changes
in
accessibility,
ability
block
cohesin
stability.
Multivariate
modelling
reveals
that
both
accessibility
contribute
independently
insulation,
however
has
stronger
effect.
have
bidirectional
such
at
sites,
reduced
cohesin-dependent,
specific
fashion.
In
addition,
each
alters
TF
an
indirect
manner,
which
impart
most
influence
rewiring
transcriptional
networks
cell's
differentiate.
Collectively,
perturbations
provide
rich
resource
for
determining
site-specific
effects.
Current Opinion in Cell Biology,
Journal Year:
2021,
Volume and Issue:
70, P. 75 - 83
Published: Jan. 9, 2021
'Structural
maintenance
of
chromosomes'
(SMC)
complexes
are
required
for
the
folding
genomic
DNA
into
loops.
Theoretical
considerations
and
single-molecule
experiments
performed
with
SMC
cohesin
condensin
indicate
that
occurs
via
loop
extrusion.
Recent
work
indicates
this
process
is
essential
assembly
antigen
receptor
genes
by
V(D)J
recombination
in
developing
B
T
cells
vertebrate
immune
system.
Here,
I
review
how
recent
studies
mouse
immunoglobulin
heavy
chain
locus
Igh
have
provided
evidence
hypothesis
formation
chromatin
loops
regulation
CTCF
Wapl
might
ensure
all
variable
gene
segments
(VH
segments)
participate
a
re-arranged
DJH
segment,
to
generation
maximally
diverse
repertoire
B-cell
receptors
antibodies.
Nature Communications,
Journal Year:
2023,
Volume and Issue:
14(1)
Published: Sept. 19, 2023
Abstract
Cohesin
regulates
gene
expression
through
context-specific
chromatin
folding
mechanisms
such
as
enhancer–promoter
looping
and
topologically
associating
domain
(TAD)
formation
by
cooperating
with
factors
cohesin
loaders
the
insulation
factor
CTCF.
We
developed
a
computational
workflow
to
explore
how
three-dimensional
(3D)
structure
are
regulated
collectively
or
individually
related
factors.
The
main
component
is
CustardPy,
which
multi-omics
datasets
compared
systematically.
To
validate
our
methodology,
we
generated
3D
genome,
transcriptome,
epigenome
data
before
after
depletion
of
effects
depletion.
observed
diverse
on
genome
changes
were
correlated
splitting
TADs
caused
loss.
also
variations
in
long-range
interactions
across
TADs,
their
epigenomic
states.
These
tools
will
be
valuable
for
studies.
Genome biology,
Journal Year:
2024,
Volume and Issue:
25(1)
Published: Jan. 31, 2024
Abstract
Background
Pervasive
usage
of
alternative
promoters
leads
to
the
deregulation
gene
expression
in
carcinogenesis
and
may
drive
emergence
new
genes
spermatogenesis.
However,
little
is
known
regarding
mechanisms
underpinning
activation
promoters.
Results
Here
we
describe
how
cancer-testis-specific
transcription
activated.
We
show
that
intergenic
intronic
CTCF
binding
sites,
which
are
transcriptionally
inert
normal
somatic
cells,
could
be
epigenetically
reprogrammed
into
active
de
novo
germ
cancer
cells.
BORIS/CTCFL,
testis-specific
paralog
ubiquitously
expressed
CTCF,
triggers
epigenetic
reprogramming
sites
units
transcription.
BORIS
initiates
recruitment
chromatin
remodeling
factor,
SRCAP,
followed
by
replacement
H2A
histone
with
H2A.Z,
resulting
a
more
relaxed
state
nucleosomes
flanking
sites.
The
relaxation
around
facilitates
multiple
additional
factors,
thereby
activating
from
given
site.
demonstrate
can
cancer-testis
genes,
long
noncoding
RNAs,
retro-pseudogenes,
dormant
transposable
elements.
Conclusions
Thus,
functions
as
factor
reprograms
clustered
transcriptional
start
promoting
both
cells
