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Werner syndrome protein positively regulates XRCC4-like factor transcription.
[werner syndrome]
XRCC
4
-
like
factor
(
XLF
)
is
involved
in
non-homologous
end
joining-mediated
repair
of
DNA
double
-strand
breaks
(
DSBs
)
.
Mutations
in
the
WRN
gene
results
in
the
development
of
Werner
syndrome
(
WS
)
,
a
rare
autosomal
recessive
disorder
characterized
by
premature
ageing
and
genome
instability
.
In
the
present
study
,
it
was
identified
that
XLF
protein
levels
were
lower
in
WRN
-
deficient
fibroblasts
,
compared
with
normal
fibroblasts
.
Depletion
of
WRN
in
HeLa
cells
led
to
a
decrease
of
XLF
mRNA
and
its
promoter
activity
.
Chromatin
immunoprecipitation
assays
demonstrated
that
WRN
was
associated
with
the
XLF
promoter
.
Depletion
of
XLF
in
normal
human
fibroblasts
increased
the
percentage
of
β-galactosidase
(
β-gal
)
staining-
positive
cells
,
indicating
acceleration
in
cellular
senescence
.
Taken
together
,
the
results
suggest
that
XLF
is
a
transcriptional
target
of
WRN
and
may
be
involved
in
the
regulation
of
cellular
senescence
.
