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Drosophila brakeless interacts with atrophin and is required for tailless-mediated transcriptional repression in early embryos.
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Complex
gene
expression
patterns
in
animal
development
are
generated
by
the
interplay
of
transcriptional
activators
and
repressors
at
cis-regulatory
DNA
modules
(
CRMs
)
.
How
repressors
work
is
not
well
understood
,
but
often
involves
interactions
with
co
-repressors
.
We
isolated
mutations
in
the
brakeless
gene
in
a
screen
for
maternal
factors
affecting
segmentation
of
the
Drosophila
embryo
.
Brakeless
,
also
known
as
Scribbler
,
or
Master
of
thickveins
,
is
a
nuclear
protein
of
unknown
function
.
In
brakeless
embryos
,
we
noted
an
expanded
expression
pattern
of
the
Krüppel
(
Kr
)
and
knirps
(
kni
)
genes
.
We
found
that
Tailless-mediated
repression
of
kni
expression
is
impaired
in
brakeless
mutants
.
Tailless
and
Brakeless
bind
each
other
in
vitro
and
interact
genetically
.
Brakeless
is
recruited
to
the
Kr
and
kni
CRMs
,
and
represses
transcription
when
tethered
to
DNA
.
This
suggests
that
Brakeless
is
a
novel
co
-repressor
.
Orphan
nuclear
receptors
of
the
Tailless
type
also
interact
with
Atrophin
co
-repressors
.
We
show
that
both
Drosophila
and
human
Brakeless
and
Atrophin
interact
in
vitro
,
and
propose
that
they
act
together
as
a
co
-repressor
complex
in
many
developmental
contexts
.
We
discuss
the
possibility
that
human
Brakeless
homologs
may
influence
the
toxicity
of
polyglutamine-expanded
Atrophin-
1
,
which
causes
the
human
neurodegenerative
disease
dentatorubral-pallidoluysian
atrophy
(
DRPLA
)
.
