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Cloning Tags > Tag based links for Zygote
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- The enigma of
ATCE1, an
acrosome-assoc
iated
transcription
factor.: Dev Biol, Vol.
298, No. 1. (1
October 2006),
pp.
201-211.Atce1
belongs to the
CREB3/LZIP
subtype of the
ATF/CREB
transcription
factor gene
family. Its
transcription
has previously
been shown to
be
testis-specifi
c and within
the testis to
be restricted
to haploid
spermatids. In
this study, we
characterized
the protein's
distribution
in the testis
and found that
it accumulates
in late round
and in
elongating
spermatids,
corresponding
to
developmental
stages
considered
transcriptiona
lly silent.
ATCE1
accumulation
is
acrosome-speci
fic and
persists up to
mature
epididymal
cells, at
which stage
the protein
remained
associated
with the inner
acrosome
membrane even
after
acrosomal
reaction. No
nuclear
localization
was evident at
any
spermatogenic
stage.
Expression of
full-length
ATCE1 in
various cell
lines revealed
ER and Golgi
localization
whereas
truncation of
the C-terminus
allowed
entrance into
the nucleus.
Potent
transcriptiona
l activation
activity, from
kB-containing
regulatory
elements (but
not from CRE
elements as
one might
expect), was
observed using
the
C-terminally
truncated
nuclear form
of ATCE1.
These results
raise the
question of
why would a
transcription
factor be
specifically
anchored to
the acrosome
inner
membrane? An
intriguing
speculation
that ATCE1
might be
paternally
delivered to
the newly
formed zygote
is discussed.S
Gil, D Yosef,
N Golan, J Don
Source: Dev Biol, Vol. 298, No. 1. (1 October 2006), pp. 201-211. - A genetic
mosaic screen
of essential
zygotic genes
in
Caenorhabditis
elegans.: Genetics, Vol.
128 (1991),
pp. 281-292.We
have devised a
simple genetic
mosaic screen,
which
circumvents
the
difficulties
posed by
phenotypic
analysis of
early lethal
mutants, to
analyze
essential
zygotic genes
in
Caenorhabditis
elegans. The
screen
attempts to
distinguish
genes involved
in cell type
and/or lineage
specific
processes such
as
determination,
differentiatio
n or
morphogenesis
from genes
involved in
general
processes such
as
intermediary
metabolism by
using the
pattern of
gene function
to classify
genes: genes
required in
one or a
subset of
early
blastomeres
may have
specific
functions,
whereas genes
required in
all early
blastomeres
may have
general
functions. We
found that 12
of 17 genes
examined
function in
specific early
blastomeres,
suggesting
that many
zygotic genes
contribute to
specific early
processes. We
discuss the
advantages and
limitations of
this screen,
which is
applicable to
other regions
of the C.
elegans
genome.EA
Bucher, IS
Greenwald
Source: Genetics, Vol. 128 (1991), pp. 281-292. - The mog-1 gene
is required
for the switch
from
spermatogenesi
s to oogenesis
in
Caenorhabditis
elegans.: Genetics, Vol.
133 (1993),
pp.
919-931.Caenor
habditis
elegans
hermaphrodites
make first
sperm, then
oocytes. By
contrast,
animals
homozygous for
any of six
loss-of-functi
on mutations
in the gene
mog-1 (for
masculinizatio
n of the germ
line) make
sperm
continuously
and do not
switch into
oogenesis.
Therefore, in
mog-1 mutants,
germ cells
that normally
would become
oocytes are
transformed
into sperm. By
contrast,
somatic sexual
fates are
normal,
suggesting
that mog-1
plays a germ
line-specific
role in sex
determination.
Analyses of
double mutants
suggest that
mog-1
negatively
regulates the
fem genes
and/or fog-1:
mog-1; fem and
mog-1; fog-1
double mutants
all make
oocytes rather
than sperm.
Therefore, we
propose that
wild-type
mog-1 is
required in
the
hermaphrodite
germ line for
regulation of
the switch
from
spermatogenesi
s to oogenesis
rather than
for
specification
of oogenesis
per se. In
addition to
its role in
germline sex
determination,
maternal mog-1
is required
for
embryogenesis:
most progeny
of a mog-1;
fem or mog-1;
fog-1 mother
die as
embryos. How
might the
roles of mog-1
in the
sperm/oocyte
switch and
embryogenesis
be linked?
Previous work
showed that
fem-3 is
regulated
post-transcrip
tionally to
achieve the
sperm/oocyte
switch. We
speculate that
mog-1 may
function in
the
post-transcrip
tional
regulation of
numerous
germ-line
RNAs,
including
fem-3. A loss
of mog-1 might
inappropriatel
y activate
fem-3 and
thereby
abolish the
sperm/oocyte
switch; its
loss might
also lead to
misregulation
of maternal
RNAs and thus
embryonic
death.PL
Graham, JE
Kimble
Source: Genetics, Vol. 133 (1993), pp. 919-931. - The SL1
trans-spliced
leader RNA
performs an
essential
embryonic
function in
Caenorhabditis
elegans that
can also be
supplied by
SL2 RNA.: Genes and
Development,
Vol. 10
(1996), pp.
1543-1556.Cova
lent joining
of leader RNA
exons to
pre-mRNAs by
trans-splicing
has been
observed in
protists and
invertebrates,
and can occur
in cultured
mammalian
cells. In the
nematode
Caenorhabditis
elegans,
approximately
60% of mRNA
species are
trans-spliced
to the
22-nucleotide
SL1 leader,
and another
approximately
10% of mRNAs
receive the
22-nucleotide
SL2 leader. We
have isolated
deletions that
remove the
rrs-1 cluster,
a gene complex
that contains
approximately
110 tandem
copies of a
repeat
encoding both
SL1 RNA and 5S
rRNA. An
SL1-encoding
gene alone
rescues the
embryonic
lethality
caused by
these
deletions.
Mutations
within the
Sm-binding
site of SL1
RNA, which is
required for
trans-splicing
, eliminate
rescue,
suggesting
that the
ability of the
SL1 leader to
be
trans-spliced
is required
for its
essential
activity. We
observe
pleiotropic
defects in
embryos
lacking SL1
RNA,
suggesting
that multiple
mRNAs may be
affected by
the absence of
an SL1 leader.
We found,
however, that
SL1-receiving
messages are
expressed
without an SL1
leader.
Surprisingly,
when
overexpressed,
SL2 RNA, which
performs a
distinct
function from
that of SL1
RNA in
wild-type
animals, can
rescue the
lethality of
embryos
lacking SL1
RNA. Moreover,
in these
mutant
embryos, we
detect SL2
instead of SL1
leaders on
normally
SL1-trans-spli
ced messages;
this result
suggests that
the mechanism
that
discriminates
between SL1
and
SL2-trans-spli
cing may
involve
competition
between SL1
and
SL2-specific
trans-splicing
. Our findings
demonstrate
that SL1 RNA
is essential
for
embryogenesis
in C. elegans
and that SL2
RNA can
substitute for
SL1 RNA in
vivo.KC
Ferguson, PJ
Heid, JH
Rothman
Source: Genes and Development, Vol. 10 (1996), pp. 1543-1556. - Specification
and
development of
the germline
in
Caenorhabditis
elegans.: Ciba
Foundation
Symposium,
Vol. 182
(1994), pp.
31-45.Maternal
-effect
sterile (mes)
genes encode
maternal
components
that are
required for
establishment
and
development of
the germline.
Five such
genes have
been
identified in
the nematode
Caenorhabditis
elegans.
Mutations in
one of the
genes result
in defects in
the asymmetric
division and
cytoplasmic
partitioning
that generate
the primordial
germ cell P4
at the
16-24-cell
stage of
embryogenesis.
As a result of
these defects,
the P4 cell is
transformed
into a muscle
progenitor and
mutant embryos
develop into
sterile adults
with extra
body muscles.
Mutations in
the other four
mes genes do
not affect
formation of
the germline
during
embryogenesis,
but result in
drastically
reduced
proliferation
of the
germline
during
post-embryonic
stages and in
an absence of
gametes in
adults. The
failure to
form gametes
may reflect a
defect in
germline
specification
or may be a
consequence of
reduced
germline
proliferation.
We are
currently
testing these
two
possibilities.
In addition to
the mes gene
products,
wild-type
function of
the zygotic
gene glp-4 is
required for
normal
post-embryonic
proliferation
of the
germline. Germ
cells in glp-4
mutant worms
are arrested
in prophase of
the mitotic
cell cycle and
are unable to
enter meiosis
and form
gametes. Thus,
following
establishment
of the germ
lineage in the
early embryo,
both maternal
and zygotic
gene products
work in
concert to
promote the
extensive
proliferation
of the
germline and
to enable germ
cells to
generate
functional
gametes.S
Strome, CM
Garvin, JE
Paulsen, EE
Capowski, PR
Martin, MJ
Beanan
Source: Ciba Foundation Symposium, Vol. 182 (1994), pp. 31-45. - Maternal
depletion of
CTCF reveals
multiple
functions
during oocyte
and
preimplantatio
n embryo
development.: Development
(Cambridge,
England) (9
July 2008)CTCF
is a
multifunctiona
l nuclear
factor
involved in
epigenetic
regulation.
Despite recent
advances that
include the
systematic
discovery of
CTCF-binding
sites
throughout the
mammalian
genome, the in
vivo roles of
CTCF in adult
tissues and
during
embryonic
development
are largely
unknown. Using
transgenic
RNAi, we
depleted
maternal
stores of CTCF
from growing
mouse oocytes,
and identified
hundreds of
misregulated
genes.
Moreover, our
analysis
suggests that
CTCF
predominantly
activates or
derepresses
transcription
in oocytes.
CTCF depletion
causes meiotic
defects in the
egg, and
mitotic
defects in the
embryo that
are
accompanied by
defects in
zygotic gene
expression,
and culminate
in apoptosis.
Maternal
pronuclear
transfer and
CTCF mRNA
microinjection
experiments
indicate that
CTCF is a
mammalian
maternal
effect gene,
and that
persistent
transcriptiona
l defects
rather than
persistent
chromosomal
defects
perturb early
embryonic
development.
This is the
first study
detailing a
global and
essential role
for CTCF in
mouse oocytes
and
preimplantatio
n
embryos.Le-Ben
Wan, Hua Pan,
Sridhar
Hannenhalli,
Yong Cheng,
Jun Ma, Andrew
Fedoriw,
Victor
Lobanenkov,
Keith E
Latham,
Richard M
Schultz,
Marisa S
Bartolomei
Source: Development (Cambridge, England) (9 July 2008) - Structural
differences in
centromeric
heterochromati
n are
spatially
reconciled on
fertilisation
in the mouse
zygote: Chromosoma,
Vol. 116, No.
4. (August
2007), pp.
403-415.Probst
, Aline,
Santos,
Fatima, Reik,
Wolf,
Almouzni,
Genevieve,
Dean, Wendy
Source: Chromosoma, Vol. 116, No. 4. (August 2007), pp. 403-415. - A
maternal-zygot
ic effect
gene, Zfp57,
maintains both
maternal and
paternal
imprints.: Developmental
cell, Vol. 15,
No. 4.
(October
2008), pp.
547-557.The
mechanisms
responsible
for
maintaining
genomic
methylation
imprints in
mouse embryos
are not
understood. We
generated a
knockout mouse
in the Zfp57
locus encoding
a KRAB zinc
finger
protein. Loss
of just the
zygotic
function of
Zfp57 causes
partial
neonatal
lethality,
whereas
eliminating
both the
maternal and
zygotic
functions of
Zfp57 results
in a highly
penetrant
embryonic
lethality. In
oocytes,
absence of
Zfp57 results
in failure to
establish
maternal
methylation
imprints at
the Snrpn
imprinted
region.
Intriguingly,
methylation
imprints are
reacquired
specifically
at the
maternally
derived Snrpn
imprinted
region when
the zygotic
Zfp57 is
present in
embryos. This
suggests that
there may be
DNA
methylation-in
dependent
memory for
genomic
imprints.
Zfp57 is also
required for
the
postfertilizat
ion
maintenance of
maternal and
paternal
methylation
imprints at
multiple
imprinted
domains. The
effects on
genomic
imprinting are
consistent
with the
maternal-zygot
ic lethality
of Zfp57
mutants.X Li,
M Ito, F Zhou,
N Youngson, X
Zuo, P Leder,
AC
Ferguson-Smith
Source: Developmental cell, Vol. 15, No. 4. (October 2008), pp. 547-557.
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