Biology Reference
In-Depth Information
Table 8.1 H3K9/HP1 components
M. musculus
D. melanogaster
A. thaliana
Suv39h1/
KMT1A,
Suv39h2/
KMT1B
DKO animals: viable,
reduced size, impaired
gametogenesis, increased
incidence of lymphoma
(
Braig et al., 2005; Peters
et al., 2001
).
DKO ESCs: Normal
proliferation, loss of
H3K9me3 and HP1
binding on
chromocenter, replaced
by H3K27me3
(
Lehnertz et al., 2003;
Peters et al., 2001
).
Su(var)
3-9
Flies are viable,
phenotype similar to
mammals, HP1 binding
is lost on chromocenters
(
Schotta et al., 2002;
Tschiersch et al., 1994
).
SUVH4/
KYP,
SUVH2
Associate with
chromocenters. Mutants
show loss of
heterochromatic marks,
loss of gene silencing.
Heterochromatinization
if overexpressed (
Jackson,
Lindroth, Cao, &
Jacobsen, 2002;
Naumann et al., 2005
).
SUVR4
a
G9a/Ehmt2/
KMT1C,
Glp/Ehmt1/
KMT1D
Embryo: Both
G9a
and
Glp
single KO are lethal
around E9.5 due to
severe growth defects.
Conditional germ line
KO impairs
development of germ
cells and leads to defects
in meiosis (
Tachibana,
Matsumura, Fukuda,
Kimura, & Shinkai,
2008; Tachibana,
Nozaki, Takeda, &
Shinkai, 2007;
Tachibana et al., 2002
).
ESC: Regulation of
euchromatic genes,
imprinted genes, rDNA
repeats, and transposons.
Reduction of DNA
methylation in
G9a
KO
cells can be rescued by
catalytically dead G9a
(
Dong et al., 2008;
Est`ve et al., 2006;
Tachibana et al., 2002;
Wagschal et al., 2008
).
dG9a
Suppressor of PEV,
also regulates
euchromatic genes.
Mutants show
developmental defects
but are viable, more
severe effects when
combined with
Su(var)
3-9
mutation (
Kato,
Kato, Tachibana,
Shinkai, & Yamaguchi,
2008; Mis, Ner, &
Grigliatti, 2006; Seum,
Reo, et al., 2007
).
Contributes to the
silencing of transposons
and rDNA repeats
(
Thorstensen et al., 2006;
Veiseth et al., 2011
).
