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In mammals, knockout of HP1g induces a dramatic reduction in the
number of PGCs due to cell cycle defects ( Abe et al., 2011 ). These animals
are sterile and exhibit defects in centromere clustering and synapsis in sper-
matocytes ( Brown et al., 2010; Naruse et al., 2007; Takada et al., 2011 ).
Takada and colleagues further show that Suv39h1 / 2 H3K9-dependent
methylation at PCH serves as a platform to recruit HP1 g , which then
recruits G9a, highlighting a putative cooperative role between H3K9
KMTs and HP1 for meiotic progression. Strikingly, HP1 g and HP1 b ,
but not HP1 a associate with the transcriptionally silent XY body during
male meiosis, suggesting possibly isoform-specific functions ( Metzler-
Guillemain, Luciani, Depetris, Guichaoua, & Mattei, 2003 ). Recently, it
was shown that the SETDB1 homologue in worms, MET-2, is involved
in MSCI and protects the germline from undergoing apoptosis ( Checchi
& Engebrecht, 2011 ). Such function has not yet been described for mam-
malian SETDB1 and SETDB2 proteins. In murine embryonic ovary and
postnatal testis, Setdb2 expression correlates with that of Stra8 , a gene
involved in the onset of meiosis in germ cells ( Hogarth, Mitchell,
Evanoff, Small, & Griswold, 2011 ), suggesting a potential role for Setdb2
in mitotic to meiotic transition in germ cells.
In the mouse female germline, HP1b is the predominantly expressed iso-
form, and so far, no report indicates that its inactivation induces defects in
this lineage ( Aucott et al., 2008 ). In Drosophila , among the five isoforms of
HP1, HP1d and HP1e show a germline-specific expression in female ovary
and male testis, respectively ( Vermaak, Henikoff, & Malik, 2005; Volpe,
Horowitz, Grafer, Jackson, & Berg, 2001 ). HP1d , also named Rhino , was
found in a screen for female sterile mutant flies. HP1d / Rhino mutant flies
are characterized by defects in polytene chromosome structure of nurse cells
and egg polarity defects. HP1d/Rhino is thought to act as a safeguard of the
female germline against mobile elements through modulation of the piRNA
pathway ( Klattenhoff et al., 2009 ). Even though there is less information
about HP1e, it is hypothesized to have a function similar to HP1d but in
the male germline ( Vermaak et al., 2005 ).
Among the H3K9 KMTs in Drosophila , only dSETDB1, has been shown
to have a crucial role in the female germline ( Clough, Moon, Wang, Smith, &
Hazelrigg, 2007; Koch, Honemann-Capito, Egger-Adam, & Wodarz, 2009;
Wang et al., 2011; Yoon et al., 2008 ). dSETDB1 is expressed most strongly at
early stages of oogenesis, in germ cells in the germarium. dSETDB1 mutant
ovaries primarily exhibit germ cell differentiation defects and apoptosis in
young females, and gradually the niche of germ stem cells is lost, indicating
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