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PSC subunit, yet binding to the nucleosomes is independent of the histone
N-terminal tails. In a cell line based
in vivo
system, the PRC1 subunit
RING1B was essential for full compaction of mammalian
Hox
clusters, as
seen by fluorescent microscopy (
Eskeland et al., 2010
). Intriguingly, how-
ever, this compaction is independent from the H2AK199 ubiquitin ligase
activity of RING1B, suggesting that the latter subunit has a dual function.
Chromatin compaction directly influences silencing, since the absence of
RING1B leads to the derepression of both the
Drosophila Ubx
and mamma-
lian
Hox
genes (
Eskeland et al., 2010; Wang, Wang, et al., 2004
).
On the other hand, a direct role for Trithorax complexes in chromatin
decompaction has not been reported. The collinear activation of
Hox
genes
coincides with the transcription of many large noncoding RNAs though,
which may indirectly induce chromatin decompaction (reviewed in
Hekimoglu & Ringrose, 2009
). When
Drosophila Hox
genes are active,
the surrounding chromatin, including the PREs, is transcribed following
a similar collinear pattern (
Bae, Calhoun, Levine, Lewis, & Drewell,
2002; Sanchez-Herrero &Akam, 1989
). Also, when enforced, the transcrip-
tion through PREs can derepress target genes and thus interfere with
Polycomb-mediated silencing (
Bender & Fitzgerald, 2002; Hogga &
Karch, 2002; Rank, Prestel, & Paro, 2002
). The production of noncoding
RNAs may thus provide
Drosophila
Trithorax complexes an indirect means
of antagonizing chromatin compaction. In mammals, many noncoding
RNAs are located within
Hox
clusters and their activities coincide with
the transcriptional state of the surrounding chromatin (
Rinn et al., 2007;
Sessa et al., 2007
), like any promoter artificially introduced at the vicinity
of
Hox
genes (see e.g.,
Herault, Kmita, Sawaya, & Duboule, 2002
). While
the transcription of surrounding chromatin in mammalian
Hox
cluster may
thus serve a similar decompacting function, functional evidences are still
lacking.
The dynamics of chromatin compaction accompanying
Hox
gene collin-
earity has been extensively studied using fluorescentmicroscopy (
Chambeyron
& Bickmore, 2004; Chambeyron, Da Silva, Lawson, & Bickmore, 2005;
Eskeland et al., 2010; Morey, Da Silva, Perry, & Bickmore, 2007
). Various
states of chromatin compaction can be visualized using differentially labeled
probes located on the 5
0
and 3
0
ends of murine
Hox
clusters. In cells where
the clusters are inactive, the inter-probes distance within the
HoxB
and
HoxD
clusters is minimal, indicating compacted states. In
in vitro
differentiated ES
cells, as well as in E9.5 embryonic cells, where 3
0
located
Hox
genes are active,
the inter-probes distances are significantly increased. Therefore, partially
