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rigid regulatory mechanism, on the contrary, there is a need of plasticity to
support the development of multicellular organisms. One way of achieving
plasticity is through the interconnection of pathways. The two major
chromatin-based silencing mechanisms that we reviewed above share many
common ways of targeting based on protein interaction, ncRNA, or recog-
nition of PTM on histones ( Fig. 8.1 ). However, they are often considered as
distinct and mutually exclusive in regard to their distribution in the nucleus
and genome wide ( de Wit et al., 2007 ). As mentioned in the beginning,
studies in T. thermophila would argue that these pathways have common
ancestral functions ( Liu et al., 2007 ). Could these two silencing mechanisms
be independent of each other? HP1 is found in an atypical PRC1 complex
Polycomb
pathway
?
PRC1
Cbx
PRC1
Rybp
PRC2
(Oct3/4 REST)
TF
Chromatin
structure
Chromatin
binding protein
H3K9me3
H3K27me3
ncRNA
(KAP1/ZNF, Rb)
Suv39h1/2
HP1
SETDB1
H3K9/HP1
pathway
G9a
Figure 8.1 Overview of targeting of Polycomb complexes and H3K9 KMT/HP1 proteins.
Polycomb and H3K9 KMT/HP1 complexes can be targeted to chromatin through many
diverse ways implicating direct interaction with modified histones, noncoding RNA
(ncRNA), chromatin structure, and DNA-binding protein like transcription factors or
zinc-finger-containing protein (ZNF). Solid lines indicate interactions. Dotted lines indi-
cate potential interactions. Some examples are indicated between brackets. See text for
details.
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