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Volume 86, Issue 1, Pages (July 1996)

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Presentation on theme: "Volume 86, Issue 1, Pages (July 1996)"— Presentation transcript:

1 Volume 86, Issue 1, Pages 13-19 (July 1996)
Chromatin Unfolds  Gary Felsenfeld  Cell  Volume 86, Issue 1, Pages (July 1996) DOI: /S (00)

2 Figure 1 Two Classes of Inactivation Models
(A) Polymerization models: a model of higher order chromatin packaging at inactivated sites derived from the yeast telomeric silencing model proposed by Moretti et al and Hecht et al The general features of this model might be shared by other systems, such as assembly of positioned nucleosomes over STE6 (Cooper et al. 1994; Roth 1995) and Polycomb-group inactivation of homeotic genes. In every case there must be a polymerization initiator bound to a specific site (RAP1 for the telomere, α2/Mcm1 for mating type locus positioning, and PRE binding protein for the Pc-G case). Additional proteins (e.g., SIR 3/SIR4) interact with this initiator to extend polymerization (and inactivation) over the adjacent chromatin, using specific interactions with the histones for this purpose. These propagator proteins may, as has been suggested for SIR4 near the telomere, also provide attachment sites within the nucleus, which may anchor the complex to the nuclear periphery (Palladino et al. 1993). The evidence for this model is quite strong in the case of the telomere. (B) Loop domain models: factors bound to DNA at specific sites located at intervals throughout the domain or at its ends interact either directly or through other proteins to isolate the domains topologically from each other and (in some models) to inactivate the genes it contains. The loop ends are sometimes thought of as bound to nuclear matrix or otherwise immobilized. This class of models has been proposed as a mechanism for Pc-G suppression (see text), for insulation, and for LCR action. It is related to models of higher order chromatin structure proposed by Laemmli (see, e.g., Saitoh and Laemmli 1994). Cell  , 13-19DOI: ( /S (00) )

3 Figure 1 Two Classes of Inactivation Models
(A) Polymerization models: a model of higher order chromatin packaging at inactivated sites derived from the yeast telomeric silencing model proposed by Moretti et al and Hecht et al The general features of this model might be shared by other systems, such as assembly of positioned nucleosomes over STE6 (Cooper et al. 1994; Roth 1995) and Polycomb-group inactivation of homeotic genes. In every case there must be a polymerization initiator bound to a specific site (RAP1 for the telomere, α2/Mcm1 for mating type locus positioning, and PRE binding protein for the Pc-G case). Additional proteins (e.g., SIR 3/SIR4) interact with this initiator to extend polymerization (and inactivation) over the adjacent chromatin, using specific interactions with the histones for this purpose. These propagator proteins may, as has been suggested for SIR4 near the telomere, also provide attachment sites within the nucleus, which may anchor the complex to the nuclear periphery (Palladino et al. 1993). The evidence for this model is quite strong in the case of the telomere. (B) Loop domain models: factors bound to DNA at specific sites located at intervals throughout the domain or at its ends interact either directly or through other proteins to isolate the domains topologically from each other and (in some models) to inactivate the genes it contains. The loop ends are sometimes thought of as bound to nuclear matrix or otherwise immobilized. This class of models has been proposed as a mechanism for Pc-G suppression (see text), for insulation, and for LCR action. It is related to models of higher order chromatin structure proposed by Laemmli (see, e.g., Saitoh and Laemmli 1994). Cell  , 13-19DOI: ( /S (00) )

4 Figure 2 A Two-State Switch
A schematic diagram showing how an all-or-none change in chromatin structure (see text) could be used to convert a slowly changing concentration of transcription factors into a sharp change of state. Cell  , 13-19DOI: ( /S (00) )


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