Stabilization of Chromatin Structure by PRC1, a Polycomb Complex

Stabilization of Chromatin Structure by PRC1, a Polycomb Complex

Vol. 98, 37–46, July 9, 1999 | Zhaohui Shao,*† Florian Raible,*‡§ Ramin Mollaaghatababa,*† Jeffrey R. Guyon,*‡ Chao-ting Wu,* Welcome Bender,* and Robert E. Kingston*‡§
The Polycomb group (PcG) genes are essential for maintaining the repression of homeotic genes during development. Mutations in these genes can be suppressed by mutations in SWI/SNF family genes. The authors purified a complex called PRC1, which contains proteins from the PcG genes *Polycomb*, *Posterior sex combs*, *polyhomeotic*, *Sex combs on midleg*, and others. Preincubation of PRC1 with nucleosomal arrays blocked the remodeling activity of SWI/SNF, suggesting that PRC1 and SWI/SNF compete for the nucleosomal template. PRC1 was active on nucleosomal arrays formed with tailless histones, indicating that it interacts with the main body of the nucleosomal proteins or DNA rather than histone tails. The results suggest that PRC1 functions by interacting with nucleosomal arrays to stabilize them against subsequent remodeling by SWI/SNF. PRC1 and SWI/SNF can block each other's function, and PRC1 must be present first on the template to block SWI/SNF. The competition between PRC1 and SWI/SNF may be a mechanism to regulate gene expression by favoring SWI/SNF unless PRC1 has already established a repressed state.The Polycomb group (PcG) genes are essential for maintaining the repression of homeotic genes during development. Mutations in these genes can be suppressed by mutations in SWI/SNF family genes. The authors purified a complex called PRC1, which contains proteins from the PcG genes *Polycomb*, *Posterior sex combs*, *polyhomeotic*, *Sex combs on midleg*, and others. Preincubation of PRC1 with nucleosomal arrays blocked the remodeling activity of SWI/SNF, suggesting that PRC1 and SWI/SNF compete for the nucleosomal template. PRC1 was active on nucleosomal arrays formed with tailless histones, indicating that it interacts with the main body of the nucleosomal proteins or DNA rather than histone tails. The results suggest that PRC1 functions by interacting with nucleosomal arrays to stabilize them against subsequent remodeling by SWI/SNF. PRC1 and SWI/SNF can block each other's function, and PRC1 must be present first on the template to block SWI/SNF. The competition between PRC1 and SWI/SNF may be a mechanism to regulate gene expression by favoring SWI/SNF unless PRC1 has already established a repressed state.
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