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Selective and antagonistic functions of SWI/SNF and Mi-2β nucleosome remodeling complexes during an inflammatory response
被引:343
作者:
Ramirez-Carrozzi, VR
Nazarian, AA
Li, CC
Gore, SL
Sridharan, R
Imbalzano, AN
Smale, ST
[1
]
机构:
[1] Univ Calif Los Angeles, Howard Hughes Med Inst, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA
[3] Univ Massachusetts, Sch Med, Dept Cell Biol, Worcester, MA 01655 USA
关键词:
inflammation;
cytokines;
chromatin;
SWI/SNF;
NuRD;
D O I:
10.1101/gad.1383206
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Studies of mammalian genes activated in response to an acute stimulus have suggested diverse mechanisms through which chromatin structure and nucleosome remodeling events contribute to inducible gene transcription. However, because of this diversity, the logical organization of the genome with respect to nucleosome remodeling and gene induction has remained obscure. Numerous proinflammatory genes are rapidly induced in macrophages in response to microbial infection. Here, we show that in lipopolysaccharide-stimulated macrophages, the catalytic BRG1/BRM subunits of the SWI/SNF class of ATP-dependent nucleosome remodeling complexes are consistently required for the activation of secondary response genes and primary response genes induced with delayed kinetics, but not for rapidly induced primary response genes. Surprisingly, a Mi-2 beta complex was selectively recruited along with the SWI/SNF complexes to the control regions of secondary response and delayed primary response genes, with the Mi-2 beta complex acting antagonistically to limit the induction of these gene classes. SWI/SNF and Mi-2 beta complexes influenced cell size in a similarly antagonistic manner. These results provide insight into the differential contributions of nucleosome remodeling complexes to the rapid induction of defined classes of mammalian genes and reveal a robust anti-inflammatory function of Mi-2 beta.
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页码:282 / 296
页数:15
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