BioProject

In this study, use of a gene-targeted mouse model that is defective for pRb-condensin II interactions, Rb1L, has revealed instances where condensin II localization in interphase nuclei is dependent on pRb. More...

In this study, use of a gene-targeted mouse model that is defective for pRb-condensin II interactions, Rb1L, has revealed instances where condensin II localization in interphase nuclei is dependent on pRb. Condensin II binding overlaps significantly with marks of active chromatin, and is enriched at the promoters of genes, including closely spaced divergent promoters. Interestingly, there are some bidirectional promoters where condensin II binds in an pRb-dependent manner and transcription of only one of the two genes is upregulated in Rb1L/L MEFs, suggesting the pRb-condensin II complex may be acting as a repressor or an insulator at distinct genomic locations to influence transcription. Chromatin conformations at these locations demonstrated that the pRb-condensin II complex may be responsible for maintaining more static, long-range interactions. In addition, pRb also recruits TFIIIC, another condensin II interactor, to many genomic loci. These recently discovered non-canonical transcriptional functions of the pRb-condensin II complex may represent an additional mechanism of pRb-mediated tumor suppression. Overall design: Four Rb1+/+ and Rb1L/L MEF pairs were used for 4C-Seq. Interactions at two different viewpoints, the bidrectional promoter between Cdca3 and Usp5 and the bidirectional promoter between Pole and Pxmp2, were examined. Less...