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Cell Cycle. 2015;14(13):2160-70. doi: 10.1080/15384101.2015.1049778.

A novel role for the condensin II complex in cellular senescence.

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a The Wistar Institute ; Philadelphia , PA USA.


Although cellular senescence is accompanied by global alterations in genome architecture, how the genome is restructured during the senescent processes is not well understood. Here, we show that the hCAP-H2 subunit of the condensin II complex exists as either a full-length protein or an N-terminus truncated variant (ΔN). While the full-length hCAP-H2 associates with mitotic chromosomes, the ΔN variant exists as an insoluble nuclear structure. When overexpressed, both hCAP-H2 isoforms assemble this nuclear architecture and induce senescence-associated heterochromatic foci (SAHF). The hCAP-H2ΔN protein accumulates as cells approach senescence, and hCAP-H2 knockdown inhibits oncogene-induced senescence. This study identifies a novel mechanism whereby condensin drives senescence via nuclear/genomic reorganization.


BrdU, bromodeoxyuridine; CDK, cyclin dependent kinase; DAPI, 4,6-diamidino-2-phenylindole; NCAPH2, non-SMC chromosome-associated protein H2 gene; RPE-1, hTERT-immortalized retinal pigment epithelial cell line; Rb, retinoblastoma protein; SA-β-gal, senescence-associated β-galactosidase; SADS, senescence-associated distension of satellites; SAHF; SAHF, senescence-associated heterochromatic foci; SMC, structural maintenance of chromosomes; cellular senescence; condensin; genome organization; hCAP-H2, human chromosome-associated protein H2; hTERT, human telomerase reverse transcriptase; human; nuclear architecture; oncogene-induced senescence; shRNA, short-hairpin RNA.; uORF, upstream open reading frame

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