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Condensin association with histone H2A shapes mitotic chromosomes (2011)

K. Tada ; H. Susumu ; T. Sakuno ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 474(7352): 477-83. doi: 10.1038/nature10179.

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Publication Date: 2011-06-03

Description: Chromosome structure is dynamically regulated during cell division, and this regulation is dependent, in part, on condensin. The localization of condensin at chromosome arms is crucial for chromosome partitioning during anaphase. Condensin is also enriched at kinetochores but its precise role and loading machinery remain unclear. Here we show that fission yeast (Schizosaccharomyces pombe) kinetochore proteins Pcs1 and Mde4--homologues of budding yeast (Saccharomyces cerevisiae) monopolin subunits and known to prevent merotelic kinetochore orientation--act as a condensin 'recruiter' at kinetochores, and that condensin itself may act to clamp microtubule binding sites during metaphase. In addition to the regional recruitment factors, overall condensin association with chromatin is governed by the chromosomal passenger kinase Aurora B. Aurora-B-dependent phosphorylation of condensin promotes its association with histone H2A and H2A.Z, which we identify as conserved chromatin 'receptors' of condensin. Condensin phosphorylation and its deposition onto chromosome arms reach a peak during anaphase, when Aurora B kinase relocates from centromeres to the spindle midzone, where the separating chromosome arms are positioned. Our results elucidate the molecular basis for the spatiotemporal regulation of mitotic chromosome architecture, which is crucial for chromosome partitioning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tada, Kenji -- Susumu, Hiroaki -- Sakuno, Takeshi -- Watanabe, Yoshinori -- England -- Nature. 2011 Jun 1;474(7352):477-83. doi: 10.1038/nature10179.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21633354" target="_blank"〉PubMed〈/a〉

Keywords: Adenosine Triphosphatases/*metabolism ; Aurora Kinase B ; Aurora Kinases ; Binding Sites ; Cell Cycle Proteins/metabolism ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosomes, Fungal/*metabolism ; DNA-Binding Proteins/*metabolism ; HeLa Cells ; Histones/*metabolism ; Humans ; Kinetochores/metabolism ; Microtubules/metabolism ; *Mitosis ; Multiprotein Complexes/*metabolism ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Binding ; Protein Transport ; Protein-Serine-Threonine Kinases/metabolism ; Schizosaccharomyces/cytology/*metabolism ; Schizosaccharomyces pombe Proteins/metabolism ; cdc25 Phosphatases/genetics/metabolism

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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The inner centromere-shugoshin network prevents chromosomal instability (2015)

Y. Tanno ; H. Susumu ; M. Kawamura ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 349(6253): 1237-40. doi: 10.1126/science.aaa2655.

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Publication Date: 2015-09-12

Description: Chromosomal instability (CIN) is a major trait of cancer cells and a potent driver of tumor progression. However, the molecular mechanisms underlying CIN still remain elusive. We found that a number of CIN(+) cell lines have impairments in the integrity of the conserved inner centromere-shugoshin (ICS) network, which coordinates sister chromatid cohesion and kinetochore-microtubule attachment. These defects are caused mostly by the loss of histone H3 lysine 9 trimethylation at centromeres and sometimes by a reduction in chromatin-associated cohesin; both pathways separately sustain centromeric shugoshin stability. Artificial restoration of the ICS network suppresses chromosome segregation errors in a wide range of CIN(+) cells, including RB- and BRCA1-deficient cells. Thus, dysfunction of the ICS network might be a key mechanism underlying CIN in human tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanno, Yuji -- Susumu, Hiroaki -- Kawamura, Miyuki -- Sugimura, Haruhiko -- Honda, Takashi -- Watanabe, Yoshinori -- New York, N.Y. -- Science. 2015 Sep 11;349(6253):1237-40. doi: 10.1126/science.aaa2655.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ; Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ; First Department of Pathology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan. ; Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ywatanab@iam.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26359403" target="_blank"〉PubMed〈/a〉

Keywords: BRCA1 Protein/genetics ; Carcinogenesis/genetics/*metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Centromere/genetics/*metabolism ; Chromatids/metabolism ; Chromatin/metabolism ; *Chromosomal Instability ; Chromosomal Proteins, Non-Histone/metabolism ; *Chromosome Segregation ; HeLa Cells ; Histones/metabolism ; Humans ; Kinetochores/metabolism ; Lysine/metabolism ; Methylation ; Microtubules/metabolism ; Retinoblastoma Protein/genetics

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics