Chromosomes articles within Nature Cell Biology

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  • News & Views |

    When transcription by RNA polymerase II is stalled by ultraviolet-induced DNA damage, it recruits repair factors, leading to excision of the damaged site and DNA synthesis to fill the gap. Three new studies show that, for aldehyde-induced DNA crosslinks, repair is activated by the same factors, but without base excision and gap filling.

    • Marco Saponaro

  • News & Views |

    The nuclear envelope participates in the spatial regulation of DNA repair, but the mechanisms behind this are unclear. A study now reports that a nuclear envelope-localized nuclease, NUMEN/ENDOD1, guides the choice of DNA-repair pathway by inhibiting the resection of DNA ends and aberrant recombination, ensuring genome stability.

    • Sylvain Audibert
    •  & Evi Soutoglou

  • News & Views |

    Cellular senescence induced by DNA replication and telomere attrition contributes to organ dysfunction, inflammation and impaired immunity. A study reveals that antigen-presenting cells provide telomeric DNA to CD4+ T cells in synaptic contact, which enables the suspension of senescence, T cell expansion and long-lived immunity.

    • Anna Carey
    • , Laura Niedernhofer
    •  & Christina Camell

  • Article |

    Das et al. show that chromatin incorporation of histone H3 variant CENP-A at centromeres in early mouse embryos depends on the maternally provided Cenpa mRNA pool and on repetitive centromere satellite DNA, rather than pre-existing CENP-A nucleosomes.

    • Arunika Das
    • , Aiko Iwata-Otsubo
    •  & Michael A. Lampson

  • Letter
    | Open Access

    Yamazaki et al. show that cell cycle-regulated changes in hyperphosphorylation of Ki-67 and NPM1 modulate alternating charge blocks in these proteins, which defines their propensity for liquid–liquid phase separation at chromatin.

    • Hiroya Yamazaki
    • , Masatoshi Takagi
    •  & Shige H. Yoshimura

  • Review Article |

    Rossiello et al. review the contributions of telomere shortening and/or dysfunction to ageing and a broad spectrum of age-associated human diseases.

    • Francesca Rossiello
    • , Diana Jurk
    •  & Fabrizio d’Adda di Fagagna

  • News & Views |

    During the repair of DNA breaks by homologous recombination, damaged DNA seeks out intact, similar in sequence segments to use as a template. In this issue, Piazza, Bordelet and colleagues describe three-dimensional chromosome architecture remodelling during homologous recombination and show that cohesin restricts homology search in cis, independently of sister chromatid cohesion.

    • Argyris Papantonis
    •  & Vassilis Roukos

  • News & Views |

    Centromere identity must be maintained through multiple generations. A new study reveals a Constitutive Centromere-Associated Network (CCAN)-dependent retention of CENP-A, a key epigenetic mark for centromeres, in centromeres during DNA replication and a replication-dependent error correction to eliminate ectopic CENP-A in chromosome arms.

    • Masatoshi Hara
    •  & Tatsuo Fukagawa

  • News & Views |

    Micronucleation of missegregated chromatin can lead to substantial chromosome rearrangements via chromothripsis. However, the molecular details of micronucleus-based chromothripsis are still unclear. Now, an elegant system that specifically induces missegregation of the Y chromosome provides insight into this process, including a role for non-homologous end joining.

    • Emily M. Hatch

  • Article |

    Durocher and colleagues find that in budding yeast, the movement of chromosomes induced by DNA breaks is due to the loss of attachment of kinetochores to spindle pole bodies and of telomeres to the nuclear periphery, and may promote checkpoint arrest.

    • Jonathan Strecker
    • , Gagan D. Gupta
    •  & Daniel Durocher

  • News & Views |

    Mitotic chromosome condensation has fascinated biologists since Flemming's early illustrations of mitosis in the late nineteenth century. Now — 130 years later — chromatid condensation is reconstituted in vitro with the minimum components. The results are remarkably and beautifully simple, requiring only core histones, three histone chaperones, topoisomerase II and condensin I.

    • Jason C. Bell
    •  & Aaron F. Straight

  • Review Article |

    Repair of a chromosome break can result in part of a chromosome attaching to a different chromosome, causing gene deregulation and disease. Roukos and Misteli discuss the spatial aspect of chromosome translocation and the role of DNA repair pathways in this process.

    • Vassilis Roukos
    •  & Tom Misteli

  • News & Views |

    Faithful genome segregation depends on the functions of the eukaryotic centromere, which is characterized by the histone variant CENP-A. Gene replacement in human cells and fission yeast has now been used to show how CENP-A biochemically encodes centromere identity, as well as reveal an unexpected role for CENP-B in centromere function.

    • Bradley T. French
    •  & Aaron F. Straight

  • Article |

    The centromere-specific histone H3 variant CENP-A is sufficient for centromere specification in many species. Cleveland and colleagues have used an elegant gene targeting strategy to define a two-step mechanism for how CENP-A acts in centromere targeting and kinetochore assembly and function.

    • Daniele Fachinetti
    • , H. Diego Folco
    •  & Don W. Cleveland

  • Article |

    Chromosome segregation requires the capture of kinetochores by microtubules, a process that in yeast mitosis is facilitated by kinetochores being tethered to spindle poles. Sato and colleagues find that in meiosis I, when kinetochores are not tethered to poles, a microtubule array associated with TACC (Alp7) and TOG proteins (Alp14 and Dis1) retrieves kinetochores in a Polo-kinase-dependent manner.

    • Yasutaka Kakui
    • , Masamitsu Sato
    •  & Masayuki Yamamoto

  • Article |

    Centrosome amplification is often seen in cancer cells and may cause aneuploidy. Basto and colleagues unexpectedly find that centrosome amplification (induced by Plk4 overexpression) in the mouse central nervous system causes microcephaly due to depletion of the neural stem cell pool through aneuploidy and cell death.

    • Véronique Marthiens
    • , Maria A. Rujano
    •  & Renata Basto

  • Article |

    Both telomerase activity and NF-κB-driven inflammation occur in tumours, and NF-κB is known to upregulate telomerase levels. Tergaonkar and colleagues now find evidence for a reciprocal direct regulation of NF-κB-dependent gene transcription by telomerase, through an interaction between telomerase and the NF-κB p65 subunit.

    • Arkasubhra Ghosh
    • , Gaye Saginc
    •  & Vinay Tergaonkar

  • News & Views |

    The diverse nature of eukaryotic centromere structure has led to a prevailing view that the kinetochore–chromatin interface is fundamentally different in distinct species. Two studies now challenge this dogma with the identification of budding yeast homologues of the vertebrate centromere DNA-binding proteins CENP-T and CENP-W.

    • Karen E. Gascoigne
    •  & Iain M. Cheeseman

  • Article |

    Multi-protein kinetochore complexes bind to the centromeric region of chromosomes to ensure accurate spindle attachment and chromosome segregation, although centromere organization differs widely between species. Westermann and colleagues now identify the budding yeast protein Cnn1 as the orthologue of mammalian CENP-T. They show that it binds to the Ndc80 kinetochore complex and functions in chromosome segregation, illustrating a conserved role for this protein.

    • Alexander Schleiffer
    • , Michael Maier
    •  & Stefan Westermann

  • Article |

    Repair of double-strand breaks (DSBs) by homologous recombination is thought to involve the movement of damaged chromosomes to facilitate pairing of homologues. Rothstein and colleagues have now followed the movement of damaged loci in diploid yeast by time-lapse microscopy, revealing the dynamics of damage-induced movement and the requirement for repair proteins in this process.

    • Judith Miné-Hattab
    •  & Rodney Rothstein

  • News & Views |

    Cellular senescence is a stable proliferation arrest induced by triggers such as short telomeres, activated oncogenes and genotoxic stress. Two studies show that cellular senescence induced by genotoxic stress depends on chronic DNA-damage signalling from irreparable damage to telomeres. Hence, dysfunctional or damaged telomeres are the initiators of multiple modes of senescence.

    • John van Tuyn
    •  & Peter D. Adams

  • Article |

    D’Adda di Fagagna and colleagues observe that, after genotoxic treatment of cells and mice, unrepaired DNA-damage foci and DNA-damage signalling persist at telomeres. They show that introducing the telomeric protein TRF2 near a double-strand break elsewhere on the chromosomes prevents repair. Unrepaired foci are also observed at telomeres of ageing animals, suggesting a role for TRF2 in senescence establishment.

    • Marzia Fumagalli
    • , Francesca Rossiello
    •  & Fabrizio d’Adda di Fagagna

  • Letter |

    The E3 ligase RNF8 is recruited to double-strand breaks in DNA to promote repair. Jacobs and colleagues discovered that RNF8 also goes to unprotected telomeres, where it mediates non-homologous end-joining of chromosome ends and contributes to telomere-induced genomic instability.

    • Marieke H. Peuscher
    •  & Jacqueline J. L. Jacobs

  • News & Views |

    The histone H3 variant CENP-A defines centromeric chromatin, but it has been unclear how CENP-A is stably maintained at centromeres. It has now been shown that the CENP-A licensing factor HsKNL2 and the small GTPases activating protein MgcRacGAP cooperate to promote the stability of newly loaded CENP-A at centromeres.

    • Lisa Prendergast
    •  & Kevin F. Sullivan

  • Perspective |

    It has been proposed that the spindle assembly checkpoint detects both unattached kinetochores and lack of tension between sister kinetochores when sister chromatids are not attached to opposite spindle poles. However, here we argue that there is only one signal — whether kinetochores are attached to microtubules or not — and this has implications for our understanding of both chromosome segregation and the control of genomic stability.

    • Alexey Khodjakov
    •  & Jonathon Pines

  • News & Views |

    Kinetochores link microtubules to DNA and provide force critical for chromosome segregation in mitosis. New data show that kinetochores are not necessary for acentrosomal meiotic chromosome segregation in Caenorhabditis elegans. Instead, CLS-2 (CLASP) generates a mid-zone bundle of microtubules that are suggested to act in pushing the chromosomes apart.

    • Xue Han
    •  & Martin Srayko

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