Chromosomes articles within Nature

Featured

  • Article |

    A chromosome conformation capture method in which single cells are first imaged and then processed enables intact genome folding to be studied at a scale of 100 kb, validated, and analysed to generate hypotheses about 3D genomic interactions and organisation.

    • Tim J. Stevens
    • , David Lando
    •  & Ernest D. Laue

  • Letter |

    A conformation capture sequencing method is developed to link multiple genomic loci into three-dimensional proximity chains called chromosomal walks (C-walks), adding to our understanding of how higher-order chromosomal structures participate in genome regulation.

    • Pedro Olivares-Chauvet
    • , Zohar Mukamel
    •  & Amos Tanay

  • Letter |

    During cell division, chromosomes are maintained as individual units; this process is shown to be mediated by the cell proliferation marker Ki-67, which has biophysical properties similar to those of surfactants.

    • Sara Cuylen
    • , Claudia Blaukopf
    •  & Daniel W. Gerlich

  • Letter |

    Using super-resolution imaging to directly observe the three-dimensional organization of Drosophila chromatin at a scale spanning sizes from individual genes to entire gene regulatory domains, the authors find that transcriptionally active, inactive and Polycomb-repressed chromatin states each have a distinct spatial organisation.

    • Alistair N. Boettiger
    • , Bogdan Bintu
    •  & Xiaowei Zhuang

  • Letter |

    Genome-wide chromosome conformation capture analysis in C. elegans reveals that the dosage compensation complex, a condensin complex, remodels the X chromosomes of hermaphrodites into a sex-specific topology distinct from autosomes while regulating gene expression chromosome-wide.

    • Emily Crane
    • , Qian Bian
    •  & Barbara J. Meyer

  • Letter |

    Next-generation sequencing technology is used to show that the error-prone polymerase θ (Polθ) is needed to promote alternative non-homologous end joining at telomeres, and during chromosomal translocations, while counteracting homologous recombination; inhibition of Polθ represents a potential therapeutic strategy for tumours that have mutations in homology-directed repair genes.

    • Pedro A. Mateos-Gomez
    • , Fade Gong
    •  & Agnel Sfeir

  • Article |

    The long elusive mammalian meiosis-specific kinetochore factor has been identified in mice; MEIKIN—which plays an equivalent role to the yeast proteins Spo13 and Moa1—ensures mono-orientation, protects sister chromatid cohesion and recruits the kinase PLK1 to the kinetochores.

    • Jihye Kim
    • , Kei-ichiro Ishiguro
    •  & Yoshinori Watanabe

  • Letter
    | Open Access

    A study of DNA replication timing in mouse and human cells reveals that replication domains (domains of the genome which replicate at the same time) share a correlation with topologically associating domains; these results reconcile cell-type-specific sub-nuclear compartmentalization with developmentally stable chromosome domains and offer a unified model for large scale chromosome structure and function.

    • Benjamin D. Pope
    • , Tyrone Ryba
    •  & David M. Gilbert

  • Letter |

    Genome-wide chromatin conformation capture (Hi-C) is used to investigate three-dimensional genome organization in Schizosaccharomyces pombe; small domains of chromatin interact locally on chromosome arms to form globules, which depend on cohesin but not heterochromatin for formation, and heterochromatin at centromeres and telomeres provides crucial structural constraints to shape genome architecture.

    • Takeshi Mizuguchi
    • , Geoffrey Fudenberg
    •  & Shiv I. S. Grewal

  • Letter |

    Generation of human induced pluripotent stem cells from patient fibroblasts containing ring chromosomes with large deletions reveals that reprogrammed cells lose the abnormal chromosome and duplicate the wild-type homologue through compensatory uniparental disomy, suggesting that cellular reprogramming may hold potential for ‘chromosome therapy’.

    • Marina Bershteyn
    • , Yohei Hayashi
    •  & Anthony Wynshaw-Boris

  • Letter |

    Meiotic crossover regulation is proposed to operate as a self-limiting system in which meiotic chromosome structures create an environment that promotes crossovers, which in turn modify chromosome structures to inhibit crossover formation at additional neighbouring sites.

    • Diana E. Libuda
    • , Satoru Uzawa
    •  & Anne M. Villeneuve

  • Article |

    A novel genomic technique, single-cell Hi-C, detects thousands of simultaneous chromatin contacts in a single cell; this is used to show that individual chromosomes maintain domain organization at the megabase scale, but that chromosome structures vary from cell to cell at larger scales.

    • Takashi Nagano
    • , Yaniv Lubling
    •  & Peter Fraser

  • Letter |

    The site of collision between two chromosome replication forks can be used to reinitiate replication independent of an active origin, with potentially pathogenic effects.

    • Christian J. Rudolph
    • , Amy L. Upton
    •  & Robert G. Lloyd

  • Article |

    In vitro and in vivo, the yeast Pif1 helicase is able to unwind four-stranded G-quadruplex (G4) DNA efficiently and suppress the genomic instability that occurs at such structures; these G4 maintenance activities are conserved among evolutionarily diverse Pif1 family helicases, including human PIF1, demonstrating the importance of this activity throughout evolution.

    • Katrin Paeschke
    • , Matthew L. Bochman
    •  & Virginia A. Zakian

  • Letter |

    The current model to explain accurate chromosome segregation after DNA replication holds that kinetochore–microtubule attachments exert tension across the centromere and are stabilized by spatial separation from inner centromere-localized Aurora B; here an alternative model is presented, wherein active Aurora B produced by clustering is sufficient to ensure biorientation through a mechanism that is intrinsic to the kinetochore.

    • Christopher S. Campbell
    •  & Arshad Desai

  • Letter |

    A mechanism to explain chromosomal instability (CIN) in colorectal cancer is demonstrated; three new CIN-suppressor genes (PIGN, MEX3C and ZNF516) encoded on chromosome 18q are identified, the loss of which leads to DNA replication stress, resulting in structural and numerical chromosome segregation errors, which are shown to be identical to phenotypes seen in CIN cells.

    • Rebecca A. Burrell
    • , Sarah E. McClelland
    •  & Charles Swanton

  • Letter |

    The telomere-biding protein TRF2 is shown to protect telomeres from activating the DNA-damage response through two mechanisms: preventing the activation ATM kinase through its dimerization domain, in addition to independently suppressing signalling events occurring downstream of ATM.

    • Keiji Okamoto
    • , Cristina Bartocci
    •  & Eros Lazzerini Denchi

  • Comment |

    A stark warning about the societal costs of stress comes from links between shortened telomeres, chronic stress and disease, say Elizabeth H. Blackburn and Elissa S. Epel.

    • Elizabeth H. Blackburn
    •  & Elissa S. Epel

  • Letter |

    The human CST complex is shown to interact with the telomeric primer and the POT1–TPP1 complex to inhibit telomerase activity in late S phase, thereby keeping unrestrained telomere lengthening in check.

    • Liuh-Yow Chen
    • , Sophie Redon
    •  & Joachim Lingner

  • Letter |

    Centromere identity is thought to be epigenetically propagated by stable inheritance of nucleosomes containing the histone variant CENP-A; the authors propose a different model here in which germline transcription defines the genomic regions that exclude CENP-A incorporation during embryogenesis in the holocentric worm Caenorhabditis elegans.

    • Reto Gassmann
    • , Andreas Rechtsteiner
    •  & Arshad Desai

  • Letter |

    The male-specific region of rhesus macaque and human Y chromosome (MSY) are sequenced and compared to the human MSY, showing that during the last 25 million years MSY gene loss in the rhesus and human lineages was limited to the youngest stratum (stratum 5), whereas gene loss in the older strata ceased more than 25 million years ago.

    • Jennifer F. Hughes
    • , Helen Skaletsky
    •  & David C. Page

  • Outlook |

    Elizabeth Blackburn gave the first lecture at the 2011 Lindau meeting, describing her Nobel prizewinning work on telomeres. These chromosomal caps are known to play a role in cancer and are implicated in ageing — but their full biological utility remains a mystery.

    • Michael Eisenstein

  • News Q&A |

    Telomeres may not predict how long we'll live, but they can still revolutionise medicine, says Nobel laureate Elizabeth Blackburn.

    • Jo Marchant

  • Letter |

    Two single-stranded DNA-binding proteins, POT1 and RPA, associate with telomeres. Binding of RPA to telomeres can activate a DNA damage response, so it was previously proposed that POT1 binds telomeres to prevent RPA association. Here, it is found that POT1–TPP1 cannot prevent RPA binding, and hnRNPA1 is identified as having this activity instead. In addition, it is shown that TERRA, a telomere-associated RNA, displaces hnRNPA1 and promotes POT1 binding after S phase, when replication is completed.

    • Rachel Litman Flynn
    • , Richard C. Centore
    •  & Lee Zou

  • Technology Feature |

    A DNA sequence isn't enough; to understand the workings of the genome, we must study chromosome structure.

    • Monya Baker

  • Letter |

    Here it is shown that reactivation of endogenous telomerase activity in mice extends telomeres, reduces DNA damage signalling, allows resumption of proliferation in quiescent cultures, and eliminates degenerative phenotypes across multiple organs including testes, spleens and intestines. Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease and the reversal of damage observed here support the development of regenerative strategies designed to restore telomere integrity.

    • Mariela Jaskelioff
    • , Florian L. Muller
    •  & Ronald A. DePinho

  • Letter |

    Two forms of X-chromosome inactivation ensure the selective silencing of female sex chromosomes in mouse embryos. Imprinted silencing begins with the detection of Xist RNA expression on the paternal X chromosome at about the four-cell stage of development. Later, a random form of inactivation silences either the paternal or the maternal X chromosome. Here it is shown that maternal deposits of the ubiquitin ligase Rnf12/RLIM are required for the imprinted form of X-chromosome inactivation.

    • JongDae Shin
    • , Michael Bossenz
    •  & Ingolf Bach

  • Letter |

    The ends of chromosomes, known as telomeres, look like ends generated by double-strand breaks, but if treated as such the DNA damage repair system would initiate a checkpoint response and cause telomere–telomere fusions. These authors show that telomeres lack two types of histone modification that are required for recruitment of Crb2b53BP1, without which the checkpoint cannot be activated even if other DNA damage response proteins are recruited to a Taz1-deficient telomere.

    • Tiago Carneiro
    • , Lyne Khair
    •  & Miguel Godinho Ferreira

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