Apoptosis articles within Nature

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  • Article |

    Caspase-7 cleaves and activates acid sphingomyelinase (ASM), which promotes the repair of gasdermin pores and thereby delays pore-driven lysis to allow other processes such as extrusion or apoptosis to occur before cell death.

    • Kengo Nozaki
    • , Vivien I. Maltez
    •  & Edward A. Miao

  • Letter |

    The stretch-activated channel Piezo1 controls homeostatic epithelial cell numbers by activating cells to divide rapidly when under stretch strain from low density, and by activating cells to extrude and die when cells are under crowding strain.

    • S. A. Gudipaty
    • , J. Lindblom
    •  & J. Rosenblatt

  • Letter |

    Wild-type Drosophila epithelial cells outcompete proto-oncogenic cells through translocation of the ligand Sas to the wild-type–tumour cell interface, where it binds the PTP10D receptor of the tumour cell, initiating pro-apoptotic signalling.

    • Masatoshi Yamamoto
    • , Shizue Ohsawa
    •  & Tatsushi Igaki

  • Letter |

    Apoptotic cell death is required for morphogenesis of the developing leg joint of fruitflies; using this model system, the authors show here that within apoptotic cells a transient pulling force exerted through a highly dynamic apico-basal myosin II cable-like structure acts as a mechanical signal to increase tissue tension and modify tissue shape.

    • Bruno Monier
    • , Melanie Gettings
    •  & Magali Suzanne

  • Letter |

    Unlike the limited post-injury neuronal regeneration in humans, severed axons in C. elegans can regenerate through a cellular fusion mechanism; this study identifies the molecular basis for this process which includes phosphatidylserine recognition and a role for specific molecules that also act in apoptosis.

    • Brent Neumann
    • , Sean Coakley
    •  & Massimo A. Hilliard

  • Article |

    The pannexin 1 channel on the plasma membrane of apoptotic cells mediates the release of find-me molecular signals to attract phagocytic cells for clearance of the apoptotic cells; here the quinolone antibiotic trovafloxacin is identified as a direct inhibitor of pannexin 1, which results in dysregulated fragmentation of apoptotic cells and may partly explain quinolone toxicity.

    • Ivan K. H. Poon
    • , Yu-Hsin Chiu
    •  & Kodi S. Ravichandran

  • Letter |

    Several death-domain-containing proteins are directly inactivated by the enteropathogenic Escherichia coli type III secretion system effector NleB; NleB functions as an N-acetylglucosamine transferase that modifies a conserved death domain arginine residue, blocking the receptor–adapter interaction.

    • Shan Li
    • , Li Zhang
    •  & Feng Shao

  • Letter |

    A mouse model is developed in which the pro-apoptotic activity of DCC is silenced and the mice are more prone to intestinal tumour progression, giving insight into the role of DCC in human colorectal cancer.

    • Marie Castets
    • , Laura Broutier
    •  & Patrick Mehlen

  • Letter |

    The ubiquitin conjugation system regulates the canonical NF-κB activation pathway, which mediates immune responses. Linear polyubiquitin chains—in which the C terminal glycine of ubiquitin is conjugated to the α-amino group of the amino-terminal methionine of another ubiquitin—are generated by a unique ubiquitin ligase complex called linear ubiquitin chain assembly complex (LUBAC) composed of two RING domain proteins called HOIL-1 and HOIP. This is one of three complementary studies identifying a novel component of the LUBAC complex called SHARPIN, which is recruited to receptor signalling complexes (RSCs) that form after TNF and CD40L stimulation. The LUBAC complex containing SHARPIN stimulates the formation of linear ubiquitin chains in vitro and in vivo and is required for the activation of NF-κB signalling.

    • Fumiyo Ikeda
    • , Yonathan Lissanu Deribe
    •  & Ivan Dikic

  • News & Views |

    Apoptotic cell death is essential for the development of multicellular organisms. Paradoxically, three proteins instrumental in apoptosis also collaborate to preserve life by preventing necrotic cell death. See Letters p.363, p.368 & p.373

    • Marcus E. Peter

  • Letter |

    Apoptotic cells discharge ATP and UTP, which act as 'find-me' signals for phagocytes that in turn engulf dying cells before potentially harmful cellular contents are released. These authors show that the release of ATP and UTP is exclusively by means of the plasma membrane channel pannexin 1, which is opened specifically by caspase activity.

    • Faraaz B. Chekeni
    • , Michael R. Elliott
    •  & Kodi S. Ravichandran

  • Letter |

    Cell death by apoptosis is crucial for tissue development and function, and occurs throughout life. Apoptotic cells must be cleared by phagocytic cells, but the mechanisms that regulate cell clearance in vivo remain unclear. Here, a conserved engulfment protein, ELMO1, is shown to be required for the phagocytic clearance of apoptotic germ cells by Sertoli cells in mouse testes. The findings make a compelling case for the relationship between engulfment and tissue homeostasis in vivo.

    • Michael R. Elliott
    • , Shuqiu Zheng
    •  & Kodi S. Ravichandran

  • Letter |

    One model for cancer development posits that the proliferating cells in a tumour can become 'addicted' to activating mutations in an oncogene. With the realization that certain microRNAs promote tumorigenesis, it has been proposed that tumours may also become dependent on such 'oncomiRs'. Here, evidence is provided that the gene encoding microRNA-21 is an oncogene, and that in its absence, tumours undergo apoptosis and regress. Thus tumours can indeed become addicted to oncomiRs.

    • Pedro P. Medina
    • , Mona Nolde
    •  & Frank J. Slack

  • Article |

    When oxygen levels drop in a tissue, the transcription factor hypoxia-inducible factor (HIF) is activated to regulate the cellular response. HIFα levels are increased in most solid tumours and this correlates with a poor prognosis, for unknown reasons. Here it is shown that HIF-1, the worm version of HIFα, protects germ cells from DNA-damage-induced death. It does this remotely, by increasing the production of the TYR-2 protein in distant neurons. Inhibiting a human TYR-2 homologue promotes apoptosis in melanoma cells.

    • Ataman Sendoel
    • , Ines Kohler
    •  & Michael O. Hengartner

  • News & Views |

    In worms, neurons respond to low levels of environmental oxygen in a way that protects distant tissues from stress-induced cell death. The molecules that mediate this cell-cell signalling may be targets for cancer treatment.

    • Jo Anne Powell-Coffman
    •  & Clark R. Coffman

  • News & Views |

    Paradoxically, the CD95 receptor, a potent inducer of apoptotic cell death, is expressed on most tumour cells. Surprisingly, it turns out to be an important promoter of various cancers.

    • Douglas R. Green

  • Letter |

    Cancer 'chemoprevention' uses substances to reverse, suppress or prevent the initial phase of carcinogenesis or the progression of neoplastic cells to cancer cells. Here it is shown that treatment with TRAIL proteins and all-trans-retinyl acetate can cause the death, in vitro and in vivo, of premalignant cells deficient in the adenomatous polyposis coli gene. Normal cells are unaffected. Selectively eliminating premalignant tumour cells in this way is thus an effective method for chemoprevention.

    • Ling Zhang
    • , Xiaoyang Ren
    •  & Xiangwei Wu

  • Letter |

    In multicellular organisms, apoptotic cells are removed from tissues by phagocytes, which recognize and engulf the dying cells. The molecular mechanisms underlying the subsequent degradation of the cells have been unclear. Here, two evolutionarily conserved genes have been identified that are required for such processing in Caenorhabditis elegans and mammals. An understanding of these events could lead to new treatments for diseases associated with poor engulfment and destruction of dying cells.

    • Jason M. Kinchen
    •  & Kodi S. Ravichandran

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