Cell death articles within Nature Communications

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  • Article
    | Open Access

    RIPK3-mediated phosphorylation of the mixed lineage kinase domain-like (MLKL) pseudokinase is thought to be the trigger for MLKL activation during necroptotic signaling. Here the authors provide evidence that the transition of human MLKL from a monomeric state to a tetramer is essential for necroptosis signalling.

    • Emma J. Petrie
    • , Jarrod J. Sandow
    •  & James M. Murphy

  • Article
    | Open Access

    Carbon-nanohorns have a unique morphology and structure yet little is known about the biocompatibility. Here, the authors investigate the biocompatibility and bio-interaction of carbon nanohorns, compare them to carbon nanotubes and show the superior biocompatibility and safety of the nanohorns.

    • Bing He
    • , Yujie Shi
    •  & Qiang Zhang

  • Article
    | Open Access

    Jun N-terminal kinase (JNK) is necessary for development in tumours, indicating it may play tumour-promoting roles; however, the experimental analysis of the role of JNK in proliferation is hindered by its pro-apoptotic activity. Here the authors carry out experiments in Drosophila with genetic backgrounds that make cells refractory to apoptosis to definitely prove the JNK pathway contribution to tumorigenesis.

    • Noelia Pinal
    • , María Martín
    •  & Ginés Morata

  • Article
    | Open Access

    The inhibitor of apoptosis (IAP) protein, BRUCE is known to ubiquitinate apoptosis regulators for proteasomal degradation. Here the authors show that BRUCE provides a bridge between LAMP2 on lysosomes and Atg8 family proteins on autophagosomes to support autophagosome-lysosome fusion.

    • Petra Ebner
    • , Isabella Poetsch
    •  & Fumiyo Ikeda

  • Article
    | Open Access

    The differences in virus-host interactions resulting in distinct pathogenicity of seasonal and pandemic influenza A viruses (IAV) are not well understood. Here, the authors show that the hemagglutinin segment from pandemic, but not seasonal, IAV suppresses RIPK3-mediated dendritic cell death, thereby reducing T cell activation.

    • Boris M. Hartmann
    • , Randy A. Albrecht
    •  & Stuart C. Sealfon

  • Article
    | Open Access

    The Tetraconata concept suggests that insects and crustaceans may share evolutionarily conserved pathways. Here, the authors describe the animal tropism and structure-function relationship of nigritoxin, showing that this protein is lethal for insects and crustaceans but harmless to other animals.

    • Yannick Labreuche
    • , Sabine Chenivesse
    •  & Frédérique Le Roux

  • Article
    | Open Access

    Bcl-2 interacting killer (Bik) decreases airway epithelial hyperplasia via apoptosis mediated by calcium release from the endoplasmic reticulum (ER), but the mechanism is unclear. Here the authors show that Bik promotes Bak enrichment at the ER to tether mitochondria for efficient calcium transfer.

    • Yohannes A. Mebratu
    • , Ivan Leyva-Baca
    •  & Yohannes Tesfaigzi

  • Article
    | Open Access

    High-grade serous ovarian cancers (HGS-OvCa) frequently develop chemotherapy resistance. Here, the authors through a systematic analysis of proteomic and drug response data of 14 HGS-OvCa PDXs demonstrate that targeting apoptosis regulators can improve response of these tumors to inhibitors of the PI3K/mTOR pathway.

    • Ioannis K. Zervantonakis
    • , Claudia Iavarone
    •  & Joan S. Brugge

  • Article
    | Open Access

    Endoplasmic reticulum (ER) stress promotes cardiac dysfunction. Here the authors uncover a pathway whereby AGGF1 blocks ER stress by inhibiting ERK1/2 activation and the transcriptional repressor ZEB1, leading to induction of miR-183-5p and down-regulation of CHOP, and show that AGGF1 can effectively treat cardiac hypertrophy and heart failure.

    • Yufeng Yao
    • , Qiulun Lu
    •  & Qing K. Wang

  • Article
    | Open Access

    Notch signalling is deregulated in several cancers; therefore, strategies targeting this pathway are currently being explored. Here the authors report a pro-apoptotic function of Notch3 in endothelial cells; consequently, when Notch3 is silenced in stroma cells, tumour growth and angiogenesis are increased.

    • Shuheng Lin
    • , Ana Negulescu
    •  & Patrick Mehlen

  • Article
    | Open Access

    Small cell lung cancer cells (SCLC) are differentially sensitive to inhibitors of the BCL-2 family. Here the authors analyse the response to BH3 mimetics in SCLC, delineate patterns of expression of apoptotic proteins correlated with differential sensitivities and demonstrate a synergistic anti-tumour activity between ABT-199 and anthracyclines or CDK9 inhibitors.

    • Akane Inoue-Yamauchi
    • , Paul S. Jeng
    •  & Emily H. Cheng

  • Article
    | Open Access

    The permeabilization of the mitochondrial outer membrane to induce apoptosis is regulated by complex interactions between Bcl-2 family members. Here the authors develop a quantitative interactome of a membrane Bcl-2 network and identify a hierarchy of protein complexes in apoptosis induction.

    • Stephanie Bleicken
    • , Annika Hantusch
    •  & Ana J. Garcia-Saez

  • Article
    | Open Access

    Spatiotemporal control of intracellular molecular self-assembly holds promise for therapeutic applications. Here the authors develop a peptide consisting of a phenylalanine dipeptide with a mitochondrial targeting moiety to form self-assembling fibrous nanostructures within mitochondria, leading to apoptosis.

    • M. T. Jeena
    • , L. Palanikumar
    •  & Ja-Hyoung Ryu

  • Article
    | Open Access

    Investigating cell death in living organisms is hampered by a lack of techniques to induce apoptosis with spatial and temporal precision without collateral damage. Here the authors develop two-photon chemical apoptotic targeted ablation (2Phatal), allowing studies of apoptosis and its functional consequencesin vivo.

    • Robert A. Hill
    • , Eyiyemisi C. Damisah
    •  & Jaime Grutzendler

  • Article
    | Open Access

    The exocyst delivers basolateral proteins from the secretory pathway to the plasma membrane of epithelial cells close to tight junctions. Here the authors show that Par3 acts as a docking site for the exocyst to regulate polarized delivery of basolateral proteins and this is essential to prevent apoptosis and promote mammary cell survival.

    • Syed Mukhtar Ahmed
    •  & Ian G. Macara

  • Article
    | Open Access

    Chlamydiae replicate in host cells within specialised vacuoles (inclusions), which are eventually ruptured to liberate the bacteria, leading to cell lysis. Here, Kerret al. use a laser ablation technique and videomicroscopy to show that inclusion rupture triggers a necrotic pathway in the host cell.

    • Markus C. Kerr
    • , Guillermo A. Gomez
    •  & Rohan D Teasdale

  • Article
    | Open Access

    Mitochondrial reactive oxygen species (ROS) promote necroptosis and the receptor interacting protein 1 (RIP1) is a key player in this form of cell death. Here, the authors show that cysteine residues in RIP1 sense ROS and oxidation of the cysteines triggers RIP1 autophosphorylation, which promotes functional necrosome formation.

    • Yingying Zhang
    • , Sheng Sean Su
    •  & Jiahuai Han

  • Article
    | Open Access

    The kinase FAK is important for integrin signalling and promotes cell survival. Here, the authors demonstrate FAK regulates adipocyte survival, and is particularly important for maintaining insulin sensitivity during adipose tissue expansion in the context of a calorie-rich diet.

    • Cynthia T. Luk
    • , Sally Yu Shi
    •  & Minna Woo

  • Article
    | Open Access

    Inhibitors of the mTORC1 pathway are considered anti-cancer drugs. Here, the authors show that on nutrient restriction, glutaminolysis-induced activation of mTORC1 induces apoptosis via inhibiting autophagy, highlighting that under such conditions inhibition of mTORC1 results in survival of cancer cells.

    • Victor H. Villar
    • , Tra Ly Nguyen
    •  & Raúl V. Durán

  • Article
    | Open Access

    DFNA5 is related to the caspase-dependent pyroptosis inducer gasdermin D. Here the authors find that DFNA5 is cleaved by caspase 3 and show this cleavage skews cells away from apoptosis into secondary necrosis, a form of cell death characterized by membrane ballooning similar to pyroptosis.

    • Corey Rogers
    • , Teresa Fernandes-Alnemri
    •  & Emad S. Alnemri

  • Article
    | Open Access

    The tumour microenvironment can be modulated to sensitize tumours to the effects of therapy. Here the authors show that radiation induced miR-103 downregulates TREX1 in endothelial cells, decreases angiogenesis and leads to the secretion of proinflammatory mediators that reduce tumour growth.

    • RaeAnna Wilson
    • , Cristina Espinosa-Diez
    •  & Sudarshan Anand

  • Article
    | Open Access

    Diabetes is characterized by prolonged hyperglycaemia and tissue damage in pancreatic islets. Here, Brereton et al. show that chronic high glucose levels lead to glycogen accumulation in β-cells, associated with reduced autophagy, impaired metabolism, insulin granule depletion and apoptosis.

    • Melissa F. Brereton
    • , Maria Rohm
    •  & Frances M. Ashcroft

  • Article
    | Open Access

    Rela is a transcription factor shown to have seemingly contradictory roles in anabolism and catabolism of cartilage. Here the authors find that Rela prevents chondrocyte apoptosis and that homozygous knockout causes accelerated osteoarthritis in adults, whereas heterozygous knockout suppresses osteoarthritis by maintaining wild-type effects on apoptosis but inhibiting catabolic gene expression.

    • Hiroshi Kobayashi
    • , Song Ho Chang
    •  & Taku Saito

  • Article
    | Open Access

    In conditions of energy stress cells reduce transcription of ribosomal RNA (rRNA) to maintain cell survival. Here, the authors show that energy stress induces an AMPK-dependent phosphorylation of Sirt7, which promotes its ubiquitin-independent degradation by REGγ, resulting in the down-regulation of rRNA transcription and cell survival.

    • Lianhui Sun
    • , Guangjian Fan
    •  & Chuangui Wang

  • Article
    | Open Access

    Reactive oxygen species (ROS) damage cell components, necessitating their clearance through autophagy. Here, the authors show that ROS can induce autophagy by triggering TRPML1 to release Ca2+from the lysosomal lumen, in turn activating the autophagy and lysosomal biogenesis regulator TFEB.

    • Xiaoli Zhang
    • , Xiping Cheng
    •  & Haoxing Xu

  • Article
    | Open Access

    Integrins are transmembrane proteins that have important roles in cell adhesion and signalling. Here the authors design a therapeutic protein that binds integrin αvβ3, has anti-angiogenic activity, and reduces tumour growth in xenograft models, while being seemingly well tolerated.

    • Ravi Chakra Turaga
    • , Lu Yin
    •  & Zhi-Ren Liu

  • Article
    | Open Access

    While non-canonical, Atg5/Atg7-independent autophagy has been reported to occur, molecular details of alternative autophagy pathways remain unknown. Here, the authors report that the protein TRIM31 mediates alternative autophagy in intestinal cells, which protects against pathogenic bacteria.

    • Eun A. Ra
    • , Taeyun A. Lee
    •  & Boyoun Park

  • Article
    | Open Access

    The transcription factor CHOP/GADD153 regulates apoptosis in response to the unfolded protein response. Here the authors show that CHOP/GADD153 regulates the expression of miR-216b, which targets c-Jun and sensitizes cells to ER stress-dependent apoptosis.

    • Zhenhua Xu
    • , Yiwen Bu
    •  & J. Alan Diehl

  • Article
    | Open Access

    Cell competition is a quality control mechanism to eliminate unfit cells. Here the authors show that physical compaction of less fit cells surrounded by healthy neighbours leads to increased expression of tumour suppressor p53 in the compacted cells, causing cell death.

    • Laura Wagstaff
    • , Maja Goschorska
    •  & Eugenia Piddini

  • Article
    | Open Access

    Natural killer cells are a major component of the innate immune response. Here, Wang et al. show that natural killer cell development requires robust activation of autophagy at the immature stage where it acts to remove damaged mitochondria and reduces levels of reactive oxygen species.

    • Shuo Wang
    • , Pengyan Xia
    •  & Zusen Fan

  • Article
    | Open Access

    Apoptosis often requires mitochondrial outer membrane permeabilization, a process targeted by Bcl-2-binding BH3 mimetics. Here the authors describe and apply 'mito-priming', a method that allows triggering mitochondrial apoptosis in a synchronous manner, facilitating the investigation of mitochondrial apoptosis and its regulation by Bcl-2 proteins.

    • Jonathan Lopez
    • , Margaux Bessou
    •  & Stephen W. G. Tait

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