Stress signalling articles within Nature Communications

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  • Article
    | Open Access

    The cellular mechanisms underlying autophagy are conserved; however it is unclear how they evolved in higher organisms. Here the authors identify two oxidation-sensitive cysteine residues in the autophagy receptor SQSTM1/p62 in vertebrates which allow activation of pro-survival autophagy in stress conditions.

    • Bernadette Carroll
    • , Elsje G. Otten
    •  & Viktor I. Korolchuk

  • Article
    | Open Access

    p53 is a pivotal tumour suppressor that is activated by various cellular stress inducers. Here, the authors show that peptidase D (PEPD) promotes the growth of cancer cells by suppressing p53 and that the complex PEPD-p53 is critical for robust p53 activation in response to stress signals.

    • Lu Yang
    • , Yun Li
    •  & Yuesheng Zhang

  • Article
    | Open Access

    OmpR is a transcription factor activated in acid and osmotic responses of Gram-negative bacteria, leading to acidification of the bacterial cytoplasm. Here the authors use single cell pH imaging to define the role of OmpR-regulated genes in the acidification response to osmotic and acid stress of Salmonella and E. coli.

    • Smarajit Chakraborty
    • , Ricksen S. Winardhi
    •  & Linda J. Kenney

  • Article
    | Open Access

    Cysteine hydropersulfides (CysSSH) are believed to have a cellular redox protective role. Here the authors show that these species can be produced from L-cysteine by cysteinyl-tRNA synthetases and that these enzymes are also involved in mitochondrial biogenesis and bioenergetics regulation.

    • Takaaki Akaike
    • , Tomoaki Ida
    •  & Hozumi Motohashi

  • Article
    | Open Access

    AMPK is involved in sensing of metabolic stress. The authors show that the autophagy initiator ULK1 phosphorylates β1-Ser108 on the regulatory β1-subunit, sensitizing AMPK to allosteric drugs, and activates signaling pathways that appear independent of Thr172 phosphorylation in the kinase activation loop.

    • Toby A. Dite
    • , Naomi X. Y. Ling
    •  & Jonathan S. Oakhill

  • Article
    | Open Access

    Heat Shock Factor 1 (HSF1) is a regulator of stress-induced transcription. Here, the authors investigate changes to transcription and chromatin organization upon stress and find that activated HSF1 binds to transcription-primed promoters and enhancers, and to CTCF occupied, untranscribed chromatin.

    • Anniina Vihervaara
    • , Dig Bijay Mahat
    •  & Lea Sistonen

  • Article
    | Open Access

    Senescent and injured cells affect tissue functions and can drive tumorigenesis. Thus, efficient elimination of these cells is pivotal for tissue integrity. Here Miyamuraet al. show that YAP acts as a cellular stress sensor and promotes the elimination of damaged cells to maintain tissue homeostasis.

    • Norio Miyamura
    • , Shoji Hata
    •  & Hiroshi Nishina

  • Article
    | Open Access

    cAMP/PKA signalling plays important roles in physiology, but there are a lack of tools to spatially distinguish cAMP. Here the authors present a FRET-based cAMP biosensor they call CUTie that can directly compare cAMP signals at multiple subcellular sites and detect nanoscale heterogeneity in cAMP in cardiac myocytes.

    • Nicoletta C. Surdo
    • , Marco Berrera
    •  & Manuela Zaccolo

  • Article
    | Open Access

    While yeasts lack dedicated photoreceptors, they nonetheless possess metabolic rhythms responsive to light. Here the authors find that light signalling in budding yeast involves the production of H2O2, which in turn regulates protein kinase A through a peroxiredoxin-thioredoxin redox relay.

    • Kristofer Bodvard
    • , Ken Peeters
    •  & Mikael Molin

  • 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

    Environmental stress causes epigenetic changes but it is unclear if such changes are transgenerational. Here, the authors show that inC. elegans, increased resistance to oxidative stress and proteotoxicity in the parental generation and linked epigenetic changes are transmitted to subsequent generations.

    • Saya Kishimoto
    • , Masaharu Uno
    •  & Eisuke Nishida

  • Article
    | Open Access

    Nucleoplasmic translocation of NPM1 is integral to nucleolar stress sensing. Here, the authors show that nucleolar oxidation is a general cellular stress response, and that oxidation-related glutathionylation of NPM1 triggers its translocation and facilitates p53 activation.

    • Kai Yang
    • , Ming Wang
    •  & Jing Yi

  • Article
    | Open Access

    The chaperone Hsp70 has a dual role, promoting both protein refolding and protein degradation. Seo and Park et al. show that Hsp70 acetylation enhances protein refolding after stress, and that subsequent deacetylation progressively promotes ubiquitin ligase binding and protein degradation.

    • Ji Hae Seo
    • , Ji-Hyeon Park
    •  & Kyu-Won Kim

  • Article
    | Open Access

    The ‘genome guardian’ p53 has a well-established role in suppressing tumour development after DNA damage. Here the authors show that expression of the ubiquitin-like protein ISG15 is regulated by p53 which in turn is modified by ISG15 to enhance binding to target gene promoters.

    • Jong Ho Park
    • , Seung Wook Yang
    •  & Chin Ha Chung

  • Article
    | Open Access

    Oxaliplatin resistance in colorectal cancers is a major clinical problem, and predictive markers are urgently needed. Here, the authors show that miR-625-3pexpression reduces the sensitivity of colorectal cancer cells to oxaliplatin by targeting the kinase MAP2K6, an activator of the MAPK14 pathway.

    • Mads Heilskov Rasmussen
    • , Iben Lyskjær
    •  & Claus Lindbjerg Andersen

  • Article
    | Open Access

    Stress granules that form in response to stress contain translationally stalled mRNPs and play important roles in cellular homeostasis. Here the authors implicate SRSF3 neddylation as an important factor in the formation of stress granules in response to arsenite exposure.

    • Aravinth Kumar Jayabalan
    • , Anthony Sanchez
    •  & Takbum Ohn

  • Article
    | Open Access

    Cancer cells under stress use acetate to maintain the acetyl-CoA pool and fuel lipid biosynthesis. Here, the authors show that acetate also promotes de novo lipid synthesis by increasing histone acetylation at the promoters of lipogenic enzymes ACACA and FASN, thus inducing their expression.

    • Xue Gao
    • , Shu-Hai Lin
    •  & Qun-Ying Lei

  • Article
    | Open Access

    The nucleolus is a specialized functional domain of the nucleus where ribosome biogenesis is initiated and also implicated in a p53-dependent anti-tumor surveillance. Here the authors use a quantitative imaging approach to detail the role of each ribosomal protein on the structural integrity of the nucleolus and p53 homeostasis.

    • Emilien Nicolas
    • , Pascaline Parisot
    •  & Denis L. J. Lafontaine

  • Article
    | Open Access

    Visceral and subcutaneous fat are associated with different metabolic risk, but mediators of such depot specific effects are not very well known. Here the authors identify the transcriptional regulator, TRIP-Br2, as a regulator of endoplasmic reticulum (ER) stress-induced inflammatory responses specifically in visceral fat.

    • Guifen Qiang
    • , Hyerim Whang Kong
    •  & Chong Wee Liew

  • Article
    | Open Access

    In response to amino acid and growth factor removal the TSC1/2 complex translocates to the lysosome to inactivate mTOR and inhibit cell growth. Here, the authors have shown that other cellular stresses also trigger this translocation to the lysosome suggesting that this is a universal mechanism in the stress response.

    • Constantinos Demetriades
    • , Monika Plescher
    •  & Aurelio A. Teleman

  • Article
    | Open Access

    Proteinuria promotes chronic kidney disease progression. Karoui et al. show that proteinuria stimulates overexpression of iron transporting protein lipocalin-2 via Ca2+release-induced ER stress, which leads to tubular apoptosis, and that inhibition of this pathway by PBA delays renal deterioration in proteinuric mice.

    • Khalil El Karoui
    • , Amandine Viau
    •  & Fabiola Terzi

  • Article
    | Open Access

    Cytoplasmic stress granules (SG) are intracellular aggregates that suppress translation and sequester apoptosis regulatory factors. Here the authors show that reactive oxygen species oxidise the SG-nucleating protein TIA1, preventing SG formation and promoting apoptosis in the presence of additional stress.

    • Kyoko Arimoto-Matsuzaki
    • , Haruo Saito
    •  & Mutsuhiro Takekawa

  • Article
    | Open Access

    Chemotherapeutic agents elicit ER and oxidative stress as part of their mode of action. Here the authors show that chemotherapy and ER stress trigger MGST2-based biosynthesis of LTC4, whose inhibition abolishes chemotherapy- and ER stress-triggered oxidative stress and DNA damage, resulting in the attenuation of cell death.

    • Efrat Dvash
    • , Michal Har-Tal
    •  & Menachem Rubinstein

  • Article
    | Open Access

    Centriolar satellites (CS) dynamically remodel in response to cellular stress. Here the authors describe a mechanism for stress-mediated remodelling, whereby CEP131 is phosphorylated downstream of p38, creating binding sites for 14-3-3 that lead to the sequestration of CEP131 in the cytoplasm and disassembly of CS.

    • Maxim A. X. Tollenaere
    • , Bine H. Villumsen
    •  & Simon Bekker-Jensen

  • Article |

    Transcription, like DNA replication, is an error-prone process. Vermulst et al.show that transcription errors increase with age in yeast, and find that prematurely increasing the error rate overwhelms the proteotoxic stress response, allowing aggregation-prone proteins to escape protein quality control.

    • Marc Vermulst
    • , Ashley S. Denney
    •  & Dorothy A. Erie

  • Article
    | Open Access

    ER stress is associated with the pathogenesis of chronic kidney disease (CKD) and new CKD therapies are needed. Here the authors show that expression of Rtn1 can control severity of renal disease and that inhibition of its expression can attenuate ER stress and CKD.

    • Ying Fan
    • , Wenzhen Xiao
    •  & John C. He

  • Article
    | Open Access

    Autophagy is a catabolic process whereby cellular components are degraded by the autophagosome, but the role of the actin cytoskeleton is not clear. Here Coutts and La Thangue show that the actin nucleator JMY is recruited to the autophagosome via binding LC3, and promotes actin nucleation that is required for autophagosome maturation.

    • Amanda S. Coutts
    •  & Nicholas B. La Thangue

  • Article
    | Open Access

    KDEL receptors are known to be involved in retrotransporting chaperones to the endoplasmic reticulum from the Golgi complex. Here the authors unravel a role of KDEL receptor 1 in regulating integrated stress responses in naïve T cells through its association with protein phosphatase 1.

    • Daisuke Kamimura
    • , Kokichi Katsunuma
    •  & Masaaki Murakami

  • Article
    | Open Access

    Stress-induced macroautophagy is initiated by the induction of reactive oxygen species (ROS). Here Qiao et al.show that the mTOR inhibitor REDD1 in a complex with pro-oxidant protein TXNIP induces ROS formation, leading to ATG4B suppression and autophagy activation in a largely mTOR-independent manner.

    • Shuxi Qiao
    • , Michael Dennis
    •  & Leif W. Ellisen

  • Article |

    ATF3, a stress mediator, regulates the activities of key cancer-associated proteins by altering their interactions with DNA or other proteins. Here, the authors report that ATF3 also regulates Tip60, a protein acetyltransferase, by promoting its enzymatic activity and increasing its protein stability.

    • Hongmei Cui
    • , Mingxiong Guo
    •  & Chunhong Yan

  • Article
    | Open Access

    FoxO transcription factors promote muscle atrophy in response to stresses such as low nutrient availability. By generating muscle-specific FoxO triple-knockout mice, Milan et al.identify mechanisms by which the FoxO transcriptional network coordinates autophagic and proteasomal protein degradation.

    • Giulia Milan
    • , Vanina Romanello
    •  & Marco Sandri

  • Article
    | Open Access

    Heat shock induces proteotoxic stress, and the cellular response is mediated by heat-shock factor 1 (HSF1). Here, Tan et al.show that following heat shock, mitochondrial SSBP1 translocates to the nucleus and binds HSF1 to enhance the expression of chaperones and support the maintenance of mitochondrial function.

    • Ke Tan
    • , Mitsuaki Fujimoto
    •  & Akira Nakai

  • Article |

    Anticancer treatments are tested in mice housed below thermoneutrality which represents chronic cold-stress. Here Eng et al. show that these mice have activated stress responses leading to therapeutic resistance and that inhibiting adrenergic signaling increases efficacy of anticancer therapies.

    • Jason W.-L. Eng
    • , Chelsey B. Reed
    •  & Bonnie L. Hylander

  • Article |

    Studies of cellular mechanotransduction commonly use elastic substrates, whereas biological substrates are viscoelastic, exhibiting stress relaxation. Here, the authors show through computational modelling and experiments that viscoelastic substrates can stimulate cell spreading to a greater extent than purely elastic substrates with the same initial stiffness.

    • Ovijit Chaudhuri
    • , Luo Gu
    •  & David J. Mooney

  • Article |

    Increasing the activity of the proteasome can prevent the accumulation of protein aggregates within the cell. Han et al.show that nanoparticle-mediated delivery of purified proteasomes to cells reduces proteotoxic stress resulting from tau overexpression, and prevents to accumulation of tau aggregates.

    • Dong Hoon Han
    • , Hee-Kyung Na
    •  & Min Jae Lee

  • Article |

    Focal adhesion kinase (FAK) is a scaffold and tyrosine kinase protein, critical for proper cardiac function under stress conditions. Here the authors show that the small heat–shock protein αB-crystallin interacts with FAK and protects it from calpain-mediated proteolysis in stressed rat cardiomyocytes.

    • Michelle B. M. Pereira
    • , Aline M. Santos
    •  & Kleber G. Franchini

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