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Nature Cell Biology

Lin Li, Fan Guo, Yun Gao, Yixin Ren, Peng Yuan, Liying Yan, Rong Li, Ying Lian, Jingyun Li, Boqiang Hu, Junpeng Gao, Lu Wen, Fuchou Tang, Jie Qiao
In the version of this Resource originally published, owing to a technical error an incorrect file was used for Supplementary Table 2; this has now been replaced with the correct file.
July 18, 2018: Nature Cell Biology
Harveer Dev, Ting-Wei Will Chiang, Chloe Lescale, Inge de Krijger, Alistair G Martin, Domenic Pilger, Julia Coates, Matylda Sczaniecka-Clift, Wenming Wei, Matthias Ostermaier, Mareike Herzog, Jonathan Lam, Abigail Shea, Mukerrem Demir, Qian Wu, Fengtang Yang, Beiyuan Fu, Zhongwu Lai, Gabriel Balmus, Rimma Belotserkovskaya, Violeta Serra, Mark J O'Connor, Alejandra Bruna, Petra Beli, Luca Pellegrini, Carlos Caldas, Ludovic Deriano, Jacqueline J L Jacobs, Yaron Galanty, Stephen P Jackson
BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors. To understand the resistance mechanisms, we conducted whole-genome CRISPR-Cas9 synthetic-viability/resistance screens in BRCA1-deficient breast cancer cells treated with PARP inhibitors. We identified two previously uncharacterized proteins, C20orf196 and FAM35A, whose inactivation confers strong PARP-inhibitor resistance. Mechanistically, we show that C20orf196 and FAM35A form a complex, 'Shieldin' (SHLD1/2), with FAM35A interacting with single-stranded DNA through its C-terminal oligonucleotide/oligosaccharide-binding fold region...
July 18, 2018: Nature Cell Biology
Aline Wuidart, Alejandro Sifrim, Marco Fioramonti, Shigeru Matsumura, Audrey Brisebarre, Daniel Brown, Alessia Centonze, Anne Dannau, Christine Dubois, Alexandra Van Keymeulen, Thierry Voet, Cédric Blanpain
In the version of this Article originally published, ref. 52 was incorrectly only attributed to its corresponding author, Fre, S., and an older title was used. The correct citation should have been: Lilja, A. M. et al. Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland. Nat. Cell Biol. (2018)'. This has now been amended in all online versions of the Article.
July 17, 2018: Nature Cell Biology
Kimberly C Lin, Toshiro Moroishi, Zhipeng Meng, Han-Sol Jeong, Steven W Plouffe, Yoshitaka Sekido, Jiahuai Han, Hyun Woo Park, Kun-Liang Guan
In this Letter, the authors neglected to acknowledge funding from the Yonsei University Future-leading Research Initiative of 2017 (2017-22-007) awarded to H.W.P.
July 17, 2018: Nature Cell Biology
Swadhin Chandra Jana, Susana Mendonça, Pedro Machado, Sascha Werner, Jaqueline Rocha, António Pereira, Helder Maiato, Mónica Bettencourt-Dias
Cilia are evolutionarily conserved structures with many sensory and motility-related functions. The ciliary base, composed of the basal body and the transition zone, is critical for cilia assembly and function, but its contribution to cilia diversity remains unknown. Hence, we generated a high-resolution structural and biochemical atlas of the ciliary base of four functionally distinct neuronal and sperm cilia types within an organism, Drosophila melanogaster. We uncovered a common scaffold and diverse structures associated with different localization of 15 evolutionarily conserved components...
July 16, 2018: Nature Cell Biology
Hery Urra, Daniel R Henriquez, José Cánovas, David Villarroel-Campos, Amado Carreras-Sureda, Eduardo Pulgar, Emiliano Molina, Younis M Hazari, Celia M Limia, Sebastián Alvarez-Rojas, Ricardo Figueroa, Rene L Vidal, Diego A Rodriguez, Claudia A Rivera, Felipe A Court, Andrés Couve, Ling Qi, Eric Chevet, Ryoko Akai, Takao Iwawaki, Miguel L Concha, Álvaro Glavic, Christian Gonzalez-Billault, Claudio Hetz
Maintenance of endoplasmic reticulum (ER) proteostasis is controlled by a signalling network known as the unfolded protein response (UPR). Here, we identified filamin A as a major binding partner of the ER stress transducer IRE1α. Filamin A is an actin crosslinking factor involved in cytoskeleton remodelling. We show that IRE1α controls actin cytoskeleton dynamics and affects cell migration upstream of filamin A. The regulation of cytoskeleton dynamics by IRE1α is independent of its canonical role as a UPR mediator, serving instead as a scaffold that recruits and regulates filamin A...
July 16, 2018: Nature Cell Biology
Thach Mai, Glenn J Markov, Jennifer J Brady, Adelaida Palla, Hong Zeng, Vittorio Sebastiano, Helen M Blau
Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) is now routinely accomplished by overexpression of the four Yamanaka factors (OCT4, SOX2, KLF4, MYC (or OSKM))1 . These iPSCs can be derived from patients' somatic cells and differentiated toward diverse fates, serving as a resource for basic and translational research. However, mechanistic insights into regulators and pathways that initiate the pluripotency network remain to be resolved. In particular, naturally occurring molecules that activate endogenous OCT4 and replace exogenous OCT4 in human iPSC reprogramming have yet to be found...
July 16, 2018: Nature Cell Biology
Hamid Mohammadi, Erik Sahai
In the version of this Review originally published, owing to a technical error the text 'However, given the multitude' was incorrectly introduced after the sentence beginning 'The transition to a mesenchymal state is characterized...'. This has now been amended in all online versions of the Review.
July 10, 2018: Nature Cell Biology
Jessica B Spinelli, Marcia C Haigis
Although classically appreciated for their role as the powerhouse of the cell, the metabolic functions of mitochondria reach far beyond bioenergetics. In this Review, we discuss how mitochondria catabolize nutrients for energy, generate biosynthetic precursors for macromolecules, compartmentalize metabolites for the maintenance of redox homeostasis and function as hubs for metabolic waste management. We address the importance of these roles in both normal physiology and in disease.
June 27, 2018: Nature Cell Biology
Hamid Mohammadi, Erik Sahai
The physical characteristics of tumours are intricately linked to the tumour phenotype and difficulties during treatment. Many factors contribute to the increased stiffness of tumours; from increased matrix deposition, matrix remodelling by forces from cancer cells and stromal fibroblasts, matrix crosslinking, increased cellularity, and the build-up of both solid and interstitial pressure. Increased stiffness then feeds back to increase tumour invasiveness and reduce therapy efficacy. Increased understanding of this interplay is offering new therapeutic avenues...
June 27, 2018: Nature Cell Biology
(no author information available yet)
No abstract text is available yet for this article.
June 27, 2018: Nature Cell Biology
Javier Garcia-Bermudez, Lou Baudrier, Konnor La, Xiphias Ge Zhu, Justine Fidelin, Vladislav O Sviderskiy, Thales Papagiannakopoulos, Henrik Molina, Matija Snuderl, Caroline A Lewis, Richard L Possemato, Kıvanç Birsoy
As oxygen is essential for many metabolic pathways, tumour hypoxia may impair cancer cell proliferation1-4 . However, the limiting metabolites for proliferation under hypoxia and in tumours are unknown. Here, we assessed proliferation of a collection of cancer cells following inhibition of the mitochondrial electron transport chain (ETC), a major metabolic pathway requiring molecular oxygen 5 . Sensitivity to ETC inhibition varied across cell lines, and subsequent metabolomic analysis uncovered aspartate availability as a major determinant of sensitivity...
June 25, 2018: Nature Cell Biology
Accalia Fu, Nika N Danial
No abstract text is available yet for this article.
June 25, 2018: Nature Cell Biology
Lucas B Sullivan, Alba Luengo, Laura V Danai, Lauren N Bush, Frances F Diehl, Aaron M Hosios, Allison N Lau, Sarah Elmiligy, Scott Malstrom, Caroline A Lewis, Matthew G Vander Heiden
Defining the metabolic limitations of tumour growth will help to develop cancer therapies 1 . Cancer cells proliferate slower in tumours than in standard culture conditions, indicating that a metabolic limitation may restrict cell proliferation in vivo. Aspartate synthesis can limit cancer cell proliferation when respiration is impaired2-4 ; however, whether acquiring aspartate is endogenously limiting for tumour growth is unknown. We confirm that aspartate has poor cell permeability, which prevents environmental acquisition, whereas the related amino acid asparagine is available to cells in tumours, but cancer cells lack asparaginase activity to convert asparagine to aspartate...
June 25, 2018: Nature Cell Biology
Frédéric Lessard, Sebastian Igelmann, Christian Trahan, Geneviève Huot, Emmanuelle Saint-Germain, Lian Mignacca, Neylen Del Toro, Stéphane Lopes-Paciencia, Benjamin Le Calvé, Marinieve Montero, Xavier Deschênes-Simard, Marina Bury, Olga Moiseeva, Marie-Camille Rowell, Cornelia E Zorca, Daniel Zenklusen, Léa Brakier-Gingras, Véronique Bourdeau, Marlene Oeffinger, Gerardo Ferbeyre
Cellular senescence is a tumour suppressor programme characterized by a stable cell cycle arrest. Here we report that cellular senescence triggered by a variety of stimuli leads to diminished ribosome biogenesis and the accumulation of both rRNA precursors and ribosomal proteins. These defects were associated with reduced expression of several ribosome biogenesis factors, the knockdown of which was also sufficient to induce senescence. Genetic analysis revealed that Rb but not p53 was required for the senescence response to altered ribosome biogenesis...
June 25, 2018: Nature Cell Biology
Krushna C Patra, Yasutaka Kato, Yusuke Mizukami, Sebastian Widholz, Myriam Boukhali, Iulia Revenco, Elizabeth A Grossman, Fei Ji, Ruslan I Sadreyev, Andrew S Liss, Robert A Screaton, Kei Sakamoto, David P Ryan, Mari Mino-Kenudson, Carlos Fernandez-Del Castillo, Daniel K Nomura, Wilhelm Haas, Nabeel Bardeesy
G protein αs (GNAS) mediates receptor-stimulated cAMP signalling, which integrates diverse environmental cues with intracellular responses. GNAS is mutationally activated in multiple tumour types, although its oncogenic mechanisms remain elusive. We explored this question in pancreatic tumourigenesis where concurrent GNAS and KRAS mutations characterize pancreatic ductal adenocarcinomas (PDAs) arising from intraductal papillary mucinous neoplasms (IPMNs). By developing genetically engineered mouse models, we show that GnasR201C cooperates with KrasG12D to promote initiation of IPMN, which progress to invasive PDA following Tp53 loss...
June 25, 2018: Nature Cell Biology
Qiang Zhuang, Wenjuan Li, Christina Benda, Zhijian Huang, Tanveer Ahmed, Ping Liu, Xiangpeng Guo, David P Ibañez, Zhiwei Luo, Meng Zhang, Mazid Md Abdul, Zhongzhou Yang, Jiayin Yang, Yinghua Huang, Hui Zhang, Dehao Huang, Jianguo Zhou, Xiaofen Zhong, Xihua Zhu, Xiuling Fu, Wenxia Fan, Yulin Liu, Yan Xu, Carl Ward, Muhammad Jadoon Khan, Shahzina Kanwal, Bushra Mirza, Micky D Tortorella, Hung-Fat Tse, Jiayu Chen, Baoming Qin, Xichen Bao, Shaorong Gao, Andrew P Hutchins, Miguel A Esteban
In the version of this Article originally published, in Fig. 2c, the '+' sign and 'OSKM' were superimposed in the label '+OSKM'. In Fig. 4e, in the labels, all instances of 'Ant' should have been 'Anti-'. And, in Fig. 7a, the label '0.0' was misplaced; it should have been on the colour scale bar. These figures have now been corrected in the online versions.
June 15, 2018: Nature Cell Biology
Huilin Huang, Hengyou Weng, Wenju Sun, Xi Qin, Hailing Shi, Huizhe Wu, Boxuan Simen Zhao, Ana Mesquita, Chang Liu, Celvie L Yuan, Yueh-Chiang Hu, Stefan Hüttelmaier, Jennifer R Skibbe, Rui Su, Xiaolan Deng, Lei Dong, Miao Sun, Chenying Li, Sigrid Nachtergaele, Yungui Wang, Chao Hu, Kyle Ferchen, Kenneth D Greis, Xi Jiang, Minjie Wei, Lianghu Qu, Jun-Lin Guan, Chuan He, Jianhua Yang, Jianjun Chen
In the version of this Article originally published, the authors incorrectly listed an accession code as GES90642. The correct code is GSE90642 . This has now been amended in all online versions of the Article.
June 7, 2018: Nature Cell Biology
Verónica Eisner, Martin Picard, György Hajnóczky
No abstract text is available yet for this article.
July 2018: Nature Cell Biology
Pablo E Hollstein, Reuben J Shaw
No abstract text is available yet for this article.
July 2018: Nature Cell Biology
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