显示样式:     当前期刊: Nature Cell Biology    加入关注    导出
我的关注
我的收藏
您暂时未登录!
登录
  • Transient Scute activation via a self-stimulatory loop directs enteroendocrine cell pair specification from self-renewing intestinal stem cells
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2018-01-15
    Jun Chen, Na Xu, Chenhui Wang, Pin Huang, Huanwei Huang, Zhen Jin, Zhongsheng Yu, Tao Cai, Renjie Jiao, Rongwen Xi

    The process through which multiple types of cell-lineage-restricted progenitor cells are specified from multipotent stem cells is unclear. Here we show that, in intestinal stem cell lineages in adult Drosophila, in which the Delta-Notch-signalling-guided progenitor cell differentiation into enterocytes is the default mode, the specification of enteroendocrine cells (EEs) is initiated by transient Scute activation in a process driven by transcriptional self-stimulation combined with a negative feedback regulation between Scute and Notch targets. Scute activation induces asymmetric intestinal stem cell divisions that generate EE progenitor cells. The mitosis-inducing and fate-inducing activities of Scute guide each EE progenitor cell to divide exactly once prior to its terminal differentiation, yielding a pair of EEs. The transient expression of a fate inducer therefore specifies both type and numbers of committed progenitor cells originating from stem cells, which could represent a general mechanism used for diversifying committed progenitor cells from multipotent stem cells.

    更新日期:2018-01-15
  • Segregation of mitochondrial DNA heteroplasmy through a developmental genetic bottleneck in human embryos
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2018-01-15
    Vasileios I. Floros, Angela Pyle, Sabine Dietmann, Wei Wei, Walfred W. C. Tang, Naoko Irie, Brendan Payne, Antonio Capalbo, Laila Noli, Jonathan Coxhead, Gavin Hudson, Moira Crosier, Henrik Strahl, Yacoub Khalaf, Mitinori Saitou, Dusko Ilic, M. Azim Surani, Patrick F. Chinnery

    Mitochondrial DNA (mtDNA) mutations cause inherited diseases and are implicated in the pathogenesis of common late-onset disorders, but how they arise is not clear1,2. Here we show that mtDNA mutations are present in primordial germ cells (PGCs) within healthy female human embryos. Isolated PGCs have a profound reduction in mtDNA content, with discrete mitochondria containing ~5 mtDNA molecules. Single-cell deep mtDNA sequencing of in vivo human female PGCs showed rare variants reaching higher heteroplasmy levels in late PGCs, consistent with the observed genetic bottleneck. We also saw the signature of selection against non-synonymous protein-coding, tRNA gene and D-loop variants, concomitant with a progressive upregulation of genes involving mtDNA replication and transcription, and linked to a transition from glycolytic to oxidative metabolism. The associated metabolic shift would expose deleterious mutations to selection during early germ cell development, preventing the relentless accumulation of mtDNA mutations in the human population predicted by Muller’s ratchet. Mutations escaping this mechanism will show shifts in heteroplasmy levels within one human generation, explaining the extreme phenotypic variation seen in human pedigrees with inherited mtDNA disorders.

    更新日期:2018-01-15
  • Myosin-Va is required for preciliary vesicle transportation to the mother centriole during ciliogenesis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2018-01-15
    Chien-Ting Wu, Hsin-Yi Chen, Tang K. Tang

    Primary cilia play essential roles in signal transduction and development. The docking of preciliary vesicles at the distal appendages of a mother centriole is an initial/critical step of ciliogenesis, but the mechanisms are unclear. Here, we demonstrate that myosin-Va mediates the transportation of preciliary vesicles to the mother centriole and reveal the underlying mechanism. We also show that the myosin-Va-mediated transportation of preciliary vesicles is the earliest event that defines the onset of ciliogenesis. Depletion of myosin-Va significantly inhibits the attachment of preciliary vesicles to the distal appendages of the mother centriole and decreases cilia assembly. Myosin-Va functions upstream of EHD1- and Rab11-mediated ciliary vesicle formation. Importantly, dynein mediates myosin-Va-associated preciliary vesicle transportation to the pericentrosomal region along microtubules, while myosin-Va mediates preciliary vesicle transportation from the pericentrosomal region to the distal appendages of the mother centriole via the Arp2/3-associated branched actin network.

    更新日期:2018-01-15
  • EXD2 governs germ stem cell homeostasis and lifespan by promoting mitoribosome integrity and translation
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2018-01-15
    Joana Silva, Suvi Aivio, Philip A. Knobel, Laura J. Bailey, Andreu Casali, Maria Vinaixa, Isabel Garcia-Cao, Étienne Coyaud, Alexis A. Jourdain, Pablo Pérez-Ferreros, Ana M. Rojas, Albert Antolin-Fontes, Sara Samino-Gené, Brian Raught, Acaimo González-Reyes, Lluís Ribas de Pouplana, Aidan J. Doherty, Oscar Yanes, Travis H. Stracker

    Mitochondria are subcellular organelles that are critical for meeting the bioenergetic and biosynthetic needs of the cell. Mitochondrial function relies on genes and RNA species encoded both in the nucleus and mitochondria, and on their coordinated translation, import and respiratory complex assembly. Here, we characterize EXD2 (exonuclease 3′–5′ domain-containing 2), a nuclear-encoded gene, and show that it is targeted to the mitochondria and prevents the aberrant association of messenger RNAs with the mitochondrial ribosome. Loss of EXD2 results in defective mitochondrial translation, impaired respiration, reduced ATP production, increased reactive oxygen species and widespread metabolic abnormalities. Depletion of the Drosophila melanogaster EXD2 orthologue (CG6744) causes developmental delays and premature female germline stem cell attrition, reduced fecundity and a dramatic extension of lifespan that is reversed with an antioxidant diet. Our results define a conserved role for EXD2 in mitochondrial translation that influences development and ageing.

    更新日期:2018-01-15
  • Author Correction: TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2018-01-08
    John J. H. Shin, Alison K. Gillingham, Farida Begum, Jessica Chadwick, Sean Munro

    Author Correction: TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi Author Correction: TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi, Published online: 08 January 2018; doi:10.1038/s41556-017-0026-7 Author Correction: TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi

    更新日期:2018-01-08
  • Defining murine organogenesis at single-cell resolution reveals a role for the leukotriene pathway in regulating blood progenitor formation
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2018-01-08
    Ximena Ibarra-Soria, Wajid Jawaid, Blanca Pijuan-Sala, Vasileios Ladopoulos, Antonio Scialdone, David J. Jörg, Richard C. V. Tyser, Fernando J. Calero-Nieto, Carla Mulas, Jennifer Nichols, Ludovic Vallier, Shankar Srinivas, Benjamin D. Simons, Berthold Göttgens, John C. Marioni

    During gastrulation, cell types from all three germ layers are specified and the basic body plan is established1. However, molecular analysis of this key developmental stage has been hampered by limited cell numbers and a paucity of markers. Single-cell RNA sequencing circumvents these problems, but has so far been limited to specific organ systems2. Here, we report single-cell transcriptomic characterization of >20,000 cells immediately following gastrulation at E8.25 of mouse development. We identify 20 major cell types, which frequently contain substructure, including three distinct signatures in early foregut cells. Pseudo-space ordering of somitic progenitor cells identifies dynamic waves of transcription and candidate regulators, which are validated by molecular characterization of spatially resolved regions of the embryo. Within the endothelial population, cells that transition from haemogenic endothelial to erythro-myeloid progenitors specifically express Alox5 and its co-factor Alox5ap, which control leukotriene production. Functional assays using mouse embryonic stem cells demonstrate that leukotrienes promote haematopoietic progenitor cell generation. Thus, this comprehensive single-cell map can be exploited to reveal previously unrecognized pathways that contribute to tissue development.

    更新日期:2018-01-08
  • PERK links the clock and protein stress in cancer
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-21
    Miguel Sanchez-Alvarez, Chris Bakal

    PERK links the clock and protein stress in cancer PERK links the clock and protein stress in cancer, Published online: 21 December 2017; doi:10.1038/s41556-017-0019-6 The unfolded protein response (UPR) regulates cell metabolism and survival in response to stress, yet how the UPR is connected to other signalling pathways is poorly understood. PERK is now shown to regulate Bmal1 and Clock proteins to promote cancer cell survival, revealing a link between growth regulation and circadian rhythms.

    更新日期:2017-12-21
  • Sugar fuels T-cell memory
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-21
    Joanna Olivas, Tiffany Horng

    Sugar fuels T-cell memory Sugar fuels T-cell memory, Published online: 21 December 2017; doi:10.1038/s41556-017-0014-y Previous work has highlighted the role of metabolic shifts in regulating the formation of memory T cells, which are generated during a primary infection to provide long-lasting immunity. A study now shows that memory T cells rely on a gluconeogenesis–glycogenolysis cycle to provide antioxidant defence and support their survival.

    更新日期:2017-12-21
  • Mechanoreciprocity in cell migration
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-21
    Sjoerd van Helvert, Cornelis Storm, Peter Friedl

    Cell migration is an adaptive process that depends on and responds to physical and molecular triggers. Moving cells sense and respond to tissue mechanics and induce transient or permanent tissue modifications, including extracellular matrix stiffening, compression and deformation, protein unfolding, proteolytic remodelling and jamming transitions. Here we discuss how the bi-directional relationship of cell–tissue interactions (mechanoreciprocity) allows cells to change position and contributes to single-cell and collective movement, structural and molecular tissue organization, and cell fate decisions.

    更新日期:2017-12-21
  • Supporting the sharing of research
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-21

    Supporting the sharing of research Supporting the sharing of research, Published online: 21 December 2017; doi:10.1038/s41556-017-0025-8 Nature Cell Biology supports the wide dissemination of scientific findings both prior to and following publication of primary research manuscripts.

    更新日期:2017-12-21
  • Muscling toward therapy with ERBB3 and NGFR
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-21
    Andrew T. V. Ho, Helen M. Blau

    Muscling toward therapy with ERBB3 and NGFR Muscling toward therapy with ERBB3 and NGFR, Published online: 21 December 2017; doi:10.1038/s41556-017-0015-x To overcome the finite supply of muscle stem cells available for cell therapy, a study now describes a strategy for obtaining an unlimited source of myogenic progenitors derived from human pluripotent cells. Two neuronal cell surface receptors facilitate the selection of a population with enhanced regenerative potential.

    更新日期:2017-12-21
  • Unresolved recombination intermediates lead to ultra-fine anaphase bridges, chromosome breaks and aberrations
    Nat. Cell. Biol. (IF 20.06) Pub Date : 
    Ying Wai Chan, Kasper Fugger, Stephen C. West

    Unresolved recombination intermediates lead to ultra-fine anaphase bridges, chromosome breaks and aberrations Unresolved recombination intermediates lead to ultra-fine anaphase bridges, chromosome breaks and aberrations, Published online: 18 December 2017; doi:10.1038/s41556-017-0011-1 Chan et al. show that unresolved recombination intermediates form a previously unappreciated type of ultra-fine bridge. These bridges are broken upon cell division, leading to chromosome breaks and instability.

    更新日期:2017-12-18
  • The autophagy receptor ALLO-1 and the IKKE-1 kinase control clearance of paternal mitochondria in Caenorhabditis elegans
    Nat. Cell. Biol. (IF 20.06) Pub Date : 
    Miyuki Sato, Katsuya Sato, Kotone Tomura, Hidetaka Kosako, Ken Sato

    The autophagy receptor ALLO-1 and the IKKE-1 kinase control clearance of paternal mitochondria in Caenorhabditis elegans The autophagy receptor ALLO-1 and the IKKE-1 kinase control clearance of paternal mitochondria in Caenorhabditis elegans , Published online: 18 December 2017; doi:10.1038/s41556-017-0008-9 Sato et al. identify ALLO-1 as an autophagy receptor required for paternal organelle clearance in Caenorhabditis elegans, and this process is dependent on ALLO-1 phosphorylation by the TBK1 family kinase IKKE-1.

    更新日期:2017-12-18
  • Mechanical cues control mutant p53 stability through a mevalonate–RhoA axis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 
    Eleonora Ingallina, Giovanni Sorrentino, Rebecca Bertolio, Kamil Lisek, Alessandro Zannini, Luca Azzolin, Luisa Ulloa Severino, Denis Scaini, Miguel Mano, Fiamma Mantovani, Antonio Rosato, Silvio Bicciato, Stefano Piccolo, Giannino Del Sal

    Mechanical cues control mutant p53 stability through a mevalonate–RhoA axis Mechanical cues control mutant p53 stability through a mevalonate–RhoA axis, Published online: 18 December 2017; doi:10.1038/s41556-017-0009-8 Ingallina et al. show that mutant p53 is protected from degradation in response to matrix stiffness in a manner dependent on RhoA geranylgeranylation and actomyosin dynamics.

    更新日期:2017-12-18
  • ERBB3 and NGFR mark a distinct skeletal muscle progenitor cell in human development and hPSCs
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-18
    Michael R. Hicks, Julia Hiserodt, Katrina Paras, Wakana Fujiwara, Ascia Eskin, Majib Jan, Haibin Xi, Courtney S. Young, Denis Evseenko, Stanley F. Nelson, Melissa J. Spencer, Ben Van Handel, April D. Pyle

    Human pluripotent stem cells (hPSCs) can be directed to differentiate into skeletal muscle progenitor cells (SMPCs). However, the myogenicity of hPSC-SMPCs relative to human fetal or adult satellite cells remains unclear. We observed that hPSC-SMPCs derived by directed differentiation are less functional in vitro and in vivo compared to human satellite cells. Using RNA sequencing, we found that the cell surface receptors ERBB3 and NGFR demarcate myogenic populations, including PAX7 progenitors in human fetal development and hPSC-SMPCs. We demonstrated that hPSC skeletal muscle is immature, but inhibition of transforming growth factor-β signalling during differentiation improved fusion efficiency, ultrastructural organization and the expression of adult myosins. This enrichment and maturation strategy restored dystrophin in hundreds of dystrophin-deficient myofibres after engraftment of CRISPR–Cas9-corrected Duchenne muscular dystrophy human induced pluripotent stem cell-SMPCs. The work provides an in-depth characterization of human myogenesis, and identifies candidates that improve the in vivo myogenic potential of hPSC-SMPCs to levels that are equal to directly isolated human fetal muscle cells.

    更新日期:2017-12-18
  • A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-11
    Yiwen Bu, Akihiro Yoshida, Nilesh Chitnis, Brian J. Altman, Feven Tameire, Amanda Oran, Victoria Gennaro, Kent E. Armeson, Steven B. McMahon, Gerald B. Wertheim, Chi V. Dang, Davide Ruggero, Constantinos Koumenis, Serge Y. Fuchs, J. Alan Diehl

    The unfolded protein response (UPR) is a stress-activated signalling pathway that regulates cell proliferation, metabolism and survival. The circadian clock coordinates metabolism and signal transduction with light/dark cycles. We explore how UPR signalling interfaces with the circadian clock. UPR activation induces a 10 h phase shift in circadian oscillations through induction of miR-211, a PERK-inducible microRNA that transiently suppresses both Bmal1 and Clock, core circadian regulators. Molecular investigation reveals that miR-211 directly regulates Bmal1 and Clock via distinct mechanisms. Suppression of Bmal1 and Clock has the anticipated impact on expression of select circadian genes, but we also find that repression of Bmal1 is essential for UPR-dependent inhibition of protein synthesis and cell adaptation to stresses that disrupt endoplasmic reticulum homeostasis. Our data demonstrate that c-Myc-dependent activation of the UPR inhibits Bmal1 in Burkitt’s lymphoma, thereby suppressing both circadian oscillation and ongoing protein synthesis to facilitate tumour progression.

    更新日期:2017-12-11
  • A Pck1-directed glycogen metabolic program regulates formation and maintenance of memory CD8+ T cells
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-11
    Ruihua Ma, Tiantian Ji, Huafeng Zhang, Wenqian Dong, Xinfeng Chen, Pingwei Xu, Degao Chen, Xiaoyu Liang, Xiaonan Yin, Yuying Liu, Jingwei Ma, Ke Tang, Yi Zhang, Yue’e Peng, Jinzhi Lu, Yi Zhang, Xiaofeng Qin, Xuetao Cao, Yonghong Wan, Bo Huang

    CD8+ memory T (Tm) cells are fundamental for protective immunity against infections and cancers1,2,3,4,5. Metabolic activities are crucial in controlling memory T-cell homeostasis, but mechanisms linking metabolic signals to memory formation and survival remain elusive. Here we show that CD8+ Tm cells markedly upregulate cytosolic phosphoenolpyruvate carboxykinase (Pck1), the hub molecule regulating glycolysis, tricarboxylic acid cycle and gluconeogenesis, to increase glycogenesis via gluconeogenesis. The resultant glycogen is then channelled to glycogenolysis to generate glucose-6-phosphate and the subsequent pentose phosphate pathway (PPP) that generates abundant NADPH, ensuring high levels of reduced glutathione in Tm cells. Abrogation of Pck1–glycogen–PPP decreases GSH/GSSG ratios and increases levels of reactive oxygen species (ROS), leading to impairment of CD8+ Tm formation and maintenance. Importantly, this metabolic regulatory mechanism could be readily translated into more efficient T-cell immunotherapy in mouse tumour models.

    更新日期:2017-12-11
  • Systematic analysis of ribophagy in human cells reveals bystander flux during selective autophagy
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-11
    Heeseon An, J. Wade Harper

    Ribosomes are abundant cellular machines1,2 that are regulated by assembly, supernumerary subunit turnover and nascent chain quality control mechanisms1,2,3,4,5. Moreover, nitrogen starvation in yeast has been reported to promote selective ribosome delivery to the vacuole in an autophagy conjugation system dependent manner, a process called ‘ribophagy’6,7. However, whether ribophagy in mammals is selective or regulated is unclear. Using Ribo–Keima flux reporters, we find that starvation or mTOR inhibition promotes VPS34-dependent ribophagic flux, which, unlike yeast, is largely independent of ATG8 conjugation and occurs concomitantly with other cytosolic protein autophagic flux reporters8,9. Ribophagic flux was not induced upon inhibition of translational elongation or nascent chain uncoupling, but was induced in a comparatively selective manner under proteotoxic stress induced by arsenite10 or chromosome mis-segregation11, dependent upon VPS34 and ATG8 conjugation. Unexpectedly, agents typically used to induce selective autophagy also promoted increased ribosome and cytosolic protein reporter flux, suggesting significant bulk or ‘bystander’ autophagy during what is often considered selective autophagy12,13. These results emphasize the importance of monitoring non-specific cargo flux when assessing selective autophagy pathways.

    更新日期:2017-12-11
  • Adhesion forces and cortical tension couple cell proliferation and differentiation to drive epidermal stratification
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-11
    Yekaterina A. Miroshnikova, Huy Q. Le, David Schneider, Torsten Thalheim, Matthias Rübsam, Nadine Bremicker, Julien Polleux, Nadine Kamprad, Marco Tarantola, Irène Wang, Martial Balland, Carien M. Niessen, Joerg Galle, Sara A. Wickström

    To establish and maintain organ structure and function, tissues need to balance stem cell proliferation and differentiation rates and coordinate cell fate with position. By quantifying and modelling tissue stress and deformation in the mammalian epidermis, we find that this balance is coordinated through local mechanical forces generated by cell division and delamination. Proliferation within the basal stem/progenitor layer, which displays features of a jammed, solid-like state, leads to crowding, thereby locally distorting cell shape and stress distribution. The resulting decrease in cortical tension and increased cell–cell adhesion trigger differentiation and subsequent delamination, reinstating basal cell layer density. After delamination, cells establish a high-tension state as they increase myosin II activity and convert to E-cadherin-dominated adhesion, thereby reinforcing the boundary between basal and suprabasal layers. Our results uncover how biomechanical signalling integrates single-cell behaviours to couple proliferation, cell fate and positioning to generate a multilayered tissue.

    更新日期:2017-12-11
  • A homeostatic apical microtubule network shortens cells for epithelial folding via a basal polarity shift
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-04
    Michiko Takeda, Mustafa M. Sami, Yu-Chiun Wang

    Epithelial folding is typically driven by localized actomyosin contractility. However, it remains unclear how epithelia deform when myosin levels are low and uniform. In the Drosophila gastrula, dorsal fold formation occurs despite a lack of localized myosin changes, while the fold-initiating cells reduce cell height following basal shifts of polarity via an unknown mechanism. We show that cell shortening depends on an apical microtubule network organized by the CAMSAP protein Patronin. Prior to gastrulation, microtubule forces generated by the minus-end motor dynein scaffold the apical cell cortex into a dome-like shape, while the severing enzyme Katanin facilitates network remodelling to ensure tissue-wide cell size homeostasis. During fold initiation, Patronin redistributes following basal polarity shifts in the initiating cells, apparently weakening the scaffolding forces to allow dome descent. The homeostatic network that ensures size/shape homogeneity is thus repurposed for cell shortening, linking epithelial polarity to folding via a microtubule-based mechanical mechanism.

    更新日期:2017-12-05
  • ABIN-1 regulates RIPK1 activation by linking Met1 ubiquitylation with Lys63 deubiquitylation in TNF-RSC
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-12-04
    Slawomir A. Dziedzic, Zhenyi Su, Vica Jean Barrett, Ayaz Najafov, Adnan K. Mookhtiar, Palak Amin, Heling Pan, Li Sun, Hong Zhu, Averil Ma, Derek W. Abbott, Junying Yuan

    Ubiquitylation of the TNFR1 signalling complex (TNF-RSC) controls the activation of RIPK1, a kinase critically involved in mediating multiple TNFα-activated deleterious events. However, the molecular mechanism that coordinates different types of ubiquitylation modification to regulate the activation of RIPK1 kinase remains unclear. Here, we show that ABIN-1/NAF-1, a ubiquitin-binding protein, is recruited rapidly into TNF-RSC in a manner dependent on the Met1-ubiquitylating complex LUBAC to regulate the recruitment of A20 to control Lys63 deubiquitylation of RIPK1. ABIN-1 deficiency reduces the recruitment of A20 and licenses cells to die through necroptosis by promoting Lys63 ubiquitylation and activation of RIPK1 with TNFα stimulation under conditions that would otherwise exclusively activate apoptosis in wild-type cells. Inhibition of RIPK1 kinase and RIPK3 deficiency block the embryonic lethality of Abin-1–/– mice. We propose that ABIN-1 provides a critical link between Met1 ubiquitylation mediated by the LUBAC complex and Lys63 deubiquitylation by phospho-A20 to modulate the activation of RIPK1.

    更新日期:2017-12-05
  • Erratum: PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    Fabao Liu, Fengfei Ma, Yuyuan Wang, Ling Hao, Hao Zeng, Chenxi Jia, Yidan Wang, Peng Liu, Irene M. Ong, Baobin Li, Guojun Chen, Jiaoyang Jiang, Shaoqin Gong, Lingjun Li, Wei Xu

    Erratum: PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis Erratum: PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis, Published online: 29 November 2017; doi:10.1038/ncb3648 Erratum: PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis

    更新日期:2017-11-29
  • Of stem cells and ethics
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29

    Of stem cells and ethics Of stem cells and ethics, Published online: 29 November 2017; doi:10.1038/ncb3652 Advances in stem cell research offer unprecedented insights into human biology and opportunities for clinical translation. They also raise many questions with social and ethical implications.

    更新日期:2017-11-29
  • RNA takes over control of DNA break repair
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    Francesca Storici, Ailone E. Tichon

    RNA takes over control of DNA break repair RNA takes over control of DNA break repair, Published online: 29 November 2017; doi:10.1038/ncb3645 Small RNAs generated at DNA break sites are implicated in mammalian DNA repair. Now, a study shows that following the formation of DNA double-strand breaks, bidirectional transcription events adjacent to the break generate small RNAs that trigger the DNA damage response by local RNA:RNA interactions.

    更新日期:2017-11-29
  • Addendum: A regulated PNUTS mRNA to lncRNA splice switch mediates EMT and tumour progression
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    Simon Grelet, Laura A. Link, Breege Howley, Clémence Obellianne, Viswanathan Palanisamy, Vamsi K. Gangaraju, J. Alan Diehl, Philip H. Howe

    Addendum: A regulated PNUTS mRNA to lncRNA splice switch mediates EMT and tumour progression Addendum: A regulated PNUTS mRNA to lncRNA splice switch mediates EMT and tumour progression, Published online: 29 November 2017; doi:10.1038/ncb3647 Addendum: A regulated PNUTS mRNA to lncRNA splice switch mediates EMT and tumour progression

    更新日期:2017-11-29
  • Corrigendum: Cholesterol and fatty acids regulate cysteine ubiquitylation of ACAT2 through competitive oxidation
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    Yong-Jian Wang, Yan Bian, Jie Luo, Ming Lu, Ying Xiong, Shu-Yuan Guo, Hui Yong, Xu Lin, Qin Li, Catherine C. Y. Chang, Ta-Yuan Chang, Bo-Liang Li, Bao-Liang Song

    Corrigendum: Cholesterol and fatty acids regulate cysteine ubiquitylation of ACAT2 through competitive oxidation Corrigendum: Cholesterol and fatty acids regulate cysteine ubiquitylation of ACAT2 through competitive oxidation, Published online: 29 November 2017; doi:10.1038/ncb3651 Corrigendum: Cholesterol and fatty acids regulate cysteine ubiquitylation of ACAT2 through competitive oxidation

    更新日期:2017-11-29
  • Capturing endosomal vesicles at the Golgi
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    J. Christopher Fromme, Mary Munson

    Capturing endosomal vesicles at the Golgi Capturing endosomal vesicles at the Golgi, Published online: 29 November 2017; doi:10.1038/ncb3649 Membrane trafficking specificity between distinct compartments ensures that cargo proteins and lipids are delivered to their target organelle. However, accurate recognition of cargo carriers by tethering factors on target membranes is poorly understood. TBC1D23 is now identified as an adaptor that links endosome-derived vesicles with golgins at the trans-Golgi.

    更新日期:2017-11-29
  • Erratum: DNA sensing in senescence
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    Marina Ruiz de Galarreta, Amaia Lujambio

    Erratum: DNA sensing in senescence Erratum: DNA sensing in senescence, Published online: 29 November 2017; doi:10.1038/ncb3644 Erratum: DNA sensing in senescence

    更新日期:2017-11-29
  • Erratum: EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-29
    Zarah M. Löf-Öhlin, Pia Nyeng, Matthew E. Bechard, Katja Hess, Eric Bankaitis, Thomas U. Greiner, Jacqueline Ameri, Christopher V. Wright, Henrik Semb

    Erratum: EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity Erratum: EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity, Published online: 29 November 2017; doi:10.1038/ncb3646 Erratum: EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity

    更新日期:2017-11-29
  • Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-27
    Flavia Michelini, Sethuramasundaram Pitchiaya, Valerio Vitelli, Sheetal Sharma, Ubaldo Gioia, Fabio Pessina, Matteo Cabrini, Yejun Wang, Ilaria Capozzo, Fabio Iannelli, Valentina Matti, Sofia Francia, G. V. Shivashankar, Nils G. Walter, Fabrizio d’Adda di Fagagna

    Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks, Published online: 27 November 2017; doi:10.1038/ncb3643 Michelini et al. show that RNA polymerase II is recruited to double-strand breaks to induce long non-coding RNAs and the generation of small DNA damage response RNAs that promote recruitment of DNA repair factors and repair.

    更新日期:2017-11-28
  • Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-11-27
    Flavia Michelini, Sethuramasundaram Pitchiaya, Valerio Vitelli, Sheetal Sharma, Ubaldo Gioia, Fabio Pessina, Matteo Cabrini, Yejun Wang, Ilaria Capozzo, Fabio Iannelli, Valentina Matti, Sofia Francia, G. V. Shivashankar, Nils G. Walter, Fabrizio d’Adda di Fagagna

    Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks, Published online: 27 November 2017; doi:10.1038/ncb3643 Michelini et al. show that RNA polymerase II is recruited to double-strand breaks to induce long non-coding RNAs and the generation of small DNA damage response RNAs that promote recruitment of DNA repair factors and repair.

    更新日期:2017-11-28
  • A transient pool of nuclear F-actin at mitotic exit controls chromatin organization
    Nat. Cell. Biol. (IF 20.06) Pub Date : 
    Christian Baarlink, Matthias Plessner, Alice Sherrard, Kohtaro Morita, Shinji Misu, David Virant, Eva-Maria Kleinschnitz, Robert Harniman, Dominic Alibhai, Stefan Baumeister, Kei Miyamoto, Ulrike Endesfelder, Abderrahmane Kaidi, Robert Grosse

    A transient pool of nuclear F-actin at mitotic exit controls chromatin organization A transient pool of nuclear F-actin at mitotic exit controls chromatin organization, Published online: 13 November 2017; doi:10.1038/ncb3641 NatureArticleSnippet(type=short-summary, markup= Baarlink et al. identify a transient pool of nuclear F-actin, the dynamics of which are controlled by cofilin-1 that accumulates after mitosis and is important for chromatin reorganization in G1. , isJats=true)

    更新日期:2017-11-13
  • A transient pool of nuclear F-actin at mitotic exit controls chromatin organization
    Nat. Cell. Biol. (IF 20.06) Pub Date : 
    Christian Baarlink, Matthias Plessner, Alice Sherrard, Kohtaro Morita, Shinji Misu, David Virant, Eva-Maria Kleinschnitz, Robert Harniman, Dominic Alibhai, Stefan Baumeister, Kei Miyamoto, Ulrike Endesfelder, Abderrahmane Kaidi, Robert Grosse

    A transient pool of nuclear F-actin at mitotic exit controls chromatin organization A transient pool of nuclear F-actin at mitotic exit controls chromatin organization, Published online: 13 November 2017; doi:10.1038/ncb3641 NatureArticleSnippet(type=short-summary, markup= Baarlink et al. identify a transient pool of nuclear F-actin, the dynamics of which are controlled by cofilin-1 that accumulates after mitosis and is important for chromatin reorganization in G1. , isJats=true)

    更新日期:2017-11-13
  • PARPi focus the spotlight on replication fork protection in cancer
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Katharina Schlacher

    PARPi focus the spotlight on replication fork protection in cancer Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3638 PARP inhibitors (PARPi) kill BRCA1/2-mutated cancers, which become resistant when DNA repair functions are restored. Now, MUS81 nuclease inhibition due to EZH2 downregulation is found to restore DNA replication fork protection but not repair, leading to PARPi-resistance in mutant BRCA2 cells and patients. This challenges the DNA repair dominance in synthetic lethality.

    更新日期:2017-10-31
  • Implantable synthetic organoid matrices for intestinal regeneration
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Jeffrey W. Brown, Jason C. Mills

    Implantable synthetic organoid matrices for intestinal regeneration Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3635 Organoids are a powerful tool to study both physiological and disease processes. A completely synthetic matrix assembled from exchangeable modular parts has been developed and not only supports proliferation of human intestinal organoids derived from pluripotent embryonic stem cells, but also augments subsequent ad vivo implantation into injured murine colon.

    更新日期:2017-10-31
  • TYRP1 mRNA goes fishing for miRNAs in melanoma
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Maria S. Soengas, Eva Hernando

    TYRP1 mRNA goes fishing for miRNAs in melanoma Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3637 A variety of non-coding RNAs have been reported as endogenous sponges for cancer-modulating miRNAs. However, miRNA trapping by transcripts with protein-coding functions is less understood. The mRNA of TYRP1 is now found to sequester the tumour suppressor miR-16 on non-canonical miRNA response elements in melanoma, thereby promoting malignant growth.

    更新日期:2017-10-31
  • Reforms spell optimism for biological research in China
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31

    Reforms spell optimism for biological research in China Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3639 A series of government reforms aim to enhance basic research efforts in China with a shift in focus from quantity to quality.

    更新日期:2017-10-31
  • Erratum: Super-resolution microscopy reveals that disruption of ciliary transition-zone architecture causes Joubert syndrome
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Xiaoyu Shi, Galo Garcia III, Julie C. Van De Weghe, Ryan McGorty, Gregory J. Pazour, Dan Doherty, Bo Huang, Jeremy F. Reiter

    Erratum: Super-resolution microscopy reveals that disruption of ciliary transition-zone architecture causes Joubert syndrome Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3622

    更新日期:2017-10-31
  • PARPi focus the spotlight on replication fork protection in cancer
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Katharina Schlacher

    PARPi focus the spotlight on replication fork protection in cancer Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3638 PARP inhibitors (PARPi) kill BRCA1/2-mutated cancers, which become resistant when DNA repair functions are restored. Now, MUS81 nuclease inhibition due to EZH2 downregulation is found to restore DNA replication fork protection but not repair, leading to PARPi-resistance in mutant BRCA2 cells and patients. This challenges the DNA repair dominance in synthetic lethality.

    更新日期:2017-10-31
  • Implantable synthetic organoid matrices for intestinal regeneration
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Jeffrey W. Brown, Jason C. Mills

    Implantable synthetic organoid matrices for intestinal regeneration Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3635 Organoids are a powerful tool to study both physiological and disease processes. A completely synthetic matrix assembled from exchangeable modular parts has been developed and not only supports proliferation of human intestinal organoids derived from pluripotent embryonic stem cells, but also augments subsequent ad vivo implantation into injured murine colon.

    更新日期:2017-10-31
  • TYRP1 mRNA goes fishing for miRNAs in melanoma
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Maria S. Soengas, Eva Hernando

    TYRP1 mRNA goes fishing for miRNAs in melanoma Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3637 A variety of non-coding RNAs have been reported as endogenous sponges for cancer-modulating miRNAs. However, miRNA trapping by transcripts with protein-coding functions is less understood. The mRNA of TYRP1 is now found to sequester the tumour suppressor miR-16 on non-canonical miRNA response elements in melanoma, thereby promoting malignant growth.

    更新日期:2017-10-31
  • Reforms spell optimism for biological research in China
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31

    Reforms spell optimism for biological research in China Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3639 A series of government reforms aim to enhance basic research efforts in China with a shift in focus from quantity to quality.

    更新日期:2017-10-31
  • Erratum: Super-resolution microscopy reveals that disruption of ciliary transition-zone architecture causes Joubert syndrome
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-31
    Xiaoyu Shi, Galo Garcia III, Julie C. Van De Weghe, Ryan McGorty, Gregory J. Pazour, Dan Doherty, Bo Huang, Jeremy F. Reiter

    Erratum: Super-resolution microscopy reveals that disruption of ciliary transition-zone architecture causes Joubert syndrome Nature Cell Biology, Published online: 31 October 2017; doi:10.1038/ncb3622

    更新日期:2017-10-31
  • TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-30
    John J. H. Shin, Alison K. Gillingham, Farida Begum, Jessica Chadwick, Sean Munro

    TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi Nature Cell Biology, Published online: 30 October 2017; doi:10.1038/ncb3627 Shin et al. identify TBC1D23 as an adaptor that interacts both with golgins and endosomal WASH and is required for the delivery of endosome-derived vesicles to the trans-Golgi.

    更新日期:2017-10-30
  • Class III phosphatidylinositol-3-OH kinase controls epithelial integrity through endosomal LKB1 regulation
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-30
    Fergal O’Farrell, Viola Hélène Lobert, Marte Sneeggen, Ashish Jain, Nadja Sandra Katheder, Eva Maria Wenzel, Sebastian Wolfgang Schultz, Kia Wee Tan, Andreas Brech, Harald Stenmark, Tor Erik Rusten

    The molecular mechanisms underlying the interdependence between intracellular trafficking and epithelial cell polarity are poorly understood. Here we show that inactivation of class III phosphatidylinositol-3-OH kinase (CIII-PI3K), which produces phosphatidylinositol-3-phosphate (PtdIns3P) on endosomes, disrupts epithelial organization. This is caused by dysregulation of endosomally localized Liver Kinase B1 (LKB1, also known as STK11), which shows delocalized and increased activity accompanied by dysplasia-like growth and invasive behaviour of cells provoked by JNK pathway activation. CIII-PI3K inactivation cooperates with RasV12 to promote tumour growth in vivo in an LKB1-dependent manner. Strikingly, co-depletion of LKB1 reverts these phenotypes and restores epithelial integrity. The endosomal, but not autophagic, function of CIII-PI3K controls polarity. We identify the CIII-PI3K effector, WD repeat and FYVE domain-containing 2 (WDFY2), as an LKB1 regulator in Drosophila tissues and human organoids. Thus, we define a CIII-PI3K-regulated endosomal signalling platform from which LKB1 directs epithelial polarity, the dysregulation of which endows LKB1 with tumour-promoting properties.

    更新日期:2017-10-30
  • Distinct kinetics of serine and threonine dephosphorylation are essential for mitosis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-30
    Jamin B. Hein, Emil P. T. Hertz, Dimitriya H. Garvanska, Thomas Kruse, Jakob Nilsson

    Distinct kinetics of serine and threonine dephosphorylation are essential for mitosis Nature Cell Biology, Published online: 30 October 2017; doi:10.1038/ncb3634 Cdk1-mediated phosphorylation of threonine and serine residues on cell cycle regulators needs to be removed after mitosis. Hein et al. show that the known preference of the PP2A–B55 phosphatase for threonine provides temporal regulation of mitotic exit.

    更新日期:2017-10-30
  • TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-30
    John J. H. Shin, Alison K. Gillingham, Farida Begum, Jessica Chadwick, Sean Munro

    TBC1D23 is a bridging factor for endosomal vesicle capture by golgins at the trans-Golgi Nature Cell Biology, Published online: 30 October 2017; doi:10.1038/ncb3627 Shin et al. identify TBC1D23 as an adaptor that interacts both with golgins and endosomal WASH and is required for the delivery of endosome-derived vesicles to the trans-Golgi.

    更新日期:2017-10-30
  • Class III phosphatidylinositol-3-OH kinase controls epithelial integrity through endosomal LKB1 regulation
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-30
    Fergal O’Farrell, Viola Hélène Lobert, Marte Sneeggen, Ashish Jain, Nadja Sandra Katheder, Eva Maria Wenzel, Sebastian Wolfgang Schultz, Kia Wee Tan, Andreas Brech, Harald Stenmark, Tor Erik Rusten

    The molecular mechanisms underlying the interdependence between intracellular trafficking and epithelial cell polarity are poorly understood. Here we show that inactivation of class III phosphatidylinositol-3-OH kinase (CIII-PI3K), which produces phosphatidylinositol-3-phosphate (PtdIns3P) on endosomes, disrupts epithelial organization. This is caused by dysregulation of endosomally localized Liver Kinase B1 (LKB1, also known as STK11), which shows delocalized and increased activity accompanied by dysplasia-like growth and invasive behaviour of cells provoked by JNK pathway activation. CIII-PI3K inactivation cooperates with RasV12 to promote tumour growth in vivo in an LKB1-dependent manner. Strikingly, co-depletion of LKB1 reverts these phenotypes and restores epithelial integrity. The endosomal, but not autophagic, function of CIII-PI3K controls polarity. We identify the CIII-PI3K effector, WD repeat and FYVE domain-containing 2 (WDFY2), as an LKB1 regulator in Drosophila tissues and human organoids. Thus, we define a CIII-PI3K-regulated endosomal signalling platform from which LKB1 directs epithelial polarity, the dysregulation of which endows LKB1 with tumour-promoting properties.

    更新日期:2017-10-30
  • Distinct kinetics of serine and threonine dephosphorylation are essential for mitosis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-30
    Jamin B. Hein, Emil P. T. Hertz, Dimitriya H. Garvanska, Thomas Kruse, Jakob Nilsson

    Distinct kinetics of serine and threonine dephosphorylation are essential for mitosis Nature Cell Biology, Published online: 30 October 2017; doi:10.1038/ncb3634 Cdk1-mediated phosphorylation of threonine and serine residues on cell cycle regulators needs to be removed after mitosis. Hein et al. show that the known preference of the PP2A–B55 phosphatase for threonine provides temporal regulation of mitotic exit.

    更新日期:2017-10-30
  • The impact of cellular metabolism on chromatin dynamics and epigenetics
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Michael A. Reid, Ziwei Dai, Jason W. Locasale

    The impact of cellular metabolism on chromatin dynamics and epigenetics Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3629 Locasale and co-authors discuss the influence of cellular metabolism on the regulation of chromatin and epigenetics.

    更新日期:2017-10-25
  • PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Fabao Liu, Fengfei Ma, Yuyuan Wang, Ling Hao, Hao Zeng, Chenxi Jia, Yidan Wang, Peng Liu, Irene M. Ong, Baobin Li, Guojun Chen, Jiaoyang Jiang, Shaoqin Gong, Lingjun Li, Wei Xu

    PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3630 Liu et al. find that PKM2 methylated by CARM1 inhibits Ca2+ influx from endoplasmic reticulum to mitochondria, thus restraining mitochondrial oxidative phosphorylation while promoting aerobic glycolysis and breast cancer growth.

    更新日期:2017-10-25
  • EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Zarah M. Löf-Öhlin, Pia Nyeng, Matthew E. Bechard, Katja Hess, Eric Bankaitis, Thomas U. Greiner, Jacqueline Ameri, Christopher V. Wright, Henrik Semb

    EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3628 In the developing mouse pancreas, EGFR regulates apical polarity via PI(3)K and Rac1 and elicits different ligand-dependent effects: BTC enables β-cell commitment and EGF inhibits polarization of epithelial progenitors during the primary transition.

    更新日期:2017-10-25
  • Synthetic hydrogels for human intestinal organoid generation and colonic wound repair
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Ricardo Cruz-Acuña, Miguel Quirós, Attila E. Farkas, Priya H. Dedhia, Sha Huang, Dorothée Siuda, Vicky García-Hernández, Alyssa J. Miller, Jason R. Spence, Asma Nusrat, Andrés J. García

    Synthetic hydrogels for human intestinal organoid generation and colonic wound repair Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3632 Cruz-Acuña et al. develop synthetic hydrogels that support the generation and expansion of viable human intestinal organoids from pluripotent stem cells and can be used as injectable vehicles for organoid engraftment and wound healing.

    更新日期:2017-10-25
  • The impact of cellular metabolism on chromatin dynamics and epigenetics
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Michael A. Reid, Ziwei Dai, Jason W. Locasale

    The impact of cellular metabolism on chromatin dynamics and epigenetics Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3629 Locasale and co-authors discuss the influence of cellular metabolism on the regulation of chromatin and epigenetics.

    更新日期:2017-10-25
  • PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Fabao Liu, Fengfei Ma, Yuyuan Wang, Ling Hao, Hao Zeng, Chenxi Jia, Yidan Wang, Peng Liu, Irene M. Ong, Baobin Li, Guojun Chen, Jiaoyang Jiang, Shaoqin Gong, Lingjun Li, Wei Xu

    PKM2 methylation by CARM1 activates aerobic glycolysis to promote tumorigenesis Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3630 Liu et al. find that PKM2 methylated by CARM1 inhibits Ca2+ influx from endoplasmic reticulum to mitochondria, thus restraining mitochondrial oxidative phosphorylation while promoting aerobic glycolysis and breast cancer growth.

    更新日期:2017-10-25
  • EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Zarah M. Löf-Öhlin, Pia Nyeng, Matthew E. Bechard, Katja Hess, Eric Bankaitis, Thomas U. Greiner, Jacqueline Ameri, Christopher V. Wright, Henrik Semb

    EGFR signalling controls cellular fate and pancreatic organogenesis by regulating apicobasal polarity Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3628 In the developing mouse pancreas, EGFR regulates apical polarity via PI(3)K and Rac1 and elicits different ligand-dependent effects: BTC enables β-cell commitment and EGF inhibits polarization of epithelial progenitors during the primary transition.

    更新日期:2017-10-25
  • Synthetic hydrogels for human intestinal organoid generation and colonic wound repair
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-23
    Ricardo Cruz-Acuña, Miguel Quirós, Attila E. Farkas, Priya H. Dedhia, Sha Huang, Dorothée Siuda, Vicky García-Hernández, Alyssa J. Miller, Jason R. Spence, Asma Nusrat, Andrés J. García

    Synthetic hydrogels for human intestinal organoid generation and colonic wound repair Nature Cell Biology, Published online: 23 October 2017; doi:10.1038/ncb3632 Cruz-Acuña et al. develop synthetic hydrogels that support the generation and expansion of viable human intestinal organoids from pluripotent stem cells and can be used as injectable vehicles for organoid engraftment and wound healing.

    更新日期:2017-10-25
  • Acute myeloid leukaemia disrupts endogenous myelo-erythropoiesis by compromising the adipocyte bone marrow niche
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-16
    Allison L. Boyd, Jennifer C. Reid, Kyle R. Salci, Lili Aslostovar, Yannick D. Benoit, Zoya Shapovalova, Mio Nakanishi, Deanna P. Porras, Mohammed Almakadi, Clinton J. V. Campbell, Michael F. Jackson, Catherine A. Ross, Ronan Foley, Brian Leber, David S. Allan, Mitchell Sabloff, Anargyros Xenocostas, Tony J. Collins, Mickie Bhatia

    Acute myeloid leukaemia disrupts endogenous myelo-erythropoiesis by compromising the adipocyte bone marrow niche Nature Cell Biology, Published online: 16 October 2017; doi:10.1038/ncb3625 Boyd et al. monitored the effects of patient-derived acute myeloid leukaemia (AML) cells on human HSPCs in vivo and found that AML impairs bone marrow adipocyte differentiation, and this in turn impedes healthy endogenous haematopoiesis.

    更新日期:2017-10-25
  • EZH2 promotes degradation of stalled replication forks by recruiting MUS81 through histone H3 trimethylation
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-16
    Beatrice Rondinelli, Ewa Gogola, Hatice Yücel, Alexandra A. Duarte, Marieke van de Ven, Roxanne van der Sluijs, Panagiotis A. Konstantinopoulos, Jos Jonkers, Raphaël Ceccaldi, Sven Rottenberg, Alan D. D’Andrea

    EZH2 promotes degradation of stalled replication forks by recruiting MUS81 through histone H3 trimethylation Nature Cell Biology, Published online: 16 October 2017; doi:10.1038/ncb3626 Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2 contributes to PARPi resistance in BRCA2-deficient tumours.

    更新日期:2017-10-25
  • A non-coding function of TYRP1 mRNA promotes melanoma growth
    Nat. Cell. Biol. (IF 20.06) Pub Date : 2017-10-09
    David Gilot, Mélodie Migault, Laura Bachelot, Fabrice Journé, Aljosja Rogiers, Emmanuelle Donnou-Fournet, Ariane Mogha, Nicolas Mouchet, Marie-Laure Pinel-Marie, Bernard Mari, Tristan Montier, Sébastien Corre, Arthur Gautron, Florian Rambow, Petra El Hajj, Rania Ben Jouira, Sophie Tartare-Deckert, Jean-Christophe Marine, Brice Felden, Ghanem Ghanem, Marie-Dominique Galibert

    A non-coding function of TYRP1 mRNA promotes melanoma growth Nature Cell Biology, Published online: 9 October 2017; doi:10.1038/ncb3623 Gilot et al. have found that TYRP1 mRNA, in addition to coding for TYRP1 protein, can promote melanoma by sequestering the tumour suppressor miR-16, thus de-repressing the mRNA transcription of miR-16 target RAB17, which is involved in melanoma cell proliferation.

    更新日期:2017-10-25
Some contents have been Reproduced with permission of the American Chemical Society.
Some contents have been Reproduced by permission of The Royal Society of Chemistry.
化学 • 材料 期刊列表